Adenomatous Polyposis Coli Protein: A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.Adenomatous Polyposis Coli: A polyposis syndrome due to an autosomal dominant mutation of the APC genes (GENES, APC) on CHROMOSOME 5. The syndrome is characterized by the development of hundreds of ADENOMATOUS POLYPS in the COLON and RECTUM of affected individuals by early adulthood.Genes, APC: Tumor suppressor genes located in the 5q21 region on the long arm of human chromosome 5. The mutation of these genes is associated with familial adenomatous polyposis (ADENOMATOUS POLYPOSIS COLI) and GARDNER SYNDROME, as well as some sporadic colorectal cancers.beta Catenin: A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.Cytoskeletal Proteins: Major constituent of the cytoskeleton found in the cytoplasm of eukaryotic cells. They form a flexible framework for the cell, provide attachment points for organelles and formed bodies, and make communication between parts of the cell possible.Glycogen Synthase Kinase 3: A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.Microtubules: Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein TUBULIN and are influenced by TUBULIN MODULATORS.Intestinal Polyps: Discrete abnormal tissue masses that protrude into the lumen of the INTESTINE. A polyp is attached to the intestinal wall either by a stalk, pedunculus, or by a broad base.Axin Protein: A scaffolding protein that is a critical component of the axin signaling complex which binds to ADENOMATOUS POLYPOSIS COLI PROTEIN; GLYCOGEN SYNTHASE KINASE 3; and CASEIN KINASE I.Adenomatous Polyps: Benign neoplasms derived from glandular epithelium. (From Stedman, 25th ed)Gardner Syndrome: A variant of ADENOMATOUS POLYPOSIS COLI caused by mutation in the APC gene (GENES, APC) on CHROMOSOME 5. It is characterized by not only the presence of multiple colonic polyposis but also extracolonic ADENOMATOUS POLYPS in the UPPER GASTROINTESTINAL TRACT; the EYE; the SKIN; the SKULL; and the FACIAL BONES; as well as malignancy in organs other than the GI tract.Osteoma: A benign tumor composed of bone tissue or a hard tumor of bonelike structure developing on a bone (homoplastic osteoma) or on other structures (heteroplastic osteoma). (From Dorland, 27th ed)alpha Catenin: A catenin that binds F-ACTIN and links the CYTOSKELETON with BETA CATENIN and GAMMA CATENIN.Catenins: A family of cytoskeletal proteins that play essential roles in CELL ADHESION at ADHERENS JUNCTIONS by linking CADHERINS to the ACTIN FILAMENTS of the CYTOSKELETON.Stem Cell Research: Experimentation on STEM CELLS and on the use of stem cells.Neurites: In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell.Cadherins: Calcium-dependent cell adhesion proteins. They are important in the formation of ADHERENS JUNCTIONS between cells. Cadherins are classified by their distinct immunological and tissue specificities, either by letters (E- for epithelial, N- for neural, and P- for placental cadherins) or by numbers (cadherin-12 or N-cadherin 2 for brain-cadherin). Cadherins promote cell adhesion via a homophilic mechanism as in the construction of tissues and of the whole animal body.Cytoskeleton: The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm.Colonic Neoplasms: Tumors or cancer of the COLON.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Colorectal Neoplasms: Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.Centrosome: The cell center, consisting of a pair of CENTRIOLES surrounded by a cloud of amorphous material called the pericentriolar region. During interphase, the centrosome nucleates microtubule outgrowth. The centrosome duplicates and, during mitosis, separates to form the two poles of the mitotic spindle (MITOTIC SPINDLE APPARATUS).Microtubule-Associated Proteins: High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.Tubulin: A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from SPERM FLAGELLUM; CILIA; and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to COLCHICINE; VINCRISTINE; and VINBLASTINE.Spindle Apparatus: A microtubule structure that forms during CELL DIVISION. It consists of two SPINDLE POLES, and sets of MICROTUBULES that may include the astral microtubules, the polar microtubules, and the kinetochore microtubules.Cell Line, Tumor: A cell line derived from cultured tumor cells.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Xenopus laevis: The commonest and widest ranging species of the clawed "frog" (Xenopus) in Africa. This species is used extensively in research. There is now a significant population in California derived from escaped laboratory animals.Xenopus Proteins: Proteins obtained from various species of Xenopus. Included here are proteins from the African clawed frog (XENOPUS LAEVIS). Many of these proteins have been the subject of scientific investigations in the area of MORPHOGENESIS and development.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Xenopus: An aquatic genus of the family, Pipidae, occurring in Africa and distinguished by having black horny claws on three inner hind toes.Cytosol: Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.Databases, Protein: Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.Mycelium: The body of a fungus which is made up of HYPHAE.Proteins: Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.Sequence Analysis, Protein: A process that includes the determination of AMINO ACID SEQUENCE of a protein (or peptide, oligopeptide or peptide fragment) and the information analysis of the sequence.EuropeModels, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Wnt Proteins: Wnt proteins are a large family of secreted glycoproteins that play essential roles in EMBRYONIC AND FETAL DEVELOPMENT, and tissue maintenance. They bind to FRIZZLED RECEPTORS and act as PARACRINE PROTEIN FACTORS to initiate a variety of SIGNAL TRANSDUCTION PATHWAYS. The canonical Wnt signaling pathway stabilizes the transcriptional coactivator BETA CATENIN.Wnt Signaling Pathway: A complex signaling pathway whose name is derived from the DROSOPHILA Wg gene, which when mutated results in the wingless phenotype, and the vertebrate INT gene, which is located near integration sites of MOUSE MAMMARY TUMOR VIRUS. The signaling pathway is initiated by the binding of WNT PROTEINS to cells surface WNT RECEPTORS which interact with the AXIN SIGNALING COMPLEX and an array of second messengers that influence the actions of BETA CATENIN.Wnt3A Protein: A Wnt protein subtype that plays a role in cell-cell signaling during EMBRYONIC DEVELOPMENT and the morphogenesis of the developing NEURAL TUBE.Wnt3 Protein: A Wnt protein subtype that plays a role in cell-cell signaling during EMBRYONIC DEVELOPMENT and the morphogenesis of the developing NEURAL TUBE. Defects in Wnt3 protein are associated with autosomal recessive tetra-AMELIA in humans.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Wnt1 Protein: A proto-oncogene protein and member of the Wnt family of proteins. It is expressed in the caudal MIDBRAIN and is essential for proper development of the entire mid-/hindbrain region.Replication Protein A: A single-stranded DNA-binding protein that is found in EUKARYOTIC CELLS. It is required for DNA REPLICATION; DNA REPAIR; and GENETIC RECOMBINATION.DNA Damage: Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.DNA Repair: The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.DNA Replication: The process by which a DNA molecule is duplicated.DNA-Binding Proteins: Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.Mitosis: A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.DNA, Single-Stranded: A single chain of deoxyribonucleotides that occurs in some bacteria and viruses. It usually exists as a covalently closed circle.Cell Cycle Proteins: Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.Recombination, Genetic: Production of new arrangements of DNA by various mechanisms such as assortment and segregation, CROSSING OVER; GENE CONVERSION; GENETIC TRANSFORMATION; GENETIC CONJUGATION; GENETIC TRANSDUCTION; or mixed infection of viruses.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
(1/711) Axin prevents Wnt-3a-induced accumulation of beta-catenin.

When Axin, a negative regulator of the Wnt signaling pathway, was expressed in COS cells, it coeluted with glycogen synthase kinase-3beta (GSK-3beta), beta-catenin, and adenomatous polyposis coli protein (APC) in a high molecular weight fraction on gel filtration column chromatography. In this fraction, GSK-3beta, beta-catenin, and APC were co-precipitated with Axin. Although beta-catenin was detected in the high molecular weight fraction in L cells on gel filtration column chromatography, addition of conditioned medium expressing Wnt-3a to the cells increased beta-catenin in the low molecular weight fraction. However, Wnt-3a-dependent accumulation of beta-catenin was greatly inhibited in L cells stably expressing Axin. Axin also suppressed Wnt-3a-dependent activation of Tcf-4 which binds to beta-catenin and acts as a transcription factor. These results suggest that Axin forms a complex with GSK-3beta, beta-catenin, and APC, resulting in the stimulation of the degradation of beta-catenin and that Wnt-3a induces the dissociation of beta-catenin from the Axin complex and accumulates beta-catenin.  (+info)

(2/711) EB1, a protein which interacts with the APC tumour suppressor, is associated with the microtubule cytoskeleton throughout the cell cycle.

The characteristics of the adenomatous polyposis coli (APC) associated protein EB1 were examined in mammalian cells. By immunocytochemistry EB1 was shown to be closely associated with the microtubule cytoskeleton throughout the cell cycle. In interphase cells EB1 was associated with microtubules along their full length but was often particularly concentrated at their tips. During early mitosis, EB1 was localized to separating centrosomes and associated microtubules, while at metaphase it was associated with the spindle poles and associated microtubules. During cytokinesis EB1 was strongly associated with the midbody microtubules. Treatment with nocodazole caused a diffuse redistribution of EB1 immunoreactivity, whereas treatment with cytochalasin D had no effect. Interestingly, treatment with taxol abolished the EB1 association with microtubules. In nocodazole washout experiments EB1 rapidly became associated with the centrosome and repolymerizing microtubules. In taxol wash-out experiments EB1 rapidly re-associated with the microtubule cytoskeleton, resembling untreated control cells within 10 min. Immunostaining of SW480 cells, which contain truncated APC incapable of interaction with EB1, showed that the association of EB1 with microtubules throughout the cell cycle was not dependent upon an interaction with APC. These results suggest a role for EB1 in the control of microtubule dynamics in mammalian cells.  (+info)

(3/711) Analysis of masked mutations in familial adenomatous polyposis.

Familial adenomatous polyposis (FAP) is an autosomal-dominant disease characterized by the development of hundreds of adenomatous polyps of the colorectum. Approximately 80% of FAP patients can be shown to have truncating mutations of the APC gene. To determine the cause of FAP in the other 20% of patients, MAMA (monoallelic mutation analysis) was used to independently examine the status of each of the two APC alleles. Seven of nine patients analyzed were found to have significantly reduced expression from one of their two alleles whereas two patients were found to have full-length expression from both alleles. We conclude that more than 95% of patients with FAP have inactivating mutations in APC and that a combination of MAMA and standard genetic tests will identify APC abnormalities in the vast majority of such patients. That no APC expression from the mutant allele is found in some FAP patients argues strongly against the requirement for dominant negative effects of APC mutations. The results also suggest that there may be at least one additional gene, besides APC, that can give rise to FAP.  (+info)

(4/711) Administration of an unconjugated bile acid increases duodenal tumors in a murine model of familial adenomatous polyposis.

Intestinal carcinogenesis involves the successive accumulation of multiple genetic defects until cellular transformation to an invasive phenotype occurs. This process is modulated by many epigenetic factors. Unconjugated bile acids are tumor promoters whose presence in intestinal tissues is regulated by dietary factors. We studied the role of the unconjugated bile acid, chenodeoxycholate, in an animal model of familial adenomatous polyposis. Mice susceptible to intestinal tumors as a result of a germline mutation in Apc (Min/+ mice) were given a 10 week dietary treatment with 0.5% chenodeoxycholate. Following this, the mice were examined to determine tumor number, enterocyte proliferation, apoptosis and beta-catenin expression. Intestinal tissue prostaglandin E2 (PGE2) levels were also assessed. Administration of chenodeoxycholate in the diet increased duodenal tumor number in Min/+ mice. Promotion of duodenal tumor formation was accompanied by increased beta-catenin expression in duodenal cells, as well as increased PGE2 in duodenal tissue. These data suggest that unconjugated bile acids contribute to periampullary tumor formation in the setting of an Apc mutation.  (+info)

(5/711) Negative regulation of Wingless signaling by D-axin, a Drosophila homolog of axin.

Wnt/Wingless directs many cell fates during development. Wnt/Wingless signaling increases the amount of beta-catenin/Armadillo, which in turn activates gene transcription. Here the Drosophila protein D-Axin was shown to interact with Armadillo and D-APC. Mutation of d-axin resulted in the accumulation of cytoplasmic Armadillo and one of the Wingless target gene products, Distal-less. Ectopic expression of d-axin inhibited Wingless signaling. Hence, D-Axin negatively regulates Wingless signaling by down-regulating the level of Armadillo. These results establish the importance of the Axin family of proteins in Wnt/Wingless signaling in Drosophila.  (+info)

(6/711) Hereditary desmoid disease in a family with a germline Alu I repeat mutation of the APC gene.

Two families with autosomal dominantly inherited desmoid tumors have recently been shown to have germline mutations at the 3' end of the APC gene. We subsequently identified an Amish family with autosomal dominantly inherited desmoid tumors. Genetic analysis performed on one family member, a 47-year-old man with multiple desmoid tumors and no colon polyps, revealed a protein truncating mutation in the middle of the APC gene. The truncating mutation is the result of a 337-bp insertion of an Alu I sequence into codon 1526 of the APC gene. The presence of a poly(A) tail at the 3' end of the insertion suggests that the Alu I sequence was inserted by a retrotranspositional event. Germline insertions of Alu I sequences have occasionally been reported to cause other genetic diseases including type I neurofibromatosis, hereditary site-specific breast cancer (BRCA2), and hemophilia B. However, this is the first report of a germline mutation of the APC gene resulting from an Alu I insertion.  (+info)

(7/711) E-cadherin binding prevents beta-catenin nuclear localization and beta-catenin/LEF-1-mediated transactivation.

Beta-catenin is a multifunctional protein found in three cell compartments: the plasma membrane, the cytoplasm and the nucleus. The cell has developed elaborate ways of regulating the level and localization of beta-catenin to assure its specific function in each compartment. One aspect of this regulation is inherent in the structural organization of beta-catenin itself; most of its protein-interacting motifs overlap so that interaction with one partner can block binding of another at the same time. Using recombinant proteins, we found that E-cadherin and lymphocyte-enhancer factor-1 (LEF-1) form mutually exclusive complexes with beta-catenin; the association of beta-catenin with LEF-1 was competed out by the E-cadherin cytoplasmic domain. Similarly, LEF-1 and adenomatous polyposis coli (APC) formed separate, mutually exclusive complexes with beta-catenin. In Wnt-1-transfected C57MG cells, free beta-catenin accumulated and was able to associate with LEF-1. The absence of E-cadherin in E-cadherin-/- embryonic stem (ES) cells also led to an accumulation of free beta-catenin and its association with LEF-1, thereby mimicking Wnt signaling. beta-catenin/LEF-1-mediated transactivation in these cells was antagonized by transient expression of wild-type E-cadherin, but not of E-cadherin lacking the beta-catenin binding site. The potent ability of E-cadherin to recruit beta-catenin to the cell membrane and prevent its nuclear localization and transactivation was also demonstrated using SW480 colon carcinoma cells.  (+info)

(8/711) Regulation of beta-catenin signaling by the B56 subunit of protein phosphatase 2A.

