Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.Databases, Protein: Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.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.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.Systems Integration: The procedures involved in combining separately developed modules, components, or subsystems so that they work together as a complete system. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.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.Sodium Azide: A cytochrome oxidase inhibitor which is a nitridizing agent and an inhibitor of terminal oxidation. (From Merck Index, 12th ed)Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).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.Antibody Specificity: The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.alpha Catenin: A catenin that binds F-ACTIN and links the CYTOSKELETON with BETA CATENIN and GAMMA CATENIN.Antibodies, Viral: Immunoglobulins produced in response to VIRAL ANTIGENS.Antibodies, Monoclonal: Antibodies produced by a single clone of cells.Sus scrofa: A species of SWINE, in the family Suidae, comprising a number of subspecies including the domestic pig Sus scrofa domestica.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.Adherens Junctions: Anchoring points where the CYTOSKELETON of neighboring cells are connected to each other. They are composed of specialized areas of the plasma membrane where bundles of the ACTIN CYTOSKELETON attach to the membrane through the transmembrane linkers, CADHERINS, which in turn attach through their extracellular domains to cadherins in the neighboring cell membranes. In sheets of cells, they form into adhesion belts (zonula adherens) that go all the way around a cell.Intercellular Junctions: Direct contact of a cell with a neighboring cell. Most such junctions are too small to be resolved by light microscopy, but they can be visualized by conventional or freeze-fracture electron microscopy, both of which show that the interacting CELL MEMBRANE and often the underlying CYTOPLASM and the intervening EXTRACELLULAR SPACE are highly specialized in these regions. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p792)Adenomatous Polyposis Coli Protein: A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.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.Ligands: A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)Cell Adhesion: Adherence of cells to surfaces or to other cells.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.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.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Moon: The natural satellite of the planet Earth. It includes the lunar cycles or phases, the lunar month, lunar landscapes, geography, and soil.Armadillo Domain Proteins: A family of proteins that contain several 42-amino acid repeat domains and are homologous to the Drosophila armadillo protein. They bind to other proteins through their armadillo domains and play a variety of roles in the CELL including SIGNAL TRANSDUCTION, regulation of DESMOSOME assembly, and CELL ADHESION.Trans-Activators: Diffusible gene products that act on homologous or heterologous molecules of viral or cellular DNA to regulate the expression of proteins.Research Report: Detailed account or statement or formal record of data resulting from empirical inquiry.Armadillos: Burrowing, chiefly nocturnal mammals of the family Dasypodidae having bodies and heads encased in small bony plates. They are widely distributed in the warmer parts of the Americas.TCF Transcription Factors: A family of DNA-binding proteins that are primarily expressed in T-LYMPHOCYTES. They interact with BETA CATENIN and serve as transcriptional activators and repressors in a variety of developmental processes.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.Awards and PrizesTranscription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.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.Linitis Plastica: A condition where the stomach wall becomes thickened, rubbery and loses its ability to distend. The stomach assumes a "leather bottle" shape. It is most often seen in adenocarcinoma of the stomach. The term is often used synonymously with diffuse adenocarcinoma of the stomach.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.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.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.Web Browser: Software application for retrieving, presenting and traversing information resources on the World Wide Web.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.Glioblastoma: A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.Epithelial-Mesenchymal Transition: Phenotypic changes of EPITHELIAL CELLS to MESENCHYME type, which increase cell mobility critical in many developmental processes such as NEURAL TUBE development. NEOPLASM METASTASIS and DISEASE PROGRESSION may also induce this transition.Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.Neurosurgery: A surgical specialty concerned with the treatment of diseases and disorders of the brain, spinal cord, and peripheral and sympathetic nervous system.Cell Line, Tumor: A cell line derived from cultured tumor cells.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.AlabamaCarcinoma, Hepatocellular: A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.TexasLiver Neoplasms: Tumors or cancer of the LIVER.Clinical Trials, Phase I as Topic: Works about studies performed to evaluate the safety of diagnostic, therapeutic, or prophylactic drugs, devices, or techniques in healthy subjects and to determine the safe dosage range (if appropriate). These tests also are used to determine pharmacologic and pharmacokinetic properties (toxicity, metabolism, absorption, elimination, and preferred route of administration). They involve a small number of persons and usually last about 1 year. This concept includes phase I studies conducted both in the U.S. and in other countries.

Alzheimer's disease: clues from flies and worms. (1/5919)

Presenilin mutations give rise to familial Alzheimer's disease and result in elevated production of amyloid beta peptide. Recent evidence that presenilins act in developmental signalling pathways may be the key to understanding how senile plaques, neurofibrillary tangles and apoptosis are all biochemically linked.  (+info)

The human F box protein beta-Trcp associates with the Cul1/Skp1 complex and regulates the stability of beta-catenin. (2/5919)

Ubiquitin-conjugation targets numerous cellular regulators for proteasome-mediated degradation. Thus, the identification of ubiquitin ligases and their physiological substrates is crucially important, especially for those cases in which aberrant levels of regulatory proteins (e.g., beta-catenin, p27) result from a deregulated ubiquitination pathway. In yeast, the proteolysis of several G1 regulators is controlled by ubiquitin ligases (or SCFs) formed by three subunits: Skp1, Cul A (Cdc53), and one of many F-box proteins. Specific F-box proteins (Fbps) recruit different substrates to the SCF. Although many Fbps have been identified in mammals, their specific substrates and the existence of multiple SCFs have not yet been reported. We have found that one human Fbp, beta-Trcp (beta-Transducin repeat containing protein), does indeed form a novel SCF with human Skp1 and Cul1. Consistent with recent reports indicating that Xenopus and Drosophila beta-Trcp homologs act as negative regulators of the Wnt/beta-catenin signaling pathway, we report here that human beta-Trcp interacts with beta-catenin in vivo. Furthermore, beta-catenin is specifically stabilized in vivo by the expression of a dominant negative beta-Trcp. These results indicate that the Cul1/Skp1/beta-Trcp complex forms a ubiquitin ligase that mediates the degradation of beta-catenin.  (+info)