Dysregulation of Wnt-beta-catenin signaling disrupts axis formation in vertebrate embryos and underlies multiple human malignancies. The adenomatous polyposis coli (APC) protein, axin, and glycogen synthase kinase 3beta form a Wnt-regulated signaling complex that mediates the phosphorylation-dependent degradation of beta-catenin. A protein phosphatase 2A (PP2A) regulatory subunit, B56, interacted with APC in the yeast two-hybrid system. Expression of B56 reduced the abundance of beta-catenin and inhibited transcription of beta-catenin target genes in mammalian cells and Xenopus embryo explants. The B56-dependent decrease in beta-catenin was blocked by oncogenic mutations in beta-catenin or APC, and by proteasome inhibitors. B56 may direct PP2A to dephosphorylate specific components of the APC-dependent signaling complex and thereby inhibit Wnt signaling.  (+info)

*  Adenomatous polyposis coli
... (APC) also known as deleted in polyposis 2.5 (DP2.5) is a protein that in humans is encoded by the ... on APC-Associated Polyposis Conditions OMIM entries on APC-Associated Polyposis Conditions Adenomatous Polyposis Coli Protein ... The (Adenomatous Polyposis Coli) APC protein normally builds a "destruction complex" with glycogen synthase kinase 3-alpha and ... Zumbrunn J, Kinoshita K, Hyman AA, Näthke IS (January 2001). "Binding of the adenomatous polyposis coli protein to microtubules ...
*  Catenin alpha-1
"The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... "The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... Oneyama C, Nakano H, Sharma SV (March 2002). "UCS15A, a novel small molecule, SH3 domain-mediated protein-protein interaction ... "Entrez Gene: CTNNA1 catenin (cadherin-associated protein), alpha 1, 102kDa". "Protein sequence of human CTNNA1 (Uniprot ID: ...
*  BUB1B
Kaplan KB, Burds AA, Swedlow JR, Bekir SS, Sorger PK, Näthke IS (2001). "A role for the Adenomatous Polyposis Coli protein in ... The protein has been localized to the kinetochore and plays a role in the inhibition of the anaphase-promoting complex/ ... Mitotic checkpoint serine/threonine-protein kinase BUB1 beta is an enzyme that in humans is encoded by the BUB1B gene. This ... Tang Z, Bharadwaj R, Li B, Yu H (2001). "Mad2-Independent inhibition of APCCdc20 by the mitotic checkpoint protein BubR1". Dev ...
*  BUB3
2001). "A role for the Adenomatous Polyposis Coli protein in chromosome segregation". Nat. Cell Biol. 3 (4): 429-32. doi: ... Mitotic checkpoint protein BUB3 is a protein that in humans is encoded by the BUB3 gene. Bub3 is a protein involved with the ... cancer adenomatous polyposis osteosarcoma familial breast cancer glioblastoma cervicitis lung cancer carcinoma Coli polyposis ... The complex of proteins which regulate the cell arrest are BUB1, BUB2, BUB3 (this protein), Mad1, Mad2, Mad3 and MPS1. At ...
*  Beta-catenin
Through its N-terminal regulator of G-protein signaling (RGS) domain, it recruits the adenomatous polyposis coli (APC) protein ... and in particular by the adenomatous polyposis coli (APC) protein, encoded by the tumour-suppressing APC gene. Therefore, ... its partner the Adenomatous Polyposis Coli (APC) protein contains 11 such motifs in tandem arrangement per protomer, thus ... "Association and regulation of casein kinase 2 activity by adenomatous polyposis coli protein". Proceedings of the National ...
*  Casein kinase 2, alpha 1
"Association and regulation of casein kinase 2 activity by adenomatous polyposis coli protein". Proc. Natl. Acad. Sci. U.S.A. 99 ... Casein kinase II is a serine/threonine protein kinase that phosphorylates acidic proteins such as casein. The kinase exists as ... Kim MS, Lee YT, Kim JM, Cha JY, Bae YS (February 1998). "Characterization of protein interaction among subunits of protein ... Allende JE, Allende CC (1995). "Protein kinases. 4. Protein kinase CK2: an enzyme with multiple substrates and a puzzling ...
*  DVL1
Rubinfeld B, Tice DA, Polakis P (2001). "Axin-dependent phosphorylation of the adenomatous polyposis coli protein mediated by ... Segment polarity protein dishevelled homolog DVL-1 is a protein that in humans is encoded by the DVL1 gene. DVL1, the human ... Fagotto F, Jho Eh, Zeng L, Kurth T, Joos T, Kaufmann C, Costantini F (1999). "Domains of axin involved in protein-protein ... Kishida S, Yamamoto H, Hino S, Ikeda S, Kishida M, Kikuchi A (1999). "DIX domains of Dvl and axin are necessary for protein ...
*  AXIN1
Many other large IDPs are affected by missense mutations, such as BRCA1, Adenomatous polyposis coli(APC), CREB-binding protein ... Rubinfeld B, Tice DA, Polakis P (2001). "Axin-dependent phosphorylation of the adenomatous polyposis coli protein mediated by ... The encoded protein interacts with adenomatosis polyposis coli, catenin (cadherin-associated protein) beta 1, glycogen synthase ... "GSK-3beta-dependent phosphorylation of adenomatous polyposis coli gene product can be modulated by beta-catenin and protein ...
*  CSNK2B
"Association and regulation of casein kinase 2 activity by adenomatous polyposis coli protein". Proc. Natl. Acad. Sci. U.S.A. ... "Characterization of protein interaction among subunits of protein kinase CKII in vivo and in vitro". Mol. Cells. KOREA. 8 (1): ... "Mapping of the interaction domain of the protein kinase CKII beta subunit with target proteins". Mol. Cells. Korea (South). 12 ... a novel pleckstrin homology domain-containing protein that interacts with protein kinase CK2". J. Biol. Chem. UNITED STATES. ...
*  SIAH1
"Siah-1 mediates a novel beta-catenin degradation pathway linking p53 to the adenomatous polyposis coli protein". Molecular Cell ... The protein is an E3 ligase and is involved in ubiquitination and proteasome-mediated degradation of specific proteins. The ... October 2005). "Towards a proteome-scale map of the human protein-protein interaction network". Nature. 437 (7062): 1173-8. doi ... E3 ubiquitin-protein ligase SIAH1 is an enzyme that in humans is encoded by the SIAH1 gene. This gene encodes for a polypeptide ...
*  TUBA4A
Zumbrunn J, Kinoshita K, Hyman AA, Näthke IS (Jan 2001). "Binding of the adenomatous polyposis coli protein to microtubules ... Tubulin alpha-4A chain is a protein that in humans is encoded by the TUBA4A gene. Microtubules of the eukaryotic cytoskeleton ... Kirsch J, Langosch D, Prior P, Littauer UZ, Schmitt B, Betz H (Nov 1991). "The 93-kDa glycine receptor-associated protein binds ... Huby RD, Carlile GW, Ley SC (Dec 1995). "Interactions between the protein-tyrosine kinase ZAP-70, the proto-oncoprotein Vav, ...
*  Plakoglobin
... and scaffold proteins adenomatous polyposis coli (APC) and axin targets plakoglobin for degradation.[31-33]. The phosphorylated ... "The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... "The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... Swope D, Cheng L, Gao E, Li J, Radice GL (Mar 2012). "Loss of cadherin-binding proteins β-catenin and plakoglobin in the heart ...
*  PPP2R5A
"ARM domain-dependent nuclear import of adenomatous polyposis coli protein is stimulated by the B56 alpha subunit of protein ... "Direct activation of protein phosphatase-2A0 by HIV-1 encoded protein complex NCp7:vpr". FEBS Letters. 401 (2-3): 197-201. doi: ... "The B56alpha regulatory subunit of protein phosphatase 2A is a target for regulation by double-stranded RNA-dependent protein ... Protein phosphatase 2A is one of the four major Ser/Thr phosphatases, and it is implicated in the negative control of cell ...
*  CTNND1
"The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... "The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... Catenin delta-1 is a protein that in humans is encoded by the CTNND1 gene. This gene encodes a member of the Armadillo protein ... The complete sequences of 100 new cDNA clones from brain which can code for large proteins in vitro". DNA Res. 4 (2): 141-50. ...
*  CDH1 (gene)
"The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha- ... Complete loss of E-cadherin protein expression in 84% of lobular breast carcinomas. Several proteins such as SNAI1/SNAIL, ... Oneyama C, Nakano H, Sharma SV (March 2002). "UCS15A, a novel small molecule, SH3 domain-mediated protein-protein interaction ... CDH1 protein, human at the US National Library of Medicine Medical Subject Headings (MeSH) GeneReviews/NCBI/NIH/UW entry on ...
*  Microtubule
This later activity is mediated by formins, the adenomatous polyposis coli protein, and EB1, a protein that tracks along the ... There are many proteins that bind to microtubules, including the motor proteins kinesin and dynein, severing proteins like ... MAP-1 proteins consists of a set of three different proteins: A, B and C. The C protein plays an important role in the ... Plus end tracking proteins are MAP proteins which bind to the tips of growing microtubules and play an important role in ...
*  MAPRE2
The protein encoded by this gene shares significant homology to the adenomatous polyposis coli (APC) protein-binding EB1 gene ... "The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules". Proc. Natl. Acad. ... a new member of the adenomatous polyposis coli-binding EB1-like gene family, is differentially expressed in activated T cells ... Microtubule-associated protein RP/EB family member 2 is a protein that in humans is encoded by the MAPRE2 gene. ...
*  PTPN13
2000). "The Adenomatous Polyposis Coli-protein (APC) interacts with the protein tyrosine phosphatase PTP-BL via an ... 2000). "The zyxin-related protein TRIP6 interacts with PDZ motifs in the adaptor protein RIL and the protein tyrosine ... The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. PTPs are known to be signaling ... 1997). "A novel GTPase-activating protein for Rho interacts with a PDZ domain of the protein-tyrosine phosphatase PTPL1". J. ...
*  MAPRE1
The protein encoded by this gene was first identified by its binding to the APC (Adenomatous polyposis coli) protein which is ... "The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules". Proc. Natl. Acad. ... Microtubule-associated protein RP/EB family member 1 is a protein that in humans is encoded by the MAPRE1 gene. ... This protein localizes to microtubules, especially the growing ends, in interphase cells. During mitosis, the protein is ...
*  Ran (gene)
... of the tumor suppressor protein adenomatous polyposis coli (APC). Its structure and its interaction with chromosome maintenance ... Ran (RAs-related Nuclear protein) also known as GTP-binding nuclear protein Ran is a protein that in humans is encoded by the ... Ran is a small G protein that is essential for the translocation of RNA and proteins through the nuclear pore complex. The Ran ... "Molecular interactions between the importin alpha/beta heterodimer and proteins involved in vertebrate nuclear protein import ...
*  XPO1
... of the tumor suppressor protein adenomatous polyposis coli (APC). Its structure and its interaction with chromosome maintenance ... a protein involved in nuclear export of proteins". J Biol Chem. 272 (47): 29742-51. doi:10.1074/jbc.272.47.29742. PMID 9368044 ... is an eukaryotic protein that mediates the nuclear export of proteins, rRNA, snRNA, and some mRNA. XPO1 (CRM1) originally was ... "Ran-binding protein 3 is a cofactor for Crm1-mediated nuclear protein export". J. Cell Biol. 153 (7): 1391-402. doi:10.1083/jcb ...
*  Akt/PKB signaling pathway
Akt phosphorylates GSK3 beta, indirectly activating microtubule binding protein adenomatous polyposis coli (APC). Endothelial ... Key proteins involved are PI3K (phosphatidylinositol 3-kinase) and Akt (Protein Kinase B). Initial stimulation by one of the ... PI3K can also be activated by G protein-coupled receptors (GPCR), via G-protein βγ dimers or Ras which bind PI3K directly. In ... Another protein important in Akt attenuation is Carboxy Terminal Modulator Protein (CTMP). CTMP binds to the regulatory domain ...
*  MiR-27
... has been found to target and inhibit gene expression of the adenomatous polyposis coli (APC) protein, enabling it to ... FOXO1 protein expression is down-regulated in breast tumour tissue samples; miR-27a has been identified as one of three miRNAS ... There is activation of Wnt signalling through nuclear accumulation of this protein, which is in response to inhibition of the ... Suppression of miR-27a results in a FOXO1 protein increase and a consequent cell number decrease. Landgraf, P; Rusu, M; ...
*  DHRS9
2004). "The tumor suppressor adenomatous polyposis coli and caudal related homeodomain protein regulate expression of retinol ... 2003). "The secreted protein discovery initiative (SPDI), a large-scale effort to identify novel human secreted and ... transmembrane proteins: a bioinformatics assessment". Genome Res. 13 (10): 2265-70. doi:10.1101/gr.1293003. PMC 403697 . PMID ...
*  Astral microtubules
It is also dependent on several microtubule-associated proteins such as EB1 and adenomatous polyposis coli (APC). Mitosis, ...
*  PSMD7
Moreover, the UPS regulates the degradation of tumor suppressor gene products such as adenomatous polyposis coli (APC) in ... To recognize protein as designated substrate, 19S complex has subunits that are capable to recognize proteins with a special ... Accordingly, misfolded proteins and damaged protein need to be continuously removed to recycle amino acids for new synthesis; ... The 19S regulatory particles can recognize ubiquitin-labeled protein as degradation substrate, unfold the protein to linear, ...
Adenomatous Polyposis Coli Protein: A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.
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Our findings implicate the APC tumor suppressor gene in the process of axial patterning in Xenopus. Since induction of the dorsoanterior axis involves the activities of embryonic signaling centers (or organizers), these findings demonstrate that APC has signal transduction activity. APC seems to act in the same signaling pathway as β-catenin. They have similar characteristics, including induction of the homeobox protein Siamois. Furthermore, APC signaling is strongly dependent on the availability of a free cytosolic pool of β-catenin, which by itself has axis-inducing activity. Moreover, APC or APC/β-catenin complexes seem to have direct positive signaling activity, since APC does not act indirectly simply by binding up β-catenin or by changing the levels of β-catenin. We propose, therefore, that axis induction by APC is due to its role in a signal transduction process in which β-catenin has been strongly implicated.. The induction of a dorsoanterior axis in Xenopus results from localized ...
A unique feature of colon cancer is that truncation mutations in the APC (adenomatous polyposis coli) gene are common to most tumours. The high penetrance of APC mutations, especially in gut epithelium, supports the idea that APC may be involved in a number of the processes that govern the normal maintenance of this tissue: differentiation, migration, proliferation and apoptosis. Indeed, APC is involved in the regulation of β-catenin and it also is an important regulator of the cytoskeleton. Thus mutations in APC lead to the accumulation of β-catenin, which causes changes in differentiation, and they also produce changes in cytoskeletal organization, which results in altered cell migration and disrupted mitotic spindles. The function of APC in cytoskeletal organization is related to its effect on microtubules and F-actin. Depleting APC from cultured cells leads to changes in cytoskeletal organization. In addition, N-terminal fragments of APC, like those commonly found in tumours, compromise ...
We show that expression of stabilized β-catenin decreased neurite initiation and elongation in NGF-treated PC12 cells (Fig. 5). Several mechanisms could explain how stabilized β-catenin inhibits neurite outgrowth in PC12 cells. When β-catenin is stabilized by Wnt signals it can promote cadherin-mediated cell-cell adhesion (Hinck et al., 1994) in addition to Tcf/Lef-mediated transcription. Experiments expressing stabilized β-catenin in whole animals or in neuronal cultures directly contacting glial cells may mask the role of β-catenin in the APC complex with its role in adhesion (Yu and Malenka, 2004; Loureiro et al., 2001; Elul et al., 2003). Previous work on the role of β-catenin in branching of axons and dendrites uses neurons in direct cell-cell contact with a glial feeder layer, and β-catenin is thought to require N-cadherin for this effect (Yu and Malenka, 2003; Yu and Malenka, 2004). PC12 cells do not form distinct axons and dendrites (Greene et al., 1998) and, if treated with NGF ...