Axin prevents Wnt-3a-induced accumulation of beta-catenin. (3/5919)

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)

Glucocorticoid down-regulation of fascin protein expression is required for the steroid-induced formation of tight junctions and cell-cell interactions in rat mammary epithelial tumor cells. (4/5919)

Glucocorticoid hormones, which are physiological regulators of mammary epithelium development, induce the formation of tight junctions in rat Con8 mammary epithelial tumor cells. We have discovered that, as part of this process, the synthetic glucocorticoid dexamethasone strongly and reversibly down-regulated the expression of fascin, an actin-bundling protein that also interacts with the adherens junction component beta-catenin. Ectopic constitutive expression of full-length mouse fascin containing a Myc epitope tag (Myc-fascin) in Con8 cells inhibited the dexamethasone stimulation of transepithelial electrical resistance, disrupted the induced localization of the tight junction protein occludin and the adherens junction protein beta-catenin to the cell periphery, and prevented the rearrangement of the actin cytoskeleton. Ectopic expression of either the carboxyl-terminal 213 amino acids of fascin, which includes the actin and beta-catenin-binding sites, or the amino-terminal 313 amino acids of fascin failed to disrupt the glucocorticoid induction of tight junction formation. Mammary tumor cells expressing the full-length Myc-fascin remained generally glucocorticoid responsive and displayed no changes in the levels or protein-protein interactions of junctional proteins or the amount of cytoskeletal associated actin filaments. However, a cell aggregation assay demonstrated that the expression of Myc-fascin abrogated the dexamethasone induction of cell-cell adhesion. Our results implicate the down-regulation of fascin as a key intermediate step that directly links glucocorticoid receptor signaling to the coordinate control of junctional complex formation and cell-cell interactions in mammary tumor epithelial cells.  (+info)

Frequent nuclear/cytoplasmic localization of beta-catenin without exon 3 mutations in malignant melanoma. (5/5919)

Beta-Catenin has a critical role in E-cadherin-mediated cell-cell adhesion, and it also functions as a downstream signaling molecule in the wnt pathway. Mutations in the putative glycogen synthase kinase 3beta phosphorylation sites near the beta-catenin amino terminus have been found in some cancers and cancer cell lines. The mutations render beta-catenin resistant to regulation by a complex containing the glycogen synthase kinase 3beta, adenomatous polyposis coli, and axin proteins. As a result, beta-catenin accumulates in the cytosol and nucleus and activates T-cell factor/ lymphoid enhancing factor transcription factors. Previously, 6 of 27 melanoma cell lines were found to have beta-catenin exon 3 mutations affecting the N-terminal phosphorylation sites (Rubinfeld B, Robbins P, Elgamil M, Albert I, Porfiri E, Polakis P: Stabilization of beta-catenin by genetic defects in melanoma cell lines. Science 1997, 275:1790-1792). To assess the role of beta-catenin defects in primary melanomas, we undertook immunohistochemical and DNA sequencing studies in 65 melanoma specimens. Nuclear and/or cytoplasmic localization of beta-catenin, a potential indicator of wnt pathway activation, was seen focally within roughly one third of the tumors, though a clonal somatic mutation in beta-catenin was found in only one case (codon 45 Ser-->Pro). Our findings demonstrate that beta-catenin mutations are rare in primary melanoma, in contrast to the situation in melanoma cell lines. Nonetheless, activation of beta-catenin, as indicated by its nuclear and/or cytoplasmic localization, appears to be frequent in melanoma, and in some cases, it may reflect focal and transient activation of the wnt pathway within the tumor.  (+info)

Expression of CD44 in Apc and Tcf mutant mice implies regulation by the WNT pathway. (6/5919)

Overexpression of cell surface glycoproteins of the CD44 family is an early event in the colorectal adenoma-carcinoma sequence. This suggests a link with disruption of APC tumor suppressor protein-mediated regulation of beta-catenin/Tcf-4 signaling, which is crucial in initiating tumorigenesis. To explore this hypothesis, we analyzed CD44 expression in the intestinal mucosa of mice and humans with genetic defects in either APC or Tcf-4, leading to constitutive activation or blockade of the beta-catenin/Tcf-4 pathway, respectively. We show that CD44 expression in the non-neoplastic intestinal mucosa of Apc mutant mice is confined to the crypt epithelium but that CD44 is strongly overexpressed in adenomas as well as in invasive carcinomas. This overexpression includes the standard part of the CD44 (CD44s) as well as variant exons (CD44v). Interestingly, deregulated CD44 expression is already present in aberrant crypt foci with dysplasia (ACFs), the earliest detectable lesions of colorectal neoplasia. Like ACFs of Apc-mutant mice, ACFs of familial adenomatous polyposis (FAP) patients also overexpress CD44. In sharp contrast, Tcf-4 mutant mice show a complete absence of CD44 in the epithelium of the small intestine. This loss of CD44 concurs with loss of stem cell characteristics, shared with adenoma cells. Our results indicate that CD44 expression is part of a genetic program controlled by the beta-catenin/Tcf-4 signaling pathway and suggest a role for CD44 in the generation and turnover of epithelial cells.  (+info)

Cadherin-11 is expressed in invasive breast cancer cell lines. (7/5919)