Amer1/WTX binds to the tumor suppressor adenomatous polyposis coli and acts as an inhibitor of Wnt signaling by inducing β-catenin degradation. We show here that Amer1 directly interacts with the armadillo repeats of β-catenin via a domain consisting of repeated arginine-glutamic acid-alanine (REA) motifs, and that Amer1 assembles the β-catenin destruction complex at the plasma membrane by recruiting β-catenin, adenomatous polyposis coli, and Axin/Conductin. Deletion or specific mutations of the membrane binding domain of Amer1 abolish its membrane localization and abrogate negative control of Wnt signaling, which can be restored by artificial targeting of Amer1 to the plasma membrane. In line, a natural splice variant of Amer1 lacking the plasma membrane localization domain is deficient for Wnt inhibition. Knockdown of Amer1 leads to the activation of Wnt target genes, preferentially in dense compared with sparse cell cultures, suggesting that Amer1 function is regulated by cell contacts. ...
Adenomatous polyposis coli protein (APC) is a ubiquitous multidomain protein that has a well documented role as a tumor suppressor. The mechanism of APC-mediated tumor suppression is still an area of active investigation; however, several studies suggest that APC is a negative regulator of the Wnt signaling pathway as it downregulates beta-catenin via interactions with Axin/GSK3-beta complex, thereby preventing transcription of genes such as MYC that contribute to cell proliferation. Defective APC proteins contribute to the initiation and proliferation of various types of cancers, including familial adenomatous polyposis. However, other studies have shown that APC interacts with a range of other proteins such as the EB1 microtubule-binding proteins, to regulate other processes such as cell migration ...
In the present study, our comprehensive behavioral test battery revealed that Apc1638T/1638T mice shows impaired learning and memory, increased locomotor activity, mildly increased depression-like behavior, reduced anxiety-like behavior and mildly decreased social interaction behavior. In the hippocampal CA1 region of Apc1638T/1638T mice, the dendritic spine density and size are reduced, the PSD was smaller, and LTP was impaired. Taken together, our findings provide the first direct evidence of neuropsychological roles for the C-terminus of Apc tumor suppressor.. Apc1638T/1638T mice showed hyperactivity, impaired memory, increased depression-like behavior, and decreased social interaction. These behavioral characteristics are often linked to symptoms of schizophrenia (see Supplementary Table 11 in [15]) and observed in many animal models of schizophrenia [15-19]. In particular, Apc1638T/1638T mice showed a marked deficit in the performance of the working memory task. Impaired working memory is ...
3.0.CO;2-R. PMID 8806074. Sheikh F, Chen Y, Chen Y, Liang X, Hirschy A, Stenbit AE, Gu Y, Dalton ND, Yajima T, Lu Y, Knowlton KU, Peterson KL, Perriard JC, Chen J (Sep 2006). "alpha-E-catenin inactivation disrupts the cardiomyocyte adherens junction, resulting in cardiomyopathy and susceptibility to wall rupture". Circulation. 114 (10): 1046-55. doi:10.1161/CIRCULATIONAHA.106.634469. PMID 16923756. Su LK, Vogelstein B, Kinzler KW (December 1993). "Association of the APC tumor suppressor protein with catenins". Science. 262 (5140): 1734-7. doi:10.1126/science.8259519. PMID 8259519. Daniel JM, Reynolds AB (September 1995). "The tyrosine kinase substrate p120cas binds directly to E-cadherin but not to the adenomatous polyposis coli protein or alpha-catenin". Mol. Cell. Biol. 15 (9): 4819-24. doi:10.1128/mcb.15.9.4819. PMC 230726 . PMID 7651399. Oyama T, Kanai Y, Ochiai A, Akimoto S, Oda T, Yanagihara K, Nagafuchi A, Tsukita S, Shibamoto S, Ito F (December 1994). "A truncated beta-catenin disrupts ...
Truncating mutations in adenomatous polyposis coli (Apc) are strongly linked to colorectal cancers. APC is a negative regulator of the Wnt pathway and constitutive Wnt activation mediated by enhanced Wnt-β-catenin target gene activation is believed to be the predominant mechanism responsible for Apc mutant phenotypes. However, recent evidence suggests that additional downstream effectors contribute to Apc mutant phenotypes. We previously identified a mechanism in cultured human cells by which APC, acting through glycogen synthase kinase-3 (GSK-3), suppresses mTORC1, a nutrient sensor that regulates cell growth and proliferation. We hypothesized that truncating Apc mutations should activate mTORC1 in vivo and that mTORC1 plays an important role in Apc mutant phenotypes. We find mTORC1 is strongly activated in apc mutant zebrafish and in intestinal polyps in Apc mutant mice. Furthermore, mTORC1 activation is essential downstream of APC as mTORC1 inhibition partially rescues Apc mutant phenotypes ...
The adenomatous polyposis coli (Apc) gene is mutated in familial adenomatous polyposis and in sporadic colorectal tumors. The Apc gene product (APC), basically a cytoplasmic protein, blocks cell cycle
AbstractPURPOSE:The aim of this study is to show that the diagnosis of attenuated adenomatous polyposis coli must be made with caution and certainly only after adequate colonic examination with dye-spray.METHODS:Four patients thought to have attenuated adenomatous polyposis coli on the basis of fami
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Familial adenomatous polyposis (FAP) is an autosomal dominant condition characterized by the development of hundreds to thousands of colorectal adenomatous polyps. In addition to the classic form, there is also attenuated polyposis (attenuated adenomatous polyposis coli; AAPC), which is characterized by a milder phenotype. FAP/AAPC is caused by germline mutations in the adenomatous polyposis coli (APC) gene. Very recently, germline mutations in the base-excision repair gene MYH have been associated with recessive inheritance of multiple colorectal adenomas in a subset of patients. APC pathogenic alterations are mostly (,95%) represented by frameshift or nonsense mutations leading to the synthesis of a truncated protein. We identified 20 APC truncating mutation carriers out of 30 FAP/AAPC patients from different Italian kindreds. In the remaining 10 patients, we searched for alterations other than truncating mutations by enzymatic mutation detection, real-time quantitative RT-PCR, and genotyping ...
Aberrant methylation of the adenomatous polyposis coli (APC) gene promoter occurs in about 40% of breast tumours and has been correlated with reduced APC protein levels. To what extent epigenetic alterations of the APC gene may differ according to specific breast cancer phenotypes, remains to be elucidated. Our aim was to explore the role of APC methylation in the inflammatory breast cancer (IBC) phenotype. The status of APC gene promoter hypermethylation was investigated in DNA from normal breast tissues, IBC and non-IBC by both conventional and real-time quantitative methylation-specific PCR (MSP). APC methylation levels were compared with APC mRNA and protein levels. Hypermethylation of the APC gene promoter was present in 71% of IBC samples (n=21) and 43% of non-IBC samples (n=30) by conventional MSP (P=0.047). The APC gene also showed an increased frequency of high methylation levels in IBC (in 74% of cases, n=19) vs non-IBC (in 46% of cases, n=35) using a qMSP assay (P=0.048). We observed ...
BACKGROUND: Familial adenomatous polyposis (FAP) is caused by germline mutation of the adenomatous polyposis coli (APC) gene on chromosome 5q. AIMS: This study assessed genotype-phenotype correlations for extraintestinal lesions in FAP. METHODS: Mutations of the APC gene were compared with the occurrence of seven extraintestinal manifestations in 475 FAP patients from 51 families. The frequency of manifestations was adjusted for different ages of patients using person years of exposure. In pedigrees without identified APC gene mutation, analysis of linkage to chromosome 5q and/or assessment of neoplasms for replication errors characteristic of mutation in mismatch repair genes were performed. RESULTS: FAP patients from the 42 families (82%) with identified mutations of the APC gene had more frequent expression of extraintestinal manifestations than affected individuals without identified mutations (risk ratio 1.2-4.0; significant difference for cutaneous cysts). The presence of a cutaneous cyst ...
What is familial adenomatous polyposis fap? Learn about familial adenomatous polyposis fap symptoms, familial adenomatous polyposis fap causes, diagnosis, and...
Compare & find the top performing anti-Rat (Rattus) Adenomatous Polyposis Coli antibody for Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)).
Regulation and Functions of Localized RNAs. It is becoming increasingly appreciated that, virtually in all polarized mammalian cells, a large number of mRNAs do not exist diffusely in the cytoplasm, but undergo specific subcellular targeting and local control of their translation. Such localized RNAs are important for various processes such as migration, epithelial cell polarity, mitotic spindle assembly and neuronal function. Defects in RNA localization are implicated in diseases such as mental retardation and cancer metastasis. Our lab aims to understand the mechanisms and regulation of RNA localization in mammalian cells, the effect of localized translation on protein function, and the contribution of these processes to disease.. A. The APC-dependent RNA localization pathway. We have identified an RNA localization pathway that targets numerous mRNAs to cellular protrusions (Mili et al, Nature 2008). A central component of this pathway is the tumor suppressor protein adenomatous polyposis coli ...
Familial adenomatous polyposis (FAP) is a well-described inherited syndrome, which is responsible for ,1% of all colorectal cancer (CRC) cases. The syndrome is characterized by the development of hundreds to thousands of adenomas in the colorectum. Almost all patients will develop CRC if they are not identified and treated at an early stage. The syndrome is inherited as an autosomal dominant trait and caused by mutations in the APC-gene. Recently a second familial adenomatous polyposis gene has been identified, the so-called MUTYH-gene, which has an autosomal recessive pattern of inheritance. In April 2006 and February 2007, a workshop was organized in Mallorca by European experts on Hereditary Gastrointestinal Cancer aiming to establish guidelines for the clinical management of FAP and to initiate collaborative studies. Twenty-eight experts from nine European countries participated in these workshops. Prior to the meeting, various participants examined the most important management issues ...
RATIONALE: Exisulind may be effective in preventing the development and growth of polyps in patients who have familial adenomatous polyposis.. PURPOSE: Randomized phase II/III trial to determine the effectiveness of exisulind in preventing the development and growth of polyps in patients who have familial adenomatous polyposis. ...
The intestinal epithelium has a remarkable capacity to regenerate after injury and DNA damage. Here, we show that the integrin effector protein Focal Adhesion Kinase (FAK) is dispensable for normal intestinal homeostasis and DNA damage signaling, but is essential for intestinal regeneration following DNA damage. Given Wnt/c-Myc signaling is activated following intestinal regeneration, we investigated the functional importance of FAK following deletion of the Apc tumor suppressor protein within the intestinal epithelium. Following Apc loss, FAK expression increased in a c-Myc-dependent manner. Codeletion of Apc and Fak strongly reduced proliferation normally induced following Apc loss, and this was associated with reduced levels of phospho-Akt and suppression of intestinal tumorigenesis in Apc heterozygous mice. Thus, FAK is required downstream of Wnt Signaling, for Akt/mTOR activation, intestinal regeneration, and tumorigenesis. Importantly, this work suggests that FAK inhibitors may suppress ...
BACKGROUND: The reported proportion of patients with familial adenomatous polyposis who have adrenal lesions varies between 7% and 13% compared with 4% in the general population; the prevalence of adrenal lesions in patients with attenuated familial adenomatous polyposis and MUTYH-associated polyposis is unknown. Data on the clinical relevance and clinical course are limited. OBJECTIVE: We aimed to report on the frequency, characteristics, and progression of adrenal lesions in polyposis patients. DESIGN: This was a historical cohort study. SETTINGS: The study was performed at the Academic Medical Center, Amsterdam. PATIENTS: All of the patients with familial adenomatous polyposis, attenuated familial adenomatous polyposis, and MUTYH-associated polyposis were included. Medical charts and imaging reports were analyzed for data on adrenal lesions. A radiologist reassessed all of the images. Patients had not routinely been screened for adrenal lesions. MAIN OUTCOME MEASURES: The frequency, ...
A small study suggests that serrated adenoma may be a form of familial adenomatous polyposis (FAP) and not a separate type of colorectal cancer.. Three serrated adenomas were found separately in three out of 11 Japanese patients from three families with FAP. Colorectal polyps numbered ,100 in each of the three, and all serrated adenomas were found in the rectum. All three patients with serrated adenomas had mutations in the adenomatous polyposis coli (APC) gene-two proximal to the site of the gene, at codon 161, 332 and the third at the most distal site, codon 1556. Mutations in the other patients were located between codons 554 and 1324.. The rate of occurrence of serrated adenoma in the study was 30 times that in the general population so APC mutation may influence pathogenesis of serrated adenoma. The genetic results are compatible with a recent report describing colonic polyposis of ,100 polyps as attenuated FAP, so serrated adenoma may actually be a phenotype of FAP.. All 11 patients had a ...
... (FAP) is a genetic condition that causes growths of tissue (polyps) to develop in the large intestine (colon) and rectum. If these polyps are not removed, the polyps will become cancerous with time. There are three forms of FAP: classic, attenuated (milder), and autosomal recessive FAP. In the classic form, a person can have thousands of polyps and usually develops colon cancer in their 30s. In attenuated FAP, colon cancer usually does not develop until a person is in their 50s. In autosomal recessive FAP, a person usually develops less than 100 polyps. In addition to polyps and colon cancer, FAP can also cause noncancerous growths in the intestines (desmoid tumors) as well as cancerous and noncancerous growths in other parts of the body, including part of the small intestine (duodenum), stomach, bones, and skin.. Both classic and attenuated FAP are caused by a change (mutation) in the APC gene, while autosomal recessive FAP is caused by mutations in the MUTYH ...
The root cause of FAP is understood to be a genetic mutation-a flaw in the bodys tumour suppressor genes that prevent development of tumours. The flaw allows numerous cells of the intestinal wall to develop into potentially cancerous polyps when they would usually reach the end of their life; inevitably one or more will eventually progress and give rise to cancer (7% risk by age 21, rising to 87% by age 45 and 93% by age 50). The flawed genes do not trigger cancer, but rather, they reduce the bodys ability to protect against the risk of aged cells becoming cancerous. Even with the flawed gene, it may still take time before a cell actually does develop that is cancerous as a result, and the gene may in some cases still partially operate to control tumours, therefore cancer from FAP takes many years to develop and is almost always an adult-onset disease. The second form of FAP, known as attenuated familial adenomatous polyposis has the APC gene functional but slightly impaired. It is therefore ...
ARHGEF4 (Rho guanine nucleotide exchange factor 4), also known as ASEF 1 (adenomatous polyposis coli - stimulated guanine nucleotide exchange factor 1) is an approximately 80 kDa cytoplasmic protein important for growth factor-mediated regulation of cell morphology and migration. Besides N-terminal adenomatous polyposis coli (APC)-binding region (ABR) it contains Dbl homology (DH), Pleckstrin homology (PH) and SH3 domains. The SH3 domain inhibits GEF activity of ARHGEF4 by intramolecular interaction with the DH domain, whereas binding of APC stimulates the GEF activity. Activated ARHGEF4 stimulates the small GTPase Cdc42, which leads to decreased cell-cell adherence and enhanced cell migration ...
Familial adenomatous polyposis - Learn about this inherited condition that increases risk of colon cancer. Highlights care at Mayo Clinic.
Learn more about Familial Adenomatous Polyposis at Medical City Dallas DefinitionCausesRisk FactorsSymptomsDiagnosisTreatmentPreventionrevision ...
Definition of familial adenomatous polyposis. Provided by Stedmans medical dictionary and Drugs.com. Includes medical terms and definitions.
The BJC is owned by Cancer Research UK, a charity dedicated to understanding the causes, prevention and treatment of cancer and to making sure that the best new treatments reach patients in the clinic as quickly as possible. The journal reflects these aims. It was founded more than fifty years ago and, from the start, its far-sighted mission was to encourage communication of the very best cancer research from laboratories and clinics in all countries. The breadth of its coverage, its editorial independence and it consistent high standards, have made BJC one of the worlds premier general cancer journals. Its increasing popularity is reflected by a steadily rising impact factor.
An adenoma is a polyp made up of tissue that looks much like the normal lining of your colon, although it is different in several important ways when it is looked at under the microscope. The growth pattern is only important because it helps determine when you will need your next colonoscopy to make sure you dont develop colon cancer in the future. Cell overgrowth resulting from mutations in the APC gene leads to the adenomatous polyps of the colon colon polyps seen in familial adenomatous polyposis. There are 2 major growth patterns: tubular and villous. In addition to this, a stroboscope (flashing light) may be used to observe the movement of the vocal folds during speech. Adenomas with a villous growth pattern are also more likely to have cancers develop in them. Erratum in: Gastroenterology. Some people have a variant of the disorder, called attenuated familial adenomatous polyposis, in which polyp growth is delayed. Larger adenomas more often have cancers developing in them. The average ...
Hyperplastic polyps of the colon are common benign lesions. They frequently arise at the crest of a mucosal fold where they present as small, sessile polyps usually measuring less than 5 mm in diameter with a smooth convex surface.1 Although traditionally regarded as non-neoplastic, recent evidence has shown hyperplastic polyps to have molecular features of neoplasia.2 Histologically they have a very characteristic appearance of elongated crypts with prominent epithelial infoldings giving a pathognomonic serrated pattern. The majority of hyperplastic polyps occur in the rectosigmoid where they may be single or often multiple; however their numbers rarely exceed 10.1 The occurrence of multiple or large hyperplastic polyps in the large bowel is termed hyperplastic polyposis coli.1 3 4 Hyperplastic polyposis coli is a rare condition characterised by the presence of large multiple hyperplastic polyps, some of which may show dysplasia, an occurrence that is felt to contribute significantly to the ...
EB1 was identified by its ability to interact with APC, a tumor suppressor protein that has been shown to associate with microtubules and promote microtubule assembly in vitro (15). We have examined the subcellular distribution of EB1 by indirect immunofluorescence and confocal microscopy, using mAbs specific for EB1. Our results indicate that EB1 decorates the centrosome and the microtubule cytoskeleton throughout the cell cycle.. Previous studies performed on RKO, a human colorectal cancer cell line, and the mouse fibroblast cell line NIH 3T3 have shown that overexpressed full-length, but not truncated, APC associated to microtubules (11). We analyzed the subcellular distribution of EB1 in SW480, a colon cancer cell line that expresses a carboxyl-terminal deleted form of APC that is unable to interact with either EB1 or microtubules; in these cells EB1 localization to microtubules and the centrosome was preserved (Fig. 1d), demonstrating that the cellular distribution of EB1 does not depend on ...
Because FAP has such an early age of onset, cancer screening often begins in childhood. In addition, genetic testing of children at risk is a special consideration. Usually, genetic tests are not an option for people who are considered minors unless there is some type of medical benefit available to justify testing. FAP is an autosomal dominant cancer genetic syndrome, which means that a child whose parent has the condition has a 50/50 chance of inheriting the familial APC gene mutation. There is equally as likely a chance the child will not inherit the familial APC mutation, which would spare the child from having to undergo annual examinations (for example, sigmoidoscopy or colonoscopy) if he or she was found to be mutation negative. Thus, since genetic testing can have an impact on medical management, genetic testing of children at risk of classic FAP is an option that can be considered.. The APC gene is a tumor suppressor gene, which usually has the job of controlling cell growth and cell ...
A polyposis Syndrome due to an autosomal dominant Mutation of the APC Genes (Genes, APC) on Chromosome 5. The Syndrome is characterized by the development of hundreds of Adenomatous Polyps in the Colon and Rectum of affected individuals by early adulthood. The lifetime Risk of colorectal cancer in these Patients reaches 100 percent by age 60 ...
4370 Maintaining apoptosis in normal colonic epithelial cells involves a regulatory function of wild type adenomatous polyposis coli (APC) protein, while APC mutations lead to disregulation of the apoptotic process. A mechanism proposed in the control of colonic apoptosis by wild type APC is down-regulation of survivin, a member of the inhibitor of apoptosis (IAP) family of proteins which prevents normal apoptosis; consistent with this view survivin is typically over-expressed in human colonic tumors. In this study we tested the hypothesis that aberrant in vivo expression of the survivin gene in intestinal epithelial cells is associated with Apc inactivation; 120-day old Apc Min/+ mice which carry a chemically induced nonsense mutation in Apc codon 450 and their normal (Apc+/+) C57BL/6 littermates were studied. Immunohistochemical and immunoblot assays of survivin were performed in intestinal tissue sections and total cell lysates respectively, using a rabbit anti-survivin antibody previously ...
MAP predisposes to colorectal adenomas and carcinoma, the numbers of adenomatous polyps being in the tens to hundreds, rather than hundreds to thousands as seen in FAP, so it overlaps clinically with FAP and attenuated FAP (AFAP) due to APC mutation. It is caused by the recessive inheritance of biallelic mutations in MUTYH, which encodes mutY-homologue, a component of the oxidative DNA damage repair pathway.. Carrier frequency in most populations is between 1/100 and 1/200, so pseudodominant inheritance is quite possible and has been observed. Note should be taken of consanguinity.. Notably, tumours due to MAP may loose MMR protein expression due to somatic hits in such tumours, and thus exhibit MSI, and appear to be due to LS when they are not (Lynch-like syndrome). In addition, as gene panel testing becomes more available, patients are being found who,intriguingly, have a single mutation in MUTYH and a variant in another colorectal adenoma/carcinoma predisposition gene.. ...
Regulating the cytosolic concentration of the protein β-catenin is an important cell proliferation control mechanism. The cytoplasmic concentration of β-catenin remains low through an interaction with a protein complex consisting of adenomatous polyposis coli (APC), Axin, protein phosphatase 2A, and glycogen synthase kinase 3β (GSK3β). Upon phosphorylation by GSK3β, β-catenin associates with a ubiquitin ligase (E3) complex, resulting in its ubiquitination and proteolysis. Activation of Wnt signaling inactivates GSK3, allowing β-catenin to accumulate in the cytoplasm and eventually to translocate to the nucleus so as to affect gene expression. Two groups report that a phosphorylation-independent mechanism can lead to the destruction of β-catenin. Matsuzawa and Reed show that a mammalian protein called Siah-1 lies at the hub of another pathway that destroys β-catenin in response to DNA damaging agents and the activation of the tumor suppressor protein p53. Siah-1 is known to interact with ...
Several lines of evidence support the role of COX-2-dependent PGE2 in colon tumorigenesis (Wang and Dubois, 2010). Thus, in FAP, the administration of the selective COX-2 inhibitor celecoxib (400 mg/b.i.d.) was associated with a significant reduction of the number of colorectal polyps by approximately one-third (Steinbach et al., 2000). However, marked variability in the response to celecoxib was noted (Steinbach et al., 2000). We hypothesized that the inhibition of vascular COX-2-dependent PGI2 may contribute to the variable response to celecoxib in this setting. In fact, PGI2 may control angiogenesis by preventing endothelial activation and platelet release of angiogenic factors present in α-granules (Menter et al., 1987). Thus, we performed the present study to investigate the biosynthesis of PGI2 and TXA2, two key mediators of CV homeostasis (Grosser et al., 2006), and PGE2, a well known mediator of inflammation and tumorigenesis (Wang and Dubois, 2010) in intestinal neoplasia. We aimed to ...
The adenomatous polyposis coli (APC) gene plays a pivotal role in the pathogenesis of colorectal carcinoma (CRC) but remains a challenge for drug development. Long noncoding RNAs (lncRNAs) are invaluable in identifying cancer pathologies and providing therapeutic options for patients with cancer. Here, we identified a lncRNA (lncRNA-APC1) activated by APC through lncRNA microarray screening and examined its expression in a large cohort of CRC tissues. A decrease in lncRNA-APC1 expression was positively associated with lymph node and/or distant metastasis, a more advanced clinical stage, as well as a poor prognosis for patients with CRC. Additionally, APC could enhance lncRNA-APC1 expression by suppressing the enrichment of PPARα on the lncRNA-APC1 promoter. Furthermore, enforced lncRNA-APC1 expression was sufficient to inhibit CRC cell growth, metastasis, and tumor angiogenesis by suppressing exosome production through the direct binding of Rab5b mRNA and a reduction of its stability. ...
Background: Colectomy and ileorectal anastomosis (IRA) or restorative proctocolectomy are performed for prophylaxis in familial adenomatous polyposis (FAP). After IRA patients may require secondary proctectomy for worsening polyposis or rectal cancer. Outcomes after IRA were evaluated and risk factors predictive of progressive rectal disease identified. Methods: Parametric survival analysis was used to identify predictors of progressive rectal disease in all patients undergoing an IRA for FAP at a single centre. Hazard ratios (HRs) were calculated for phenotype, genotype, sex, age at surgery and presence of colonic cancer. Results: Of 427 patients who underwent IRA, 48 (11.2 per cent) developed rectal cancer and 77 (18.0 per cent) required proctectomy for worsening polyposis over a median follow-up of 15 (range 7-25) years. By the age of 60 years half of the patients retained their rectum. Rectal polyp count exceeding 20 (HR 30.99, 95 per cent confidence interval 9.57 to 100.32; P , 0.001), APC ...
Adenomatous polyposis coli (APC) is a microtubule plus-end scaffolding protein important in biology and disease. APC is implicated in RNA localization, although the mechanisms and functional significance remain unclear. We show APC is an RNA-binding protein and identify an RNA interactome by HITS-CLIP. Targets were highly enriched for APC-related functions, including microtubule organization, cell motility, cancer, and neurologic disease. Among the targets is β2B-tubulin, known to be required in human neuron and axon migration. We show β2B-tubulin is synthesized in axons and localizes preferentially to dynamic microtubules in the growth cone periphery. APC binds the β2B-tubulin 3 UTR; experiments interfering with this interaction reduced β2B-tubulin mRNA axonal localization and expression, depleted dynamic microtubules and the growth cone periphery, and impaired neuron migration. These results identify APC as a platform binding functionally related protein and RNA networks, and suggest a ...
Another name for Intestinal Polyps is Intestinal Polyps. There is no way to prevent intestinal polyps, but regular screening exams help to identify polyps ...
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Prevention of carcinoma means removal of the colon and rectum with permanent ileostomy, although symptomless members of the family may find ileorectal anastomosis with diathermy removal of rectal polyps and periodic surveillance more acceptable. A variant of the FAP genetic disorder is Gardners syndrome in which exostoses (particularly mandibular) and congenital retinal hyperplasia are prominent ...
The assisted conception unit at University College Hospital is the United Kingdoms first clinic to be granted a licence to perform pre-implantation genetic diagnosis (PGD) to select embryos that are free of the genetic mutation that leads to familial adenomatous polyposis (FAP).. Four couples affected by the condition, and who have a 50% chance of passing the mutated gene to a child, will start treatment for the procedure at the end of the year.. Until now, the only reproductive option for families carrying the FAP gene has been for the fetus to be tested for the condition during pregnancy, with the option of termination if it is found to have inherited the condition.. Familial adenomatous polyposis affects between 1 in 26 000 and 1 in 44 000 people in the United Kingdom. It leads to multiple rectal and colon cancers in early adulthood for almost all of those affected by the condition.. Most opt to have prophylactic surgery to remove the colon, usually in their teens.. The new licence is the ...
The morphological features of tumors are closely related to their growth patterns [8]. Polypoid tumors are believed to exhibit a predominantly vertical growth pattern, rather than a horizontal growth pattern, while non-polypoid tumors are believed to exhibit the opposite pattern, resulting in horizontal growth. Although there are some reports that LSTs have distinct biological characteristics compared to polypoid tumors [9, 10], the mechanism by which the LST conformation is generated remains unknown.. LSTs are believed to have distinct characteristics in terms of histological and genetic features [11]. Several molecular characteristics of LSTs have been described, including alteration of the adenomatous polyposis coli (APC) gene or β-catenin [12-14] affecting the WNT/APC/β-catenin signaling pathway, mutation of v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) [12, 15-20]. However, the molecular background of LSTs has remained largely unknown [19, 21]. Most of these studies have ...
Neurology news, research and treatment studies for epilepsy, neurodegenerative disorders, patients with MS and other brain and central nervous system disorders and diseases.
Microtubules (MTs) are essential structures that organize the cytoplasm and assemble and position the mitotic spindle. Spindle orientation is critical for accurate chromosomal segregation in eukaryotic cells, and represents a major strategy to generate cell diversity by asymmetric cell division during development of metazoans (Pearson and Bloom, 2004). In Saccharomyces cerevisiae, orientation of the mitotic spindle along the mother‐bud axis is achieved by long astral MTs emanating from the spindle pole bodies (SPBs) and interacting with the bud cortex (Kusch et al, 2003).. Several components, including the adenomatous polyposis coli (APC)‐like protein Kar9p and the kinesin Kar3p and its accessory factor Cik1p, localize to SPBs and/or MT plus ends, and pull the spindle to the bud neck, thereby providing directional cues for spindle orientation (Liakopoulos et al, 2003). Kar3p is required for MT attachment to sites of polarized growth during plus‐end depolymerization (Maddox et al, 2003). In ...
APC | Colorectal Cancer Atlas| Colon Atlas | Colorectal Cancer Database | Colorectal Cancer | Proteogenomics |Proteomics | This gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It is also involved in other processes including cell migration and adhesion, transcriptional activation, and apoptosis. Defects in this gene cause familial adenomatous polyposis (FAP), an autosomal dominant pre-malignant disease that usually progresses to malignancy. Disease-associated mutations tend to be clustered in a small region designated the mutation cluster region (MCR) and result in a truncated protein product. [provided by RefSeq, Jul 2008]