In several cancers, including breast cancer, loss of E-cadherin expression is correlated with a loss of the epithelial phenotype and with a gain of invasiveness. Cells that have lost E-cadherin expression are either poorly invasive with a rounded phenotype, or highly invasive, with a mesenchymal phenotype. Most cells lacking E-cadherin still retain weak calcium-dependent adhesion, indicating the presence of another cadherin family member. We have now examined the expression of the mesenchymal cadherin, cadherin-11, in breast cancer cell lines. Cadherin-11 mRNA and protein, as well as a variant form, are expressed in the most invasive cell lines but not in any of the noninvasive cell lines. Cadherin-11 is localized to a detergent-soluble pool and is associated with both alpha- and beta-catenin. Immunocytochemistry shows that cadherin-11 is localized to the cell membrane at sites of cell-cell contact as well as at lamellipodia-like projections, which do not interact with other cells. These results suggest that cadherin-11 expression may be well correlated with the invasive phenotype in cancer cells and may serve as a molecular marker for the more aggressive, invasive subset of tumors. Cadherin-11 may mediate the interaction between malignant tumor cells and other cell types that normally express cadherin-11, such as stromal cells or osteoblasts or perhaps even with the surrounding extracellular matrix, thus facilitating tumor cell invasion and metastasis.  (+info)

Coupling assembly of the E-cadherin/beta-catenin complex to efficient endoplasmic reticulum exit and basal-lateral membrane targeting of E-cadherin in polarized MDCK cells. (8/5919)

The E-cadherin/catenin complex regulates Ca++-dependent cell-cell adhesion and is localized to the basal-lateral membrane of polarized epithelial cells. Little is known about mechanisms of complex assembly or intracellular trafficking, or how these processes might ultimately regulate adhesion functions of the complex at the cell surface. The cytoplasmic domain of E-cadherin contains two putative basal-lateral sorting motifs, which are homologous to sorting signals in the low density lipoprotein receptor, but an alanine scan across tyrosine residues in these motifs did not affect the fidelity of newly synthesized E-cadherin delivery to the basal-lateral membrane of MDCK cells. Nevertheless, sorting signals are located in the cytoplasmic domain since a chimeric protein (GP2CAD1), comprising the extracellular domain of GP2 (an apical membrane protein) and the transmembrane and cytoplasmic domains of E-cadherin, was efficiently and specifically delivered to the basal-lateral membrane. Systematic deletion and recombination of specific regions of the cytoplasmic domain of GP2CAD1 resulted in delivery of <10% of these newly synthesized proteins to both apical and basal-lateral membrane domains. Significantly, >90% of each mutant protein was retained in the ER. None of these mutants formed a strong interaction with beta-catenin, which normally occurs shortly after E-cadherin synthesis. In addition, a simple deletion mutation of E-cadherin that lacks beta-catenin binding is also localized intracellularly. Thus, beta-catenin binding to the whole cytoplasmic domain of E-cadherin correlates with efficient and targeted delivery of E-cadherin to the lateral plasma membrane. In this capacity, we suggest that beta-catenin acts as a chauffeur, to facilitate transport of E-cadherin out of the ER and the plasma membrane.  (+info)

*p21

"Rapamycin potentiates transforming growth factor beta-induced growth arrest in nontransformed, oncogene-transformed, and human ...

*RET proto-oncogene

RET is an abbreviation for "rearranged during transfection", as the DNA sequence of this gene was originally found to be rearranged within a 3T3 fibroblast cell line following its transfection with DNA taken from human lymphoma cells.[6] The human gene RET is localized to chromosome 10 (10q11.2) and contains 21 exons.[7] The natural alternative splicing of the RET gene results in the production of 3 different isoforms of the protein RET. RET51, RET43 and RET9 contain 51, 43 and 9 amino acids in their C-terminal tail respectively.[8] The biological roles of isoforms RET51 and RET9 are the most well studied in-vivo as these are the most common isoforms in which RET occurs. Common to each isoform is a domain structure. Each protein is divided into three domains: an N-terminal extracellular domain with four cadherin-like repeats and a cysteine-rich region, a hydrophobic transmembrane domain and a cytoplasmic tyrosine kinase domain, which is split by an insertion of 27 amino acids. Within the ...

*Mdm2

Wang P, Gao H, Ni Y, Wang B, Wu Y, Ji L, Qin L, Ma L, Pei G (February 2003). "Beta-arrestin 2 functions as a G-protein-coupled ... Wang P, Wu Y, Ge X, Ma L, Pei G (March 2003). "Subcellular localization of beta-arrestins is determined by their intact N ... In addition, MDM2 has p53-independent transcription factor-like effects in nuclear factor-kappa beta (NFκB) activation. ...

*SDHB

Tryptophan alpha,beta-oxidase. *Pyrroloquinoline-quinone synthase. *L-galactonolactone oxidase. 1.3.5: Quinone. *Succinate ...

*Myc

beta-catenin-TCF complex assembly. • transcription, DNA-templated. • transcription from RNA polymerase II promoter. • G1/S ... Feng XH, Liang YY, Liang M, Zhai W, Lin X (January 2002). "Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-beta ... "Mechanism for the transcriptional repression by c-Myc on PDGF beta-receptor". Journal of Cell Science. 114 (Pt 8): 1533-44. ...

*Chromosome 20

CTNNBL1: Beta-catenin-like protein 1. *DBNDD2: Dysbindin domain-containing protein 2 ...

*CDH1 (gene)

Catenin-associated Fer and Fyn tyrosine kinases regulate beta-catenin Tyr-142 phosphorylation and beta-catenin-alpha-catenin ... phosphorylated region vital to beta-catenin binding and, therefore, to E-cadherin function.[citation needed] Beta-catenin can ... increases beta-catenin-E-cadherin association, and decreases beta-catenin-sensitive transcription". Cancer Research. 61 (4): ... "The structure of the beta-catenin/E-cadherin complex and the molecular basis of diverse ligand recognition by beta-catenin". ...

*CD97

"Beta-catenin--a linchpin in colorectal carcinogenesis?". The American Journal of Pathology. 160 (2): 389-401. doi:10.1016/s0002 ... regulates the stability of β-catenin in cytoplasm and subsequently, cytosolic β-catenin moves into the nucleus to facilitate ... Transgenic expression of a CD97 in mice enhanced levels of nonphosphorylated membrane-bound β-catenin and phosphorylated Akt.[ ... It has been shown that CD97 regulates localization and degradation of β-catenin.[24] GSK-3β, inhibited in some cancer, ...

*PSEN1

... and stabilize beta-catenin.[20] Mutant of presenilin-1 that reduces the ability to stabilize beta-catenin complex leads to ... presenilin-1 was also found to play a role in beta-catenin phosphorylation.[21] Beta-catenin is coupled by presenilin-1 and ... "Presenilin couples the paired phosphorylation of beta-catenin independent of axin: implications for beta-catenin activation in ... beta-catenin binding. • protein binding. • calcium channel activity. • aspartic-type endopeptidase activity. • endopeptidase ...

*Endometrial cancer

CTNNB1 (beta-catenin; a transcription gene) mutations are found in 14-44% of endometrial cancers and may indicate a good ... Beta-catenin mutations are commonly found in endometrial cancers with squamous cells. FGFR2 mutations are found in ... The CTNNB1 (beta-catenin) gene is most commonly mutated in the squamous subtype of endometrioid adenocarcinoma. Serous ...

*Endothelial stem cell

The result is an uncontrolled production of beta-catenin, which regulates cell growth and cell mobility. With uncontrolled beta ... catenin, the cell loses its adhesive properties. As ECs get packed together to create the lining for a new blood vessel, a ...

*TBX2

Wnt/beta-catenin Pathway. The role of Tbx2 in Wnt signaling has yet to be confirmed; however, up-regulation of Tbx2 in the beta ... catenin signaling pathway leads to loss of the adhesion molecule E-cadherin. This returns cells to a mesenchymal state, and ...

*FZD6

"Wnt-4 activates the canonical beta-catenin-mediated Wnt pathway and binds Frizzled-6 CRD: functional implications of Wnt/beta- ... beta-catenin signaling cascade". The Journal of Biological Chemistry. 279 (15): 14879-88. doi:10.1074/jbc.M306421200. PMID ... catenin activity in kidney epithelial cells". Experimental Cell Research. 298 (2): 369-87. doi:10.1016/j.yexcr.2004.04.036. ...

*Cyclin-dependent kinase 8

"CDK8 is a colorectal cancer oncogene that regulates beta-catenin activity". Nature. 455 (7212): 547-51. doi:10.1038/nature07179 ... CDK8 is a colorectal cancer oncogene: the CDK8 gene is amplified in human colorectal tumors, activating β-catenin-mediated ... β-catenin signaling, but could instead be a tumor suppressor gene in cancers driven by notch or EGFR signaling. In addition, ... "The TRAP/Mediator coactivator complex interacts directly with estrogen receptors alpha and beta through the TRAP220 subunit ...

*Prostaglandin receptor

stimulates AC, raises cAMP, stimulates beta catenin and Glycogen synthase kinase 3 ...

*FZD5

Holmen SL, Robertson SA, Zylstra CR, Williams BO (2005). "Wnt-independent activation of beta-catenin mediated by a Dkk1-Fz5 ... "A novel frizzled gene identified in human esophageal carcinoma mediates APC/beta-catenin signals". Proc. Natl. Acad. Sci. U.S.A ... "Caveolin is necessary for Wnt-3a-dependent internalization of LRP6 and accumulation of beta-catenin". Dev. Cell. 11 (2): 213-23 ... amyloid-beta binding. • signal transducer activity. • Wnt-protein binding. • protein binding. • protein kinase binding. • ...

*PITX2

"Identification of a Wnt/Dvl/beta-Catenin --> Pitx2 pathway mediating cell-type-specific proliferation during development". Cell ...

*CTNNBL1

Beta-catenin-like protein 1 is a protein that in humans is encoded by the CTNNBL1 gene. The protein encoded by this gene ... "Entrez Gene: CTNNBL1 catenin, beta like 1". Human CTNNBL1 genome location and CTNNBL1 gene details page in the UCSC Genome ... In addition, the encoded protein contains Armadillo/beta-catenin-like repeats, which have been implicated in protein-protein ...

*Androgen receptor

Yang F, Li X, Sharma M, Sasaki CY, Longo DL, Lim B, Sun Z (March 2002). "Linking beta-catenin to androgen-signaling pathway". ... Masiello D, Chen SY, Xu Y, Verhoeven MC, Choi E, Hollenberg AN, Balk SP (October 2004). "Recruitment of beta-catenin by wild- ... Amir AL, Barua M, McKnight NC, Cheng S, Yuan X, Balk SP (August 2003). "A direct beta-catenin-independent interaction between ... Beta-catenin, BRCA1, C-jun, Calmodulin 1, Caveolin 1, CDK9, COX5B, CREB-binding protein, Cyclin D1, Cyclin-dependent kinase 7, ...