In the in vivo study, the team blocked APC function and found that synaptic levels of the cell adhesion proteins neuroligin and neurexin dropped considerably. Without normal levels of these proteins, synapses were less mature both structurally and functionally. Mutations in the genes for neuroligin and neurexin are associated with autism in humans, but until now, little was known about the mechanisms responsible for localizing these proteins at the synapse. "Our laboratory study is the first to show that APC is needed to recruit neuroligin and neurexin to the synapse. This finding provides new insights into the mechanisms required for proper synapse function as well as molecular changes at the synapse that likely contribute to autistic behaviors and learning deficits in people with APC loss of function gene mutations," said Jacob. ...
BACKGROUND: Response to EGFR-targeted therapies in colorectal cancer patients has been convincingly associated with Kirsten-Ras (K-Ras) mutation status. Current mandatory mutation testing for patient selection is limited to the K-Ras hotspot codons 12 and 13.. METHODS: Colorectal tumours (n = 106) were screened for additional K-Ras mutations, phenotypes compared in transformation and Ras GTPase activating assays and gene and pathway changes induced by individual K-Ras mutants identified by microarray analysis. Taqman-based gene copy number and FISH analyses were used to investigate K-Ras gene amplification.. RESULTS: Four additional K-Ras mutations (Leu(19)Phe (1 out of 106 tumours), Lys(117)Asn (1 out of 106), Ala(146)Thr (7 out of 106) and Arg(164)Gln (1 out of 106)) were identified. Lys(117)Asn and Ala(146)Thr had phenotypes similar to the hotspot mutations, whereas Leu(19)Phe had an attenuated phenotype and the Arg(164)Gln mutation was phenotypically equivalent to wt K-Ras. We additionally ...
AXIN1_HUMAN] Defects in AXIN1 are involved in hepatocellular carcinoma (HCC) [MIM:114550].[1] [2] Defects in AXIN1 are a cause of caudal duplication anomaly (CADUA) [MIM:607864]. Caudal duplication anomaly is characterized by the occurrence of duplications of different organs in the caudal region. Note=Caudal duplication anomaly is associated with hypermethylation of the AXIN1 promoter.[3] [APC_HUMAN] Defects in APC are a cause of familial adenomatous polyposis (FAP) [MIM:175100]; which includes also Gardner syndrome (GS). FAP and GS contribute to tumor development in patients with uninherited forms of colorectal cancer. FAP is characterized by adenomatous polyps of the colon and rectum, but also of upper gastrointestinal tract (ampullary, duodenal and gastric adenomas). This is a viciously premalignant disease with one or more polyps progressing through dysplasia to malignancy in untreated gene carriers with a median age at diagnosis of 40 years.[4] [5] [6] [7] [8] [9] [10] [11] [12] [13] ...
APC coding exons 1-15 and well into the 5 and 3 ends of all the introns and untranslated regions are analyzed by sequencing. Gross deletion/duplication analysis determines gene copy number for coding exons 1-15. Additionally, all promoter 1B gross deletions as well as single nucleotide substitutions within the promoter 1B YY1 binding motif are analyzed and reported. Clinically significant intronic findings beyond 5 base pairs are always reported. Intronic variants of unknown or unlikely clinical significance are not reported beyond 5 base pairs from the splice junction. Genomic deoxyribonucleic acid (gDNA) is isolated from the patients specimen using standardized methodology and quantified. Sequence enrichment of the targeted coding exons and adjacent intronic nucleotides is carried out by a bait-capture methodology, using long biotinylated oligonucleotide probes followed by polymerase chain reaction (PCR) and next generation sequencing (NGS). Sanger sequencing is performed for any regions ...
J Nat! Cancer Inst 60:753-768. Muto T, Bussey HJR, Morson B (1975) The evolution of cancer ofthe colon and rectum. Cancer 36:2251-2270. Muto T, Kamiya J, Sawada T, Agawa S, Morioka Y, Utsunomiya J (1985) Mucin abnormality of colonic mucosa in patients with familial polyposis coli:· A new tool for early detection ofthe carrier? Dis Colon Rectum 28: 147-148. Nachlas MN (1961) Histochemical observations on the polyp-carcinoma sequence. Surg Gynecol Obstet 112:534-542. Nakamura S, Kino I (1984) Morphogenesis of minute adenomas in familial polyposis coli. Cancer 34:878-888. Lipkin M, Bell B, Sherlock P (1963) Cell proliferation kinetics in the gastrointestinal tract of man. I. Cell renewal in colon and rectum. J Clin Invest 42:767-776. Makela V, Korhonen LK, Lilus G (1971) Carbohydrate-rich compounds in the colonic mucosa of man. Cancer 27:120-127. Mariani-Costantini R, Theillet C, Hutzell P, Merlo G, Schlom J, Callahan R (1989) In situ detection of c-myc mRNA in adenocarcinomas, adenomas, and ...
beta-catenin destruction complex, beta-catenin-TCF7L2 complex, catenin complex, cell cortex, cell junction, cell periphery, cell-cell adherens junction, cell-cell junction, centrosome, cytoplasm
article{cc46aab3-9097-4281-9882-554963bfe958, abstract = {Protein C (PC), a 62 kDa multi-modular zymogen, is activated to an anticoagulant serine protease (activated PC or APC) by thrombin bound to thrombomodulin on the surface of endothelial cells. PC/APC interacts with many proteins and the characterisation of these interactions is not trivial. However, molecular modelling methods help to study these complex biological processes and provide basis for rational experimental design and interpretation of the results. PC/APC consists of a Gla domain followed by two EGF modules and a serine protease domain. In this report, we present two structural models for full-length APC and two equivalent models for full-length PC, based on the X-ray structures of Gla-domainless APC and of known serine protease zymogens. The overall elongated shape of the models is further cross-validated using size exclusion chromatography which allows evaluation of the Stokes radius (rs for PC = 33.15 A; rs for APC = 34.19 ...
MCQS ADENOMATOUS GALL BLADDER ADENOMATOUS GALL BLADDER PLAB, IELTS, USMLE, GRE, AIPGMEE, AIIMS, AFMC, BHU, CMC, JIPMER, PGI, SGPGI, ...
The results of this study show that pharmacologic inhibition of VEGFR and EGFR tyrosine kinase activity with ZD6474 reduces macropolyp number, size, and burden in the small bowel in the ApcMin/+ mouse model of familial adenomatous polyposis. Micropolyps, the putative precursors to macropolyps, were also decreased in number and size by ZD6474 treatment. Qualitatively similar results were obtained when ZD6474 was given as once-daily oral administration for 28 days to 6-week-old mice (early intervention) or 10-week-old mice (late intervention). In the early intervention study, ZD6474 also significantly inhibited polyp number in the colon, a finding that is notable given the initial low polyp count in the colon.. The ApcMin/+ mouse is one of several animal models of human gastrointestinal cancer, and it is a widely used model for the study of various factors on the early stages of intestinal cancer (8, 36). From the age of 6 weeks, ApcMin/+ mice have macroscopically detectable adenomas (5). ...
This article is from a St. Marks Polyposis Newsletter - My thanks go to David for allowing the article to be reproduced below.. The Wolfson Unit for Endoscopy was established in 1996 as a national centre for flexible endoscopy. It is designed to combine a stylish and caring environment with modern high-technology facilities for outpatients and inpatients, whether NHS or private. Personal Screening. The term medical screening, or surveillance, frequently appears in the media. People often associate screening and surveillance programmes with the prevention of conditions such as cervical cancer or breast cancer.. Detecting disease. What do we actually mean when we say that a patient is part of a screening programme and how does this apply to an individual who has Familial Adenomatous Polyposis (FAP)? Broadly speaking, screening is a method for detecting disease or body dysfunction before an individual would normally seek medical advice. FAP is a condition characterised by the formation of polyps ...
Safe Order Celebrex Generic Drug. Celebrex (Celecoxib) is used to reduce pain, inflammation, and stiffness caused by osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis. Celecoxib is also used to reduce the number of adenomatous colorectal polyps in familial adenomatous polyposis (FAP), to treat acute pain, and to treat pain associated with menstruation. Celebrex is the most trusted NSAID pain reliever from Pfizer! Celebrex also Marketed As: Celecoxib, Celebra, Onsenal ...
The numbers of obese people and diabetic patients are ever increasing. Obesity and diabetes are high-risk conditions for chronic diseases, including certain types of cancer, such as colorectal cancer (CRC). The aim of this study was to develop a novel animal model in order to clarify the pathobiology of CRC development in obese and diabetic patients. We developed an animal model of obesity and colorectal cancer by breeding the C57BL/KsJ-db/db (db/db) mouse, an animal model of obesity and type II diabetes, and the C57BL/6J-ApcMin/+ (Min/+) mouse, a model of familial adenomatous polyposis. At 15 weeks of age, the N9 backcross generation of C57BL/KsJ-db/db-ApcMin/+ (db/db-Min/+) mice developed an increased incidence and multiplicity of adenomas in the intestinal tract when compared to the db/m-Min/+ and m/m-Min/+ mice. Blood biochemical profile showed significant increases in insulin (8.3-fold to 11.7-fold), cholesterol (1.2-fold to 1.7-fold), and triglyceride (1.2-fold to 1.3-fold) in the db/db-Min/+ mice
Colorectal cancer usually develops from abnormal growths, called polyps within the bowel or rectum. If these abnormal growths remain in the colon, over time, some can turn into cancer. Regular screening, or testing, is crucial in the prevention of this cancer and usually begins at age 50. Screenings can find abnormal growths in the bowel or rectum and be removed in the early stages of growth. Removal often prevents further growth that could lead to cancer. It is recommended that adults be screened up to the age of 75. Adults aged 76 to 85 should talk to their doctor as to whether they should continue to be screened. Some people younger than 50 years of age should be screened as well if they or a close relative have had colorectal polyps or colorectal cancer, or have an inflammatory bowel disease such as Crohns disease or ulcerative colitis. Those with a genetic syndrome such as familial adenomatous polyposis (FAP) or Lynch syndrome should also be tested at an earlier age. Speak with your doctor ...
A study in this issue of Cancer Prevention Research by Sheaffer and colleagues reports that extreme DNA hypomethylation can promote intestinal tumorigenesis in a mouse model system, in apparent contradiction to prior reports of reduced adenoma formation by DNA hypomethylation. Using an elegant inducible intestine-specific knockout system, the authors found that a complete knockout of Dnmt1 in the mouse intestinal epithelium led to a more than 6-fold increase in macroscopic adenoma formation in the ApcMin/+ mice (1). This observation challenges the current notion that DNA methylation inhibition represses intestinal adenoma formation by suppressing promoter CpG island (CGI) hypermethylation and may have important implications for the prevention and treatment of human cancer (2-7).. Widespread hypomethylation and CGI hypermethylation are commonly observed in human cancers (8). Besides extensive, but descriptive evidence accumulated by human cancer epigenomic profiling studies, animal studies have ...
1. A method for diagnosing familial adenomatous polyposis (FAP) or an increased risk of FAP in a test subject believed to be at risk for such cancer, the method comprising: (a) positioning a sampling area of the oral mucosa of the test subject in a system for measuring the oral mucosal vascular density (OMVD); (b) transilluminating the sampling area of the oral mucosa of the test subject with a light source from the system in a range of wavelengths from 470 nm to 700 nm for a period of time; (c) obtaining at least one or more images of the illuminated sampling area of the test subject using a camera from the system; (d) storing the at least one or more images of (c) on an electronic storage device on a computer; (e) analyzing the at least one or more images of the test subject stored on the electronic storage device to provide an oral mucosal vascular density (OMVD) value from a selected portion of the one or more images; and (f) comparing the OMVD values of the at least one or more images of ...
The 2 most common inherited bowel cancer syndromes are hereditary nonpolyposis colorectal cancer (HNPCC) and familial adenomatous polyposis (FAP). Learn more about them here.
Colonic polyps: Abnormal excess tissue growth in the colon that can become cancerous. In familial adenomatous polyposis (FAP), a genetic mutation causes thousands of these colonic polyps to grow.
Background: Patients with Ulcerative Colitis (UC) have inherent prothrombotic tendencies. It is unknown whether this necessitates the use of additional perioperative anti-thrombotic prophylaxis when such patients require major surgery. Methods: The postoperative courses of 79 patients with UC undergoing 180 major abdominal and pelvic operations were examined for clinical and radiological evidence of venous thrombosis. Eighteen patients with Familial Adenomatous Polyposis (FAP) having surgery (35 operations) of similar magnitude were also studied. Standard anti-thrombosis prophylaxis was utilised in all patients. Results: Nine patients with UC were clinically suspected of developing postoperative venous thrombosis, but only three (3.8%) had their diagnosis confirmed radiologically (all had a pulmonary embolus). Therefore, the overall postoperative thrombosis rate, on an intention to treat basis, was 1.7% (3/180). No patient with FAP developed significant venous thrombosis. Conclusion: Standard ...
The creation of a pelvic ileal reservoir is associated with inflammatory changes in the reservoir mucosa. Chronic inflammation and villous atrophy are seen in most patients with both ulcerative colitis and familial adenomatous polyposis (FAP), the two prime indications for the operation. The mucosa undergoes a form of colonic metaplasia which is demonstrable by morphological, mucin histochemical, immunohistochemical and proliferation methods. Other pathological features such as mucosal ischaemia, mucosal prolapse, granulomas and pyloric metaplasia are seen in the pouch mucosa and these changes contribute to the confusion over definitions of pouchitis ...
Prenatal diagnosis (PND) and preimplantation genetic diagnosis (PGD) for later onset and/or reduced penetrance inherited cancer predispositions, e.g. familial adenomatous polyposis, hereditary non-polyposis colorectal ...
Background : Results of epidemiologic studies suggest that there is limited evidence for the association between cigarette smoking and risk of colorectal cancer. Cigarette smoking has been shown to increase the risk of colorectal adenomatous polyps, which are recognized as precursors of colorectal cancer, while few studies have examined the...
Adenomatous gall bladder - Colon cancer: Symptoms, causes, and treatment. The idea behind a colon cleanse process is to eliminate the toxins which have built up in your digestive system.
Mutations spectrum in hereditary disorders predisposing to occurrence of intestine polyposis in Poland Andrzej Plawski, Paweł Boruń, Tomasz Banasiewicz, Jacek Paszkowski, Agnieszka Stembalska, Maria Sąsiadek, Monika Siołek, Beata Kozak Klonowska, Izabela Brozek, Janusz Limon, Dorota Nowakowska, Grzegorz Kurzawski, Tomasz Byrski, Tomasz Gach, Diana Hodorowicz-Zaniewska, Anna Bartkowiak, Ryszad Slomski, Elżbieta Czkwianianc, Krzysztof Linke, Ewa Grzybowska, Arleta Lącka-Wojciechowska, Marek Szwiec, Sabina Więcek, Alicja żabka, Agnieszka Synowiec, Anna Jakubiuk-Tomaszuk, Robert Skalski, Jan Lubinski, Piotr Krokowicz, Paweł Blecharz, Mikołaj Teisseyre, Michal Drews, Wojciech Cichy
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Scientists have known that patients colon tumors with APC mutations have an increased amount of survivin, a protein that halts apoptosis, the programmed cell death. This increase also appears to be associated with a rise in the number of stem cells found at the bottom of colonic crypts. Researchers wanted to see if there was a difference in stem cell number between normal mice and mice mutant for APC. To do this, they exposed both normal and mutant mice to radiation, testing their ability to repair the resulting DNA damage. They speculated that increased survivin in the mutant mice might enable more stem cells to survive and affect the response to radiation. The researchers asked if mice with an APC mutation are different from normal mice in radiation sensitivity and their ability to repair the damage. Normal cells can repair DNA damage from radiation, Dr. Leeper explains ...