*HDAC7

... and increased levels of active beta-catenin. Since each of these contribute to regulating cell proliferation, deletion of HDAC7 ... "Histone deacetylase 7 controls endothelial cell growth through modulation of beta-catenin". Circulation Research. 106 (7): 1202 ... One study showed that HDAC7 suppresses proliferation and β-catenin activity in chondrocytes. This was shown by knocking out ... Overall, this study demonstrated that HDAC7 once again interacts with β-catenin to keep endothelial cells in a low ...

*PDLIM1

"Identification of a Wnt/Dvl/beta-Catenin --> Pitx2 pathway mediating cell-type-specific proliferation during development". Cell ...

*Plakophilin-4

"Presenilins interact with armadillo proteins including neural-specific plakophilin-related protein and beta-catenin". J. ... A novel multiple PSD-95/Dlg-A/ZO-1 protein interacting with neural plakophilin-related armadillo repeat protein/delta-catenin ... A novel multiple PSD-95/Dlg-A/ZO-1 protein interacting with neural plakophilin-related armadillo repeat protein/delta-catenin ... local control of RhoA at the cleavage furrow by the p0071 catenin". Cell Cycle. 6 (2): 122-7. doi:10.4161/cc.6.2.3741. PMID ...

*TCF7L1

Graham TA, Weaver C, Mao F, Kimelman D, Xu W (Dec 2000). "Crystal structure of a beta-catenin/Tcf complex". Cell. 103 (6): 885- ... Balaz P, Plaschke J, Krüger S, Görgens H, Schackert HK (Aug 2010). "TCF-3, 4 protein expression correlates with beta-catenin ... These transcription factors are activated by beta catenin, mediate the Wnt signaling pathway and are antagonized by the ... "Lovastatin protects human neurons against Abeta-induced toxicity and causes activation of beta-catenin-TCF/LEF signaling". ...

*PCAF

Ge X, Jin Q, Zhang F, Yan T, Zhai Q (Jan 2009). "PCAF acetylates {beta}-catenin and improves its stability". Mol. Biol. Cell. ... Asano Y, Czuwara J, Trojanowska M (November 2007). "Transforming growth factor-beta regulates DNA binding activity of ...

*Mesenchyme

... by c-Fos estrogen receptor activation involves nuclear translocation of beta-catenin and upregulation of beta-catenin/lymphoid ... Mohamed, O. A.; Clarke, H. J.; Dufort, D (2004). "Beta-catenin signaling marks the prospective site of primitive streak ... Other deficiencies in signaling pathways, such as in Nodal (a TGF-beta protein), will lead to defective mesoderm formation.[9] ... Both formation of the primitive streak and mesenchymal tissue is dependent on the Wnt/β-catenin pathway.[12] Specific markers ...

*PDLIM1 - ويكيبيديا، الموسوعة الحرة

"Identification of a Wnt/Dvl/beta-Catenin --, Pitx2 pathway mediating cell-type-specific proliferation during development.". ...

*LMNA - 维基百科,自由的百科全书

连环蛋白(英语:Catenin). *Alpha catenin. *Beta catenin *APC ...