Im having a problem with the back end of Supreme. The first time I load a page in Pages, I can see the Swift Page Builder.. The next time I load a Page, it is gone.. The Swift Page Builder always shows up under Posts, however. Thats the strange part. If I restart Apache, Swift Page Builder comes back once. Then it vanishes again until I reboot.. It appears to be a conflict with PHPs APC, the alternative PHP cache that lends a massive speedup in PHPs serving of pages.. Is there a way you can resolve this? Id prefer to use APC rather than WordPresss caching plugins because WordPress is not the only content we are serving.. Heres my apc.ini in case theres a setting I can change to fix this:. [APC] apc.enabled = 1 apc.cache_by_default = on apc.shm_segments = 1 apc.shm_size = 96M apc.ttl = 3600 apc.user_ttl = 3600 apc.num_files_hint = 0 apc.write_lock = On apc.include_once_override = 1 apc.mmap_file_mask = /tmp/apc.XXXXXX. ...
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PURPOSE: Disconnection of an ileal pouch-anal anastomosis with repeat ileal pouch-anal anastomosis has been proposed for treatment of ileal pouch-anal anastomosis failure caused by septic or functional complications. We report our experience with repeat ileal pouch-anal anastomosis, and document functional outcome and quality of life.. METHODS: Of 101 patients undergoing laparotomy, ileoanal disconnection, and repeat ileal pouch-anal anastomosis, 80 were referred from other institutions. Indications included: chronic anastomotic leak (n=27), perineal or pouch-vaginal fistula (n=47), anastomotic stricture (n=22), dysfunction/long efferent limb of S-pouch (n=36), and previous ileal pouch-anal anastomosis excision or exclusion (n=6). In 64 cases a "septic" indication was observed. Pathologic features of Crohns disease were present in 4 patients preoperatively and 15 more after repeat ileal pouch-anal anastomosis. Four patients had clinical features of Crohns disease.. RESULTS: Three patients had ...
Pouch salvage surgeries can avoid RPC/IPAA surgery failure. Pouch salvage operations are divided to two groups: Trans perineal and trans abdominal approaches (8). In the trans abdominal approach, the surgeon mobilizes the pouch, and depending on the pouch condition and small bowel mesentery length, the pouch will be removed or left in place. Then mucosectomy of rectal mucosa down to dentate line will be performed and at the end, hand sewn pouch anal anastomosis will complete the operation. Diverting ileostomy will be performed in most cases. Trans perineal approaches include fistulotomy for very low fistulas, advancement flap or muscle transposition for high fistulas and pouch-vaginal fistulas, or rectal mucosectomy plus pouch mobilization with pouch anal anastomosis for remained rectal mucosa or stricture at pouch anal anastomosis site. Four major complications resulting in pouch surgery failure were observed with sepsis being the most common factor. Sepsis could occur early, immediately after ...
PURPOSE: Pathophysiology of pouchitis after ileal pouch-anal anastomosis is controversial because of the potential for development of carcinoma. Cyclooxygenase-2-derived prostaglandins may be involved in the inflammatory process and play a role in the pathogenesis of colon cancer. Vascular endothelial growth factor plays a major role in neoangiogenesis and is overexpressed in a number of gastrointestinal malignancies. The goal of this study was to evaluate the expression of cyclooxygenase-2 and vascular endothelial growth factor and to assess neoangiogenesis and epithelial cell proliferation in patients with ileal pouch-anal anastomosis. METHODS: Endoscopic biopsies were obtained from 15 patients with ileal pouch-anal anastomosis without pouchitis (10 biopsies from the ileal pouch and 10 from ileal nonpouch mucosa) and from 15 subjects with irritable bowel syndrome (10 biopsies from normal-appearing ileum and rectum). Cyclooxygenase-1, cyclooxygenase-2, and vascular endothelial growth factor ...
IBIROGBA, S. B. et al. The clinical and pathological features of hereditary mixed polyposis syndrome: Report on a South African family. S. Afr. j. surg. [online]. 2008, vol.46, n.3, pp.90-92. ISSN 2078-5151.. BACKGROUD: Hereditary mixed polyposis syndrome is characterised by multiple large-bowel polyps of differing histological types including a mixture of atypical juvenile polyps, hyperplastic polyps and adenomas. Affected individuals are thought to have an increased risk of malignancy, possibly via the juvenile polyposis pathway. METHODS: A 51-year-old woman (with a history of a colectomy for polyps during childhood) presented with rectal bleeding. Endoscopy demonstrated small rectal polyps which were hyperplastic on histology. A family tree was drawn up and the three children of the proband underwent flexible sigmoidoscopy. RESULTS: Endoscopic surveillance of the three children revealed one who had a similar phenotype to the mother. This child underwent colectomy and ileorectal anastomosis. ...
Adapted from http://www.genetests.org/ It is now recognized that FAP has a broad spectrum of clinical manifestations and, in addition to classic FAP, includes three phenotypes that previously were thought to be discrete clinical entities distinct from FAP: attenuated FAP, Gardner syndrome, and Turcot syndrome. Patients with classic FAP present with over 100 colorectal adenomatous polyps or less then 100 adenomatous polyps AND a relative diagnosed with FAP. Patients with attenuated FAP (AFAP) present with colonic adenomatous polyps less than 100 in number and more proximally found in the colon than in classic FAP. In patients with a fewer number of polyps (average of 30), a family history of colon cancer in persons less than age 60 years with multiple adenomatous polyps is necessary for diagnosis. The average age of colon cancer diagnosis in individuals with attenuated FAP is age 50 to 55 years, which is 10-15 years later than that observed in classic FAP. A predominance of right-sided colorectal ...
Background: Sporadic adenoma formation found on surveillance colonoscopies in patients with inflammatory bowel disease (IBD) represents a significant risk for cancer. Certain racial groups like African Americans (AA) are at increased risk of developing colorectal cancer (CRC), but there is conflicting literature on differences in sporadic adenoma formation. Some data suggests AA are at increased risk for large adenomas, more proximal lesions, and increased prevalence. These data, however, are studying the general population and to our knowledge no study has looked at differences in adenoma formation by race in IBD patients. The present retrospective study analyzes the prevalence of adenomas in IBD patients. Methods: All IBD patients who received a surveillance colonoscopy within the past year were included in the present study. Sporadic adenomas included serrated, tubular, villous, and tubulovillous adenoma formation. A database was created using Microsoft Excel and identifying information was
AIMS--To investigate colonic metaplasia of goblet and columnar epithelial cells in ileal pouch mucosa; to correlate this with the degree of morphological and inflammatory change; and to assess whether such changes are related to the presence of faecal stasis. METHODS--Biopsy specimens of ileal pouch mucosa were taken from 31 patients (30 with ulcerative colitis, one with familial adenomatous polyposis) either before (eight patients) or after (23 patients) ileostomy closure. A simple morphological technique was used to assess changes in villous height. Inflammatory change was estimated using an established scoring system for pouchitis, and acquisition of colonic antigens was determined by immunohistochemistry using three monoclonal antibodies which recognise components of the two major epithelial cell types in the colorectum. The degree of staining with the monoclonal antibodies was graded and the grades correlated with an index of villous atrophy and with the inflammatory scores. RESULTS--Five ...
Periampullary cancers encompass a mixture of cancers but in general are separated into four subtypes: cancer in the head of the pancreas, distal bile duct cancer, true ampullary cancer, and duodenal cancer. These cancers arise in the vicinity of the ampulla of Vater and are differentiated by their histologic origins (pancreatic, distal bile duct, ampulla of Vater, or duodenum). While pancreatic adenocarcinoma makes up the majority of resected periampullary cancers at 62%, ampullary cancer accounts for 19%, distal bile duct cancer 12%, and duodenal cancer 7% of resected periampullary cancers.1 Although preoperative assessment with imaging and biopsy can distinguish one subtype from the other, often times the tumor origin may be undetermined preoperatively. Moreover, duodenal cancer in the periampullary region as well as intestinal-type ampullary cancer behave in a similar fashion, whereas distal bile duct cancer and pancreaticobiliary-type ampullary cancer behave similar to one another. While 56% ...
Lynch syndrome (Hereditary Nonpolyposis Colorectal Cancer, HNPCC) is the most common hereditary syndrome predisposing to colorectal cancer, accounting for 1-3% of all colorectal cancer. This multi-organ cancer predisposition syndrome is caused by mutations in the mismatch repair (MMR) genes, especially MLH1 and MSH2, and to lesser extents MSH6 and PMS2, which lead to widespread genetic instability and thus microsatellite instability (MSI). Hereditary cancer often manifests in two or more tumours in a single individual; 35-40% of Lynch syndrome patients have synchronous or metachronous tumours of the two major Lynch syndrome-related cancers: colorectal and endometrial.. The main purposes of the work underlying this thesis were to identify persons at risk of Lynch syndrome or other types of hereditary colorectal cancer, to estimate the cancer risks associated with these predispositions and to identify the underlying genetic causes.. A population-based cohort of 78 persons with double primary ...
The ileoanal reservoir procedure is a surgical treatment option for chronic ulcerative colitis, colon cancer and familial polyposis patients who need to have their large intestine (colon) removed. An ileoanal reservoir (or pouch) is an internal pouch formed of small intestine. This pouch provides a storage place for stool in the absence of the large intestine. Anal sphincter muscles assist in holding in the stool. Several times a day, stool is passed through the anus.. Ileoanal reservoir surgery is a widely accepted surgical treatment for ulcerative colitis or familial polyposis because it eliminates the disease, gives the patient control of bowel movements and does not require a permanent ileostomy. Each patient considering this surgery is carefully evaluated to determine if this procedure is appropriate for them. This procedure is performed in one, two or three stages, but is most often done in two stages, usually 2-3 months apart.. ...
Two-photon spectral resolved imaging was used to image fresh human biopsies of colon tissue and to characterize healthy colon mucosa, adenomatous polyp and adenocarcinoma by means of a morpho-functional analysis. Morphological examination, performed using endogenous tissue fluorescence, discriminated adenomatous and adenocarcinoma tissues from normal mucosa in terms of cellular asymmetry and nucleus-to-cytoplasm ratio. Good agreement was found between multiphoton images and histological examination performed on the same samples. Further characterization, performed by means of spectral-resolved analysis of NADH and FAD fluorescence, demonstrated an altered metabolic activity in both adenomatous and adenocarcinoma tissues compared to healthy mucosa. This morpho-functional approach may represent a powerful method to be used in combination with endoscopy for in vivo optical diagnosis of colon cancer and may be extended to other tissues.. ©2013 Optical Society of America. Full Article , PDF Article ...
Generic Celebrex is used for treating rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, juvenile arthritis or menstrual pain. It is also used in familial adenomatous polyposis (FAP) to decrease the number of polyps (growths) in the rectal area.. Generic Celebrex (Celecoxib 100/200mg) $ 0.92 pill - Gastrointestinal Tract, Womens Health, Anti-inflammatories, Arthritis @ KupTania.
Buy Celebrex is used for treating rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, juvenile arthritis or menstrual pain. It is also used in familial adenomatous polyposis (FAP) to decrease the number of polyps (growths) in the rectal area.. Celebrex (Celecoxib 100/200mg) $0.69 pill - Gastrointestinal Tract, Womens Health, Anti-inflammatories, Arthritis @ Achat Medicament En Suisse En ligne - Sans Ordonnance. Acheter Medicament Sans Ordonnance en ligne en Suisse, en France, en Belgique.
Le, Q., Melmed, G., Dubinsky, M., McGovern, D., Vasiliauskas, E. A., Murrell, Z., Ippoliti, A., Shih, D., Kaur, M., Targan, S. and Fleshner, P. (2012), Surgical outcome of ileal pouch-anal anastomosis when used intentionally for well-defined Crohns disease. Inflamm Bowel Dis. doi: 10.1002/ibd.22955 ...
Ivory exostoses represent a type of osteoma that affects bones formed by membranous ossification, chiefly affecting calvarial and mandibular surfaces2,4,6,10-12,20,22,28 (Fig. 21-2). Multiple osteomas of this type are frequently associated with colonic polyposis and fibrous soft tissue tumors, including mesenteric fibromatosis and epidermal inclusion cysts in the familial disorder known as Gardners syndrome.13,14,17,24,29 Some patients also had distinct hyperplastic changes of the retinal pigmented epithelium.22,32,33 The development of ocular lesions may precede the development of colonic and osseous manifestations. The polyps of the gastrointestinal tract are adenomatous and typically involve the colon but can also be present in the duodenum and stomach. The adenomatous polyps of the gastrointestinal tract have a high propensity for malignant transformation. In fact, colon cancer develops in all affected individuals unless prophylactic colectomy is performed.23 The disorder is transmitted by ...
BACKGROUND: Restorative proctocolectomy is an operative procedure that in principle means proctocolectomy, preserving the anal sphincters and construction of an ileal pouch which is sutured to the dentate line. The method is used mostly in case of su
FUNCTION: On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for BMP-2 and BMP-4. Positively regulates chondrocyte differentiation through GDF5 interaction (By similarity). CATALYTIC ACTIVITY: ATP + [receptor-protein] = ADP + [receptor- protein] phosphate. SUBUNIT: Interacts with low affinity with GDF5; positively regulates chondrocyte differentiation. TISSUE SPECIFICITY: Highly expressed in skeletal muscle. DISEASE: Juvenile polyposis syndrome (JPS) OMIM: Autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of ...
Polyps tend to cluster in families so that having a first degree relative ( sibling, parent or child ) with colon polyps raises ones chances of having polyps. The familial cancer syndromes such as Lynch Syndromes I and II ( rare ) carry a high risk of the development of colon and other cancers. Family adenomatous polyposis or FAP, is a rare condition characterized by thousands of adenomatous polyps throughout the large bowel. People with 1st degree relatives with inflammatory bowel disease are at increased risk and those who have a first degree relative with colon cancer have a fourfold increase in risk over the general population and should be screened earlier with colonoscopy and more often than the proposed outline for screening suggested by the American Cancer Society. There is an association of cancer risk with meat, fat or protein consumption which appear to break down in the gut into cancer causing compounds called carcinogens. A personal history of ovarian, endometrial, or breast cancer ...