*Craniopharyngioma

December 2002). "Craniopharyngiomas of adamantinomatous type harbor beta-catenin gene mutations". Am. J. Pathol. 161 (6): 1997- ...
Aberrant activation of Wnt/beta-catenin signaling is recognized as a critical factor in the etiology of colorectal cancer. Evidence has suggested that dysregulated beta-catenin activity is associated with the majority of colon cancers via activation of the expression of Wnt regulated oncogenes. In the nucleus, beta-catenin regulates transcription by recruiting additional coactivators. These coactivators all have distinct and unique functions on Wnt/beta-catenin target gene activation. Here we report two coactivators for beta-catenin-mediated transcription: CCAR1 (Cell Cycle and Apoptosis Regulator 1) and CARM1 (coactivator-associated-protein-arginine-methyltransferase 1). We show that both CCAR1 and CARM1 interact with beta-catenin and positively modulate beta-catenin-mediated gene expression. In colorectal cancer cells, which have constitutively high Wnt/beta-catenin activity, depletion of CCAR1 or CARM1 inhibits the expression of Wnt/beta-catenin-mediated oncogenes and suppresses ...
Aberrant beta-catenin expression as determined by assessment of its subcellular localization constitutes a surrogate marker of Wnt signalling pathway activation and has been reported in a subset of breast cancers. The association of beta-catenin/Wnt pathway activation with clinical outcome and the mechanisms leading to its activation in breast cancers still remain a matter of controversy. The aims of this study were to address the distribution of beta-catenin expression in invasive breast cancers, the correlations between beta-catenin expression and clinicopathological features and survival of breast cancer patients, and to determine whether aberrant beta-catenin expression is driven by CTNNB1 (beta-catenin encoding gene) activating mutations. Immunohistochemistry was performed on a tissue microarray containing 245 invasive breast carcinomas from uniformly treated patients, using two anti-beta-catenin monoclonal antibodies. Selected samples were subjected to CTNNB1 exon 3 mutation analysis by ...
SMAD4 has been suggested to inhibit the activity of WNT/beta-catenin signaling pathway in cancer. However, the mechanism by which SMAD4 antagonizes WNT/beta-catenin signaling in cancer remains largely unknown. Aurora A kinase (AURKA), which is frequently overexpressed in cancer, increases the transcriptional activity of beta-catenin/T cell factor (TCF) complex by stabilizing beta-catenin through the inhibition of GSK-3beta. Here, SMAD4 modulated AURKA in a TGF-beta-independent manner. Overexpression of SMAD4 significantly suppressed AURKA function including colony formation, migration, and invasion of cell lines. In addition, SMAD4 bound to AURKA, induced degradation of AURKA by the proteasome. A luciferase activity assay revealed that the transcriptional activity of the beta-catenin/TCF complex was elevated by AURKA, but decreased by SMAD4 overexpression. Moreover, target gene analysis showed that SMAD4 abrogated the AURKA-mediated increase of beta-catenin target genes. However, this inhibitory ...
In the canonical Wnt signaling pathway, beta-catenin activates target genes through its interactions with Tcf/Lef-family transcription factors and additional transcriptional coactivators. The crystal structure of ICAT, an inhibitor of beta-catenin-mediated transcription, bound to the armadillo repeat domain of beta-catenin, has been determined. ICAT contains an N-terminal helilical domain that binds to repeats 11 and 12 of beta-catenin, and an extended C-terminal region that binds to repeats 5-10 in a manner similar to that of Tcfs and other beta-catenin ligands. Full-length ICAT dissociates complexes of beta-catenin, Lef-1, and the transcriptional coactivator p300, whereas the helical domain alone selectively blocks binding to p300. The C-terminal armadillo repeats of beta-catenin may be an attractive target for compounds designed to disrupt aberrant beta-catenin-mediated transcription associated with various cancers. ICAT inhibits beta-catenin binding to Tcf/Lef-family transcription factors ...
By means of the fluorescent differential display method, we isolated novel mouse and human genes, Drctnnb1a and DRCTNNB1A, the expression levels of which were inversely correlated to the amount of β-catenin present in cells. Recent reports have identified a number of mammalian genes including c-myc (6) , cyclin D1 (7) , matrilysin (8) , WISP (9) , c-jun, fra-1, uPAR, ZO-1 (10) , and NBL4 (11) that are regulated by stabilization and activation of β-catenin. In Xenopus or Drosophila, target genes for Wnt signaling include the nodal-related 3 gene, Xnr3 (17) , a member of the transforming growth factor-β superfamily, and homeobox genes engrailed (18) , goosecoid, siamois (17) , twin (19) , ultrabithorax (20) , and fibronectin (21) . Among those reported molecules, all but ZO-1 appeared to be up-regulated byβ -catenin through transactivation of Tcf/Lef transcription factors. Hence, DRCTNNB1A is only the second gene to be identified as down-regulated by the accumulation of β-catenin. ...
The PNU-74654 (PNU) compound is a non-FDAapproved drug which prevents that Tcf from binding to beta-catenin, acting as a Wnt/beta-catenin antagonist. In NCI-H295 cells,PNU-74654 significantly decreases cell proliferation 96 h after treatment, increases early and late apoptosis, decreases nuclear betacatenin accumulation, impairs CTNNB1/beta-catenin expression and increases betacatenin target genes 48 h after treatment. No effects are observed on HeLa cells. In NCI-H295 cells, PNU-74654 decreases cortisol, testosterone and androstenedione secretion 24 and 48 h after treatment. Additionally, in NCI-H295 cells, PNU-74654 decreases SF1 and CYP21A2 mRNA expression as well as the protein levels of STAR and aldosterone synthase 48 h after treatment. In Y1 cells, PNU-74654 impairs corticosterone secretion 24 h after treatment but does not decrease cell viability[2]. ...
Billin et al. (23) observed that TSA activated TOPflash reporter activity in HEK293 cells in the presence and absence of exogenous β-catenin and LEF1, and provided evidence that HDAC1 switches LEF1 from a repressor to a transcriptional activator. Our results confirm that TSA increases TOPflash reporter activity, and demonstrate that the effect of HDAC1 on LEF1 can be extended to TCF4, the major form of TCF/LEF in colonic mucosa. Thus, under certain circumstances, HDAC1 might influence whether TCF4 acts as a transcriptional activator or repressor in the Wnt signaling pathway. The present results also show that TOPflash reporter activity can be used as an indirect measure of HDAC activity, with an increase in reporter activity corresponding to a decrease in HDAC activity in cells treated with TSA or SFN.. SFN is an effective cancer chemopreventive agent in several animal models (10, 11, 12) and is thought to induce phase 2 detoxification enzymes through the interaction of Nrf-2 with the ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
Sigma-Aldrich offers abstracts and full-text articles by [Laurent Pangon, Dessislava Mladenova, Lauren Watkins, Christa Van Kralingen, Nicola Currey, Sam Al-Sohaily, Patrick Lecine, Jean-Paul Borg, Maija R J Kohonen-Corish].
Beta-catenin is a multifunctional protein involved both in cell adhesion and in activation of transcription. Calcium-dependent intercellular adhesion transmembrane glycoprotein E-cadherin interacts by its cytoplasmic domain with reciprocally bound alpha, beta and gamma catenin. Beta-catenin links this complex through alpha-actinin to the cytoskeleton. Functional cadherin-catenin system is important for invasiveness of tumour cells. Beta-catenin level in cytoplasm is controlled by glycogen synthase kinase-3 beta. When activity of this kinase is blocked (e.g. by excessive stimulation of Wnt signaling pathway), hypophosphorylated stable form of beta-catenin accumulates in the cytoplasm, translocates to the nucleus and activates transcription of genes including those that are involved in cell cycle control. As a result, cell division and neoplastic transformation are promoted ...
14-3-3ζ has been found to associate with β-catenin (Tian et al., 2004). Later, it was found that Akt phosphorylates β-catenin at serine 552, which appears to enhance its interaction with 14-3-3ζ (Fang et al., 2007). In both cases, ectopic expression of 14-3-3ζ resulted in a moderate activation (two- to fourfold) of β-catenin-dependent transcription in TopFlash assays. We found that 14-3-3ζ enhances, whereas 14-3-3η and ε isoforms repress, β-catenin activation of the TopFlash reporter (Fig. 5 A). One possible explanation for this observation is that 14-3-3 overexpression exerts complex biological effects, which makes our interpretation of the TopFlash results difficult. In fact, 14-3-3 proteins have been shown to interact with a plethora of target proteins ranging from transcription factors to various signaling molecules (Dougherty and Morrison, 2004; Pozuelo Rubio et al., 2004). However, it is interesting to note that, consistent with our results (Fig. 7 C), ectopic expression of ...
In Xenopus, Wnt signals and their transcriptional effector beta-catenin are required for the development of dorsal axial structures. In zebrafish, previous loss-of-function studies have not identified an essential role for beta-catenin in dorsal axis
Chandran K C ♦ December 11, 2015 ♦ Leave a comment Scientists and cancer researchers have lately identified a particular biological molecule in our body known as BETA CATENIN as an ideal molecular target for anti-cancer therapy. They have been trying to develop drugs that could inhibit the over-expressions and aberrations of BETA CATENIN, which is recognized to be playing a big role in the biochemical processes underlying various types of cancers. Their attempts have not been so far successful, since any chemical compound they develop to target BETA CATENIN will inevitably have serious harmful effects upon the organism, since it is an essential biological molecule having diverse roles normal vital processes, and its complete inhibition may lead to be very dangerous consequences.. BETA CATENIN is a protein found as part of molecular complexes in forming cadherin cell adhesion factors of animal cells. It belongs to a family of biological compounds known as catenins, consisting of alpha ...
View Notes - 2011_Questions_Week_14_Answers from BIO 349 at University of Texas. 1. What happens when you deplete beta catenin in planarians? -The organism is no longer able to form a posterior side
Background: β‐Catenin is an important signaling molecule in the Wnt pathway that plays a key role in tumorgenesis. In the absence of Wnt signaling, the cytoplasmic level of β‐catenin is kept low due to rapid proteasomal‐mediated degradation of GSK3β phosphorylated β‐catenin. Activation of Wnt signaling leads to the inactivation of GSK3β, resulting in stabilization and accumulation of β‐catenin in the cytoplasm. Consequently, β‐catenin translocates into the nucleus, where it binds with members of the T‐cell factor (Tcf)/lymphocyte enhancer‐binding factor family of transcription factors and activates the expression of many target genes important for cancer development. Most colon cancers have activating mutations in the APC tumor suppressor or in β‐catenin itself. Furthermore, activating β‐catenin mutations have been found in a variety of other tumors such as melanomas, hepatocellular carcinomas, skin, breast, and prostate cancer, whereas β‐catenin is not activated ...
J:215487 Thompson CL, Ng L, Menon V, Martinez S, Lee CK, Glattfelder K, Sunkin SM, Henry A, Lau C, Dang C, Garcia-Lopez R, Martinez-Ferre A, Pombero A, Rubenstein JL, Wakeman WB, Hohmann J, Dee N, Sodt AJ, Young R, Smith K, Nguyen TN, Kidney J, Kuan L, Jeromin A,Kaykas A, Miller J, Page D, Orta G, Bernard A, Riley Z, Smith S, Wohnoutka P, Hawrylycz MJ, Puelles L, Jones AR, A high-resolution spatiotemporal atlas of gene expression of the developing mouse brain. Neuron. 2014 Jul 16;83(2):309-23 ...
J:90567 Akiyama H, Lyons JP, Mori-Akiyama Y, Yang X, Zhang R, Zhang Z, Deng JM, Taketo MM, Nakamura T, Behringer RR, McCrea PD, de Crombrugghe B, Interactions between Sox9 and beta-catenin control chondrocyte differentiation. Genes Dev. 2004 May 1;18(9):1072-87 ...
Rabbit polyclonal beta Catenin (phospho Y489) antibody validated for WB, ICC and tested in Human. Immunogen corresponding to synthetic peptide
If you know of any papers that use this antibody, please contact us at antibodies [at] alzforum [dot] org for consideration in the References section.. ...
Looking for online definition of Beta catenin in the Medical Dictionary? Beta catenin explanation free. What is Beta catenin? Meaning of Beta catenin medical term. What does Beta catenin mean?