IMBELLONI, Luiz Eduardo; BEATO, Lúcia; ORNELLAS, Arídio and BORGES, Carlos Roberto Junqueira. Extreme intraoperative hemodilution in Jehovah s witness patient submitted total proctocolectomy: case report. Rev. Bras. Anestesiol. [online]. 2005, vol.55, n.5, pp.538-545. ISSN 0034-7094. http://dx.doi.org/10.1590/S0034-70942005000500009.. BACKGROUND AND OBJECTIVES: Homologous blood transfusion risks are well known and some patients may refuse blood transfusions on religious grounds. This report aimed at describing a case of total proctocolectomy in Jehovah s Witness patient with 4 g/dL hemoglobin. CASE REPORT: Male patient, 17 years old, with family history of adenomatous polyposis. The disease was manifested at eight years of age, characterized by bleeding. At 13 years of age he was submitted to total colectomy. At 17 years of age he was submitted to total proctocolectomy. Patient was prepared with erythropoietin, folic acid, infusion of iron and vitamin B12. Red blood cell count revealed He = ...
Background: The transition from normal epithelium to adenoma and, to invasive carcinoma in the human colon is associated with acquired molecular events taking 5-10 years for malignant transformation. We discovered CCAT1, a non-coding RNA over-expressed in colon cancer (CC), but not in normal tissues, thereby making it a potential disease-specific biomarker. We aimed to define and validate CCAT1 as a CC-specific biomarker, and to study CCAT1 expression across the adenoma-carcinoma sequence of CC tumorigenesis.Methods: Tissue samples were obtained from patients undergoing resection for colonic adenoma(s) or carcinoma. Normal colonic tissue (n = 10), adenomatous polyps (n = 18), primary tumor tissue (n = 22), normal mucosa adjacent to primary tumor (n = 16), and lymph node(s) (n = 20), liver (n = 8), and peritoneal metastases (n = 19) were studied. RNA was extracted from all tissue samples, and CCAT1 expression was analyzed using quantitative real time-PCR (qRT-PCR) with confirmatory in-situ ...
Colorectal cancer (CRC) continues to be a major cause of morbidity and mortality. Although the factors underlying CRC development and progression are multifactorial, there is an important role for tumor-host interactions, especially interactions with myeloid cells. There is also increasing evidence that cyclooxygenase-derived prostaglandins are important mediators of CRC development and growth. Although prevention trials with either nonselective NSAIDs or COX-2 selective agents have shown promise, the gastrointestinal or cardiovascular side effects of these agents have limited their implementation. The predominant prostaglandin involved in CRC pathogenesis is PGE2. Since myeloid cells express high levels of the PGE2 receptor subtype, EP4, we selectively ablated EP4 in myeloid cells and studied adenoma formation in a mouse model of intestinal adenomatous polyposis, ApcMin/+ mice. ApcMin/+mice with selective myeloid cell deletion of EP4 had marked inhibition of both adenoma number and size, with ...
Polyps are growths either of normal lining of the gastrointestinal tract or abnormal lining. The most common type of gastric polyps (polyps of the stomach) are found in the proximal half of the stomach. They are fundal type polyps because they are found in the fundus of the stomach. They are characteristically cystic. Although they may be single, frequently they are multiple. These polyps are benign and need not be removed, as distinct from pre-malignant (adenomatous polyps) that are commonly seen in the colon. Adenomatous polyps, where ever they are found, should be removed because they are precursors to cancer. All polyps, however particular stomach polyps, may cause chronic gastro-intestinal bleeding. Cystic gland polyps are friable and break off readily from food causing very small amounts of bleeding. If the physician is not certain what type of polyp it is, removal and pathological examination under the microscope will determine the type definitively. - Stock Image M240/0629
Screening for colorectal cancer with fecal occult blood testing and lower endoscopy with removal of polyps reduce the mortality rate from colorectal cancer. Screening with flexible sigmoidoscopy is becoming standard for asymptomatic persons older than 50 years. Because adenomatous polyps found in the distal colon have been associated with adenomatous polyps in the proximal colon, full colonoscopy is generally recommended for patients with distal adenomas. Small polyps (less than 1 cm) seem to have a lower risk of malignant transformation than do larger polyps and are less likely to be malignant or to have high-grade histologic features. With increasing data, it appears that there is a low prevalence of histologically advanced polyps in the proximal colon among patients with small distal tubular adenomas. Wallace and associates conducted a study to determine the prevalence of advanced adenomatous polyps in the proximal colon among patients with small tubular adenomas found on flexible ...
A60 The scientific potential of numerous unique animal models of carcinogenesis has not been fully realized due to our limited ability to monitor tumor growth in vivo. Establishment of a method for the accurate measurement of colon lesion size is needed to both characterize the dynamics of tumor growth and monitor responsiveness to therapeutic interventions. The goal of the present study was to develop an endoscopy-based protocol for the accurate estimation of tumor size in vivo from images obtained during colonoscopic examinations. This technology was established using a unique strain of Multiple Intestinal Neoplasia (Min) mice established at Fox Chase Cancer Center (Apc+/Min-FCCC), which spontaneously develop multiple colorectal tumors. Anesthetized Apc+/Min-FCCC mice received colonoscopic examinations, using a rigid endoscope. The endoscope (1.5 mm diameter) was inserted anally, and high-resolution images of 10 colon adenomas (from 8 animals) were captured using a CCD camera. Lesion size was ...
For more than 20 years, BroadcastMed has been innovating digital strategies for healthcare organizations. The company was first in the world to broadcast live surgeries on the internet using its ORLive solution which provides an intimate look inside the operating room.. ...
The Peutz-Jeghers Syndrome (PJS) and Juvenile Polyposis Syndrome (JPS) Online Support Group provides information and support for individuals with PJS and JPS, their families, friends, interested medical professionals and researchers ...
Factors associated with an increased or high risk of colorectal cancer can be divided into two categories: personal, and hereditary or familial. Personal risk factors include: a history of colorectal cancer that has been completely removed and, to a lesser extent, a history of ovarian, uterine or breast cancer; a history of polyps, especially large adenomatous polyps; a history of inflammatory bowel disease, particularly ulcerative colitis and Crohns disease; a high fat, low-fiber diet; a sedentary life-style; obesity; cigarette smoking, both currently and in the past; heavy alcohol use; and diabetes. Other possible personal risk factors for colorectal cancer include a history of working the night-shift several nights a week for at least 15 years and previous radiation treatment for prostate cancer. Familial and hereditary risk factors include: having a close relative who had colorectal cancer before age 60; family history of polyposis syndromes and hereditary non-polyposis syndromes; ...
Bone Morphogenetic Protein Receptor 1A (BMPR1A) and Juvenile Polyposis Syndrome Cara Davidson March 18, 2004. What is BMPR1A?. A receptor serine-threonine kinase Located on plasma membrane Part of the TGF- ß receptor superfamily Slideshow 6740035 by shay-young
How to Treat Nasal Polyps: Nasal Polyposis From Pathogenesis To Treatment An Update. Nasal Polyps Site, Info, tips and treatments for Nasal Polyps.
We report on 2 infants with PHHI for whom focal lesions of the pancreas were diagnosed during laparoscopy and laparoscopically enucleated. Both children were cured at the age of 1 month. One year after surgery, both patients are well and normoglycemic. Functional data from patient tissue analyses and genotyping in both cases revealed that PHHI was a consequence of defects in β-cell KATP channels. For both children, mutations in the SUR1 gene were found; the mutations were of paternal origin in both cases, as reported for focal hyperinsulinism. The focal origins of PHHI were confirmed with histologic diagnoses.. Focal adenomatous hyperplasia as a cause of PHHI was observed first by Kloppel et al7 in 1975 and was noted by Goossens et al8 in 1989 in a large study of 24 pancreata from surgically treated patients with PHHI. Since those observations, focal lesions as a cause of intractable hyperinsulinism have been consistently reported. The presumed incidence may be as high as 30% to 60% of cases of ...
Womens health Thyroid Conditions question and answers about what is cytomorphologic fatures consistent with adenomatous goiter mean? and what is the treatment needed?
Thank you for your interest in spreading the word about The BMJ.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
Mutations of APC appear to initiate sporadic and inherited forms of human colorectal cancer. Although these mutations have been well characterized, little is known about the function of the APC gene product. Two cellular proteins that associate with APC were identified by nucleotide sequence analysis and peptide mapping as the E-cadherin-associated proteins alpha- and beta-catenin. A 27-residue fragment of APC containing a 15-amino acid repeat was sufficient for the interaction with the catenins. These results suggest an important link between tumor initiation and cell adhesion. ...
Colon tumor > Familial polyposis syndromes > Peutz-Jeghers syndrome by Michael Feely, D.O., Editorial Board Review by Raul S. Gonzalez, M.D. ...
Background: The population-wise variation in proneness of Colorectal Cancer (CRC) has been studied in the manuscript. A population wise analysis of responsiveness towards colorectal cancer is carried out with genetic, epigenetic, metagenomic and environmental factors associated with APC mutation mainly responsible for CRC among eight different populations. Methods and Material: The APC mutation has been obtained using the human gene mutation database-HGMD and the international cancer genome consortium-ICGC Data Portal. The epigenetic factors affecting colon cancer have been identified through EpiGRAPH tool. The human oral microbiome database (HOMD) and comparative toxicogenomics database (CTD) are used to find the metagenomic factors affecting CRC. Results: Variants of APC gene from the selected ethnic classes chosen from Argentina, France, Germany, India, Poland, Romania, UK and USA were characterized, where the chromosome positions 112102966-112177228 are found to be affected. It has ...
adenomatous polyposis coli protein  adenomatous polyposis coli protein
proteins that are involved in organizing this network, and we show that end-binding protein 1 (EB1), adenomatous polyposis coli ... b>Adenomatous polyposis coli protein (APC) is a well-characterized tumor suppressor protein [1] [2] [3]... ... Truncation mutations in the adenomatous polyposis coli protein (APC) are responsible for familial polyposis, a form of ... ARM domain-dependent nuclear import of adenomatous polyposis coli protein is stimulated by the B56 alpha subunit of protein ...
more infohttps://www.labome.org/topics/chemicals/and/proteins/cytoskeletal/adenomatous-polyposis-coli-protein-14404.html
Adenomatous Polyposis Coli Protein
     Summary Report | CureHunter  Adenomatous Polyposis Coli Protein Summary Report | CureHunter
A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME. ... Adenomatous Polyposis Coli Protein. Subscribe to New Research on Adenomatous Polyposis Coli Protein ... Adenomatous Polyposis Coli (Familial Adenomatous Polyposis) 01/01/2008 - "The adenomatous polyposis coli gene functions as a ... Amino Acids, Peptides, and Proteins*Proteins: 90489*Cytoskeletal Proteins: 557*Adenomatous Polyposis Coli Protein: 29 ...
more infohttp://www.curehunter.com/public/keywordSummaryD025601-Adenomatous-Polyposis-Coli-Protein.do
Neurite outgrowth involves adenomatous polyposis coli protein and β-catenin | Journal of Cell Science  Neurite outgrowth involves adenomatous polyposis coli protein and β-catenin | Journal of Cell Science
A candidate protein for controlling neurite extension is the adenomatous polyposis coli (APC) protein, which regulates membrane ... Neurite outgrowth involves adenomatous polyposis coli protein and β-catenin. Violet Votin, W. James Nelson, Angela I. M. Barth ... Neurite outgrowth involves adenomatous polyposis coli protein and β-catenin. Violet Votin, W. James Nelson, Angela I. M. Barth ... Neurite outgrowth involves adenomatous polyposis coli protein and β-catenin. Violet Votin, W. James Nelson, Angela I. M. Barth ...
more infohttp://jcs.biologists.org/content/118/24/5699
Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal...  Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal...
Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal ... Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal ... Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal ... Relationship between the role of the adenomatous polyposis coli protein in colon cancer and its contribution to cytoskeletal ...
more infohttp://www.biochemsoctrans.org/content/33/4/694
Adenomatous Polyposis Coli Tumor Suppressor Protein Has Signaling Activity in Xenopus laevis Embryos Resulting in the Induction...  Adenomatous Polyposis Coli Tumor Suppressor Protein Has Signaling Activity in Xenopus laevis Embryos Resulting in the Induction...
The adenomatous polyposis coli (APC)1 gene is a tumor suppressor gene linked to familial adenomatous polyposis (FAP) and to the ... Adenomatous Polyposis Coli Tumor Suppressor Protein Has Signaling Activity in Xenopus laevis Embryos Resulting in the Induction ... 1996) The adenomatous polyposis coli tumor suppressor protein localizes to plasma membrane sites involved in active cell ... Adenomatous Polyposis Coli Tumor Suppressor Protein Has Signaling Activity in Xenopus laevis Embryos Resulting in the Induction ...
more infohttp://jcb.rupress.org/content/136/2/411
Adenomatous polyposis coli (Apc) tumor suppressor gene as a multifunctional gene | SpringerLink  Adenomatous polyposis coli (Apc) tumor suppressor gene as a multifunctional gene | SpringerLink
The Apc gene product (APC), basically a cytoplasmic protein, blocks cell cycle ... gene is mutated in familial adenomatous polyposis and in sporadic colorectal tumors. ... The adenomatous polyposis coli (Apc) gene is mutated in familial adenomatous polyposis and in sporadic colorectal tumors. The ... Kaplan KB, Burds AA, Swedlow JR, Bekir SS, Sorger PK, Näthke IS (2001) A role for the adenomatous polyposis coli protein in ...
more infohttps://link.springer.com/article/10.1111%2Fj.1447-073x.2005.00106.x
Final Diagnosis -- Case 340  Final Diagnosis -- Case 340
A role for the Adenomatous Polyposis Coli protein in chromosome segregation Kaplan, et al. (2001), Nature Cell Biol 3:429-432 * ... Familial Adenomatous Polyposis (FAP), also known as adenomatous polyposis coli (APC), is an autosomal dominant (AD) disorder ... Rapid detection of translation-terminating mutations at the adenomatous polyposis coli (APC) gene by direct protein truncation ... Final Diagnosis -- Familial adenomatous polyposis. FINAL DIAGNOSIS: FAMILIAL ADENOMATOUS POLYPOSIS, ATTENUATED TYPE.. ...
more infohttp://path.upmc.edu/cases/case340/dx.html
Targeted deletion of the C-terminus of the mouse adenomatous polyposis coli tumor suppressor results in neurologic phenotypes...  Targeted deletion of the C-terminus of the mouse adenomatous polyposis coli tumor suppressor results in neurologic phenotypes...
Loss of adenomatous polyposis coli (APC) gene function results in constitutive activation of the canonical Wnt pathway and ... a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and development ... Mutations of the tumor suppressor gene adenomatous polyposis coli (APC) are responsible for familial adenomatous polyposis (FAP ... Loss of adenomatous polyposis coli (APC) gene function results in constitutive activation of the canonical Wnt pathway and ...
more infohttps://molecularbrain.biomedcentral.com/articles/10.1186/1756-6606-7-21
Familial adenomatous polyposis - Wikipedia  Familial adenomatous polyposis - Wikipedia
The APC is a tumour suppressor gene responsible for the production of adenomatous polyposis coli (APC), a large multifunction ... APC regulates β-catenin, a protein that plays a crucial role in cell communication, signalling, growth, and controlled ... Familial adenomatous polyposis (FAP) is an autosomal dominant inherited condition in which numerous adenomatous polyps form ... The third variant, autosomal recessive familial adenomatous polyposis or MYH-associated polyposis, is also milder and, as its ...
more infohttps://en.m.wikipedia.org/wiki/Familial_adenomatous_polyposis
Tanneberger K et al. (2011), 
		
		
			Structural and functional characterization of t... -
		
		Xenbase Paper
	  Tanneberger K et al. (2011), Structural and functional characterization of t... - Xenbase Paper
Amer1/WTX binds to the tumor suppressor adenomatous polyposis coli and acts as an inhibitor of Wnt signaling by inducing β- ... The data suggest that Amer1 exerts its negative regulatory role in Wnt signaling by acting as a scaffold protein for the β- ... adenomatous polyposis coli, and Axin/Conductin. Deletion or specific mutations of the membrane binding domain of Amer1 abolish ...
more infohttp://www.xenbase.org/literature/article.do?method=display&articleId=43661
RCSB PDB - Protein Feature View 









 - Adenomatous polyposis coli protein - P25054 (APC HUMAN)  RCSB PDB - Protein Feature View - Adenomatous polyposis coli protein - P25054 (APC HUMAN)
The PDB archive contains information about experimentally-determined structures of proteins, nucleic acids, and complex ... This protein in other organisms (by gene name): P25054 - Homo sapiens 25 * Q93042 - Homo sapiens no matching PDB entries ... Protein disorder predictions are based on JRONN (Troshin, P. and Barton, G. J. unpublished), a Java implementation of RONN * ... The Protein Feature View requires a browser that supports SVG (Scalable Vector Graphics). Mouse over tracks and labels for more ...
more infohttp://www.rcsb.org/pdb/protein/P25054
Expression of Adenomatous Polyposis Coli Protein in Reactive Astrocytes in Hippocampus of Kainic Acid-Induced Rat | Springer...  Expression of Adenomatous Polyposis Coli Protein in Reactive Astrocytes in Hippocampus of Kainic Acid-Induced Rat | Springer...
The adenomatous polyposis coli gene (APC) was initially identified through its link to colon cancer. It is associated with the ... Expression of Adenomatous Polyposis Coli Protein in Reactive Astrocytes in Hippocampus of Kainic Acid-Induced Rat. ... Näthke IS (2004) The adenomatous polyposis coli protein: the Achilles heel of the gut epithelium. Annu Rev Cell Dev Biol 20:337 ... Senda T, Iino S, Matsushita K et al (1998) Localization of the adenomatous polyposis coli tumour suppressor protein in the ...
more infohttps://rd.springer.com/article/10.1007/s11064-009-0036-3
The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules | PNAS  The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules | PNAS
The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules. Lisbeth Berrueta, ... The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules ... The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules ... The adenomatous polyposis coli-binding protein EB1 is associated with cytoplasmic and spindle microtubules ...
more infohttps://www.pnas.org/content/95/18/10596?ijkey=86ca88e0e1cef3cddc4dda3ffda41e4e62ce6159&keytype2=tf_ipsecsha
Adenomatous Polyposis Coli (APC) Protein Moves along Microtubules and Concentrates at Their Growing Ends in Epithelial Cells |...  Adenomatous Polyposis Coli (APC) Protein Moves along Microtubules and Concentrates at Their Growing Ends in Epithelial Cells |...
... adenomatous polyposis coli; GFP, green fluorescent protein; MAP, microtubule-associated protein; MT, microtubule; pAb, ... Adenomatous Polyposis Coli (APC) Protein Moves along Microtubules and Concentrates at Their Growing Ends in Epithelial Cells. ... Adenomatous polyposis coli (APC) tumor suppressor protein has been shown to be localized near the distal ends of microtubules ( ... 1996) The adenomatous polyposis coli tumor suppressor protein localizes to plasma membrane sites involved in active cell ...
more infohttp://jcb.rupress.org/content/148/3/505?ijkey=9f526ecc567d7ba2756be6681d9e05480e12b08c&keytype2=tf_ipsecsha
Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)...  Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)...
Adenomatous Polyposis Coli/pathology. *Adenomatous Polyposis Coli Protein/genetics. *Adenomatous Polyposis Coli Protein/ ... The majority of sporadic colorectal cancers are triggered by mutations in the adenomatous polyposis coli (APC) tumor suppressor ... Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)- ... Cross-Species Comparison of Human and Mouse Intestinal Polyps Reveals Conserved Mechanisms in Adenomatous Polyposis Coli (APC)- ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/18403596?dopt=Abstract
Adenomatous polyposis coli (APC)  family (IPR026818) | InterPro | EMBL-EBI  Adenomatous polyposis coli (APC) family (IPR026818) | InterPro | EMBL-EBI
We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their ... InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites ... Adenomatous polyposis coli (APC) family (IPR026818) *Adenomatous polyposis coli (IPR026836). *Adenomatous polyposis coli 2 ( ... The adenomatous polyposis coli protein family also includes APC2 [PMID: 10021369, PMID: 11691822] and APC-related protein 1 [ ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR026818
PDB 1jpp structure summary ‹ Protein Data Bank in Europe (PDBe) ‹ EMBL-EBI  PDB 1jpp structure summary ‹ Protein Data Bank in Europe (PDBe) ‹ EMBL-EBI
Molecular mechanisms of beta-catenin recognition by adenomatous polyposis coli revealed by the structure of an APC-beta-catenin ... Adenomatous polyposis coli protein Chains: C, D Molecule details › Chains: C, D. Length: 15 amino acids. Theoretical weight: ... The Structure of a beta-Catenin Binding Repeat from Adenomatous Polyposis Coli (APC) in Complex with beta-Catenin. ... Molecular mechanisms of beta-catenin recognition by adenomatous polyposis coli revealed by the structure of an APC-beta-catenin ...
more infohttp://www.ebi.ac.uk/pdbe/entry/pdb/1jpp
Activation of Wnt/β-catenin signalling affects differentiation of cells arising from the cerebellar ventricular zone.  Activation of Wnt/β-catenin signalling affects differentiation of cells arising from the cerebellar ventricular zone.
0/Adenomatous Polyposis Coli Protein; 0/Biological Markers; 0/SOX9 Transcription Factor; 147336-22-9/Green Fluorescent Proteins ... Adenomatous Polyposis Coli Protein / metabolism. Animals. Apoptosis. Biological Markers / metabolism. Cell Differentiation*. ... Ivaniutsin U,, Chen Y,, Mason JO,, Price DJ,, Pratt T, (Year: 2009) Adenomatous polyposis coli is required for early events in ... Benchabane H,, Ahmed Y, (Year: 2009) The adenomatous polyposis coli tumor suppressor and Wnt signaling in the regulation of ...
more infohttp://www.biomedsearch.com/nih/Activation-Catenin-Signalling-Affects-Differentiation/22880037.html
Anti-APC antibody [CC-1] (ab16794) | Abcam  Anti-APC antibody [CC-1] (ab16794) | Abcam
Adenomatous Polyposis Coli antibody. *Adenomatous polyposis coli protein antibody. *Apc antibody. *APC_HUMAN antibody ... Belongs to the adenomatous polyposis coli (APC) family.. Contains 7 ARM repeats. ... Defects in APC are a cause of familial adenomatous polyposis (FAP) [MIM:175100]; which includes also Gardner syndrome (GS). FAP ... Desmoid tumors appears also as a complication of familial adenomatous polyposis.. Defects in APC are a cause of medulloblastoma ...
more infohttps://www.abcam.com/apc-antibody-cc-1-ab16794.html
  • Because familial polyposis develops very gradually over years, and can also manifest in an 'attenuated' form even more gradually, polyps resulting from FAP can lead to cancer developing at any point from adolescence to old age. (wikipedia.org)
  • Three variants are known to exist, FAP and attenuated FAP (originally called hereditary flat adenoma syndrome ) are caused by APC gene defects on chromosome 5 while autosomal recessive FAP (or MYH-associated polyposis ) is caused by defects in the MUTYH gene on chromosome 1. (wikipedia.org)
  • This protein also helps ensure that the chromosome number in cells produced through cell division is correct. (wikipedia.org)
  • The protein has been localized to the kinetochore and plays a role in the inhibition of the anaphase-promoting complex/cyclosome (APC/C), delaying the onset of anaphase and ensuring proper chromosome segregation. (wikipedia.org)
  • Consistent with the idea that such dominant effects are normally balanced by interactions within the full-length molecule, protein interactions of N-terminal fragments expressed in tumour cells can be altered by binding to C-terminal regions of APC commonly lost in tumours. (biochemsoctrans.org)
  • Identification of APC2, a homologue of the adenomatous polyposis coli tumour suppressor. (ebi.ac.uk)
  • In addition, RINGdb offers various user-friendly query functions to answer different questions about RGS proteins and GPCRs such as their possible contribution to disease processes, the putative direct or indirect relationship between RGS proteins and GPCRs. (biomedcentral.com)
  • The APC gene encodes a 300-kD protein, consisting of 2,843 amino acids, which has several structural domains. (rupress.org)
  • The middle part of the protein contains three successive 15-amino acid (aa) repeats, followed by seven related but distinct 20-aa repeats. (rupress.org)
  • The full-length human protein comprises 2,843 amino acids with a (predicted) molecular mass of 311646 Da. (wikipedia.org)
  • It is not known if this large predicted unstructured region from amino acid 800 to 2843 persists in vivo or would form stabilised complexes - possibly with yet unidentified interacting proteins. (wikipedia.org)
  • This mutation results in the substitution of the amino acid lysine for isoleucine at position 1307 in the APC protein (also written as I1307K or Ile1307Lys). (wikipedia.org)
  • This mutation replaces the amino acid isoleucine with the amino acid lysine at position 1307 in the APC protein (written as Ile1307Lys or I1307K). (nih.gov)
  • Leroy K, Duyckaerts C, Bovekamp L et al (2001) Increase of adenomatous polyposis coli immunoreactivity is a marker of reactive astrocytes in Alzheimer's disease and in other pathological conditions. (springer.com)
  • The (Adenomatous Polyposis Coli) APC protein normally builds a "destruction complex" with glycogen synthase kinase 3-alpha and or beta (GSK-3α/β) and axin via interactions with the 20 AA and SAMP repeats[citation needed]. (wikipedia.org)
  • The deactivation of the APC protein can take place after certain chain reactions in the cytoplasm are started, e.g. through the Wnt signals that destroy the conformation of the complex[citation needed]. (wikipedia.org)
  • The Apc gene product (APC), basically a cytoplasmic protein, blocks cell cycle progression and plays crucial roles in development. (springer.com)
  • Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesis. (nih.gov)
  • Suppression of intestinal polyposis in Apc delta716 knockout mice by inhibition of cyelooxygenase2 (COX-2). (springer.com)
  • Like endogenous APC and EB1, fluorescent protein fusions of APC and EB1 localize preferentially to the mother centriole. (biologists.org)
  • Through its C-terminus, APC binds to post-synaptic density discs large zonula occludens domain-containing proteins, such as discs large (DLG) and post-synaptic density (PSD)-95, and may play important roles in epithelial morphogenesis, brain development and neuronal functions. (springer.com)
  • The structure of the APC protein provides many hints about its possible cellular function. (rupress.org)
  • The protein made by the APC gene plays a critical role in several cellular processes that determine whether a cell may develop into a tumor. (wikipedia.org)
  • This short protein cannot suppress the cellular overgrowth that leads to the formation of polyps, which can become cancerous. (wikipedia.org)
  • The APC gene provides instructions for making the APC protein, which plays a critical role in several cellular processes. (nih.gov)
  • These cytoskeletal systems differ from each other in a variety of fundamental ways, and each is associated with characteristic accessory and regulatory proteins. (keystonesymposia.org)