Lymphoid enhancer-binding factor 1 (LEF1) is a protein that in humans is encoded by the LEF1 gene. Lymphoid enhancer-binding factor-1 (LEF1) is a 48-kD nuclear protein that is expressed in pre-B and T cells. It binds to a functionally important site in the T-cell receptor-alpha (TCRA) enhancer and confers maximal enhancer activity. LEF1 belongs to a family of regulatory proteins that share homology with high mobility group protein-1 (HMG1). LEF1 is highly overexpressed and associated with disease progression and poor prognosis in B-cell chronic lymphocytic leukemia. It is also a promising potential drug target. Lymphoid enhancer-binding factor 1 has been shown to interact with: ALX4, AML-1, CTNNB1, EP300, MITF PIAS4, SMAD2, and SMAD3. GRCh38: Ensembl release 89: ENSG00000138795 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000027985 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". Milatovich A, Travis A, Grosschedl R, Francke U (Mar 1992). "Gene for lymphoid ...
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 ...
The Wnt signal transduction pathway is important in a wide variety of developmental processes as well as in the genesis of human cancer. Vertebrate Wnt pathways can be functionally separated into two classes, the canonical Wnt/beta-catenin pathway and the non-canonical Wnt/Ca2+ pathway. Supporting differences in Wnt signaling, gain of function of Wnt-1 in C57mg mouse mammary epithelial cells leads to their morphological transformation while loss of function of Wnt-5a leads to the same transformation. Many downstream target genes of the Wnt/beta-catenin pathway have been identified. In contrast, little is known about the Wnt/Ca2+ pathway and whether it regulates gene expression. To test the hypothesis that a specific cell line can respond to distinct Wnts with different patterns of gene expression, we over-expressed Wnt-5a and Rfz-2 in C57mg mammary epithelial cells and compared this cell line to C57mg cells over-expressing Wnt-1. These Wnts were chosen since previous studies suggest that C57mg cells
Akt-regulated pathways enhance cell division and cell survival. Metabolic regulation through Akt and its targets is important for insulin and insulin-like growth factor I-coupled responses. Inhibition of glycogen synthase kinase-3 by Akt-dependent phosphorylation promotes accumulation of β-catenin, which forms complexes with T-cell factor/lymphoid enhancer factor transcription factors and transcriptionally up-regulates cyclin D1, Myc, and other positive growth regulators. Cyclin D1 is also inhibited by glycogen synthase kinase-3 through effects on stability and localization (7) . Concomitantly, Akt phosphorylation of cyclin-dependent protein kinase inhibitors p21Cip1 and p27Kip1 interferes with negative growth regulation (3 , 8) .. Phosphorylation of Mdm2 by Akt enhances nuclear entry, which promotes ubiquitin-dependent proteolysis of p53, and impedes p53-dependent growth suppression and apoptosis (9) . Akt directly forestalls apoptosis by phosphorylation of proapoptotic Bad and caspase-9, ...
Catenin Beta 1, CTNNB are cell adhesion molecules called (p120*␠-catenin) cadherins (the (CDH1) E-cadherin/catenin complex) include the beta-catenins a multifunctional molecule Locus: 3p22.1 [§§; ^]. Neurons also exhibited a higher CTNNB/TCF pathway association (concentration versus accumulation) with cadherins; CAS-chromosome segregation 1-like (yeast) binds with E-cadherin but not with beta-catenin. Which interacts with (Tcf-T-cell factor where a…
A key component of the Wnt pathway, beta-catenin combines with alpha-catenin and regulates cell-cell adhesion. It also interacts with alpha-catenin in the nucleus.. The alpha-catenin component of this beta-catenin/alpha-catenin complex has an inhibitory effect on beta-catenin that helps keep tumor cell migration and invasion in check. This inhibition is lost, however, when the EGFR pathway is activated. Upon activation, beta-catenin becomes untethered from alpha-catenin and translocates to the cell nucleus, where it increases expression of key target genes involved in tumor cell invasion and metastasis.. New Pathway Regulates Beta-Catenin Transactivation. The M. D. Anderson-led team made a surprising discovery: Beta-catenin also can travel to the nucleus via activation of the EGFR pathway-and it does so independently of Wnt signaling or mutations. The newly described pathway disrupts the beta-catenin/alpha catenin complex through an EGFR-extracellular receptor kinase (ERK)-protein kinase CK2- ...
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
The canonical Wnt/beta-catenin pathway plays a key role in the regulation of bone remodeling in mice and humans. Two transmembrane proteins that are involved in decreasing the activity of this pathway by binding to extracellular antagonists, such as Dickkopf 1 (Dkk1), are the low-density lipoprotein receptor related protein 5 (Lrp5) and Kremen 2 (Krm2). Lrp 5 deficiency (Lrp5(-/-)) as well as osteoblast-specific overexpression of Krm2 in mice (Col1a1-Krm2) result in severe osteoporosis occurring at young age. In this study, we analyzed the influence of Lrp5 deficiency and osteoblast-specific overexpression of Krm2 on fracture healing in mice using flexible and semi-rigid fracture fixation. We demonstrated that fracture healing was highly impaired in both mouse genotypes, but that impairment was more severe in Col1a1-Krm2 than in Lrp5(-/-) mice and particularly evident in mice in which the more flexible fixation was used. Bone formation was more reduced in Col1a1-Krm2 than in Lrp5(-/-) mice, whereas
3.0.CO;2-P. PMID 10580987. McCrea PD, Turck CW, Gumbiner B (November 1991). "A homolog of the armadillo protein in Drosophila (plakoglobin) associated with E-cadherin". Science. 254 (5036): 1359-61. doi:10.1126/science.1962194. PMID 1962194. Kemler R (September 1993). "From cadherins to catenins: cytoplasmic protein interactions and regulation of cell adhesion". Trends in Genetics. 9 (9): 317-21. doi:10.1016/0168-9525(93)90250-l. PMID 8236461. Gottardi CJ, Peifer M (March 2008). "Terminal regions of beta-catenin come into view". Structure. 16 (3): 336-8. doi:10.1016/j.str.2008.02.005. PMC 2329800 . PMID 18334207. Xing Y, Takemaru K, Liu J, Berndt JD, Zheng JJ, Moon RT, Xu W (March 2008). "Crystal structure of a full-length beta-catenin". Structure. 16 (3): 478-87. doi:10.1016/j.str.2007.12.021. PMC 4267759 . PMID 18334222. Vleminckx K, Kemler R, Hecht A (March 1999). "The C-terminal transactivation domain of beta-catenin is necessary and sufficient for signaling by the LEF-1/beta-catenin complex ...
Component of the beta-catenin destruction complex required for regulating CTNNB1 levels through phosphorylation and ubiquitination, and modulating Wnt-signaling (By similarity). Controls dorsoventral patterning via two opposing effects; down-regulates CTNNB1 to inhibit the Wnt signaling pathway and ventralize embryos, but also dorsalizes embryos by activating a Wnt-independent JNK signaling pathway. In Wnt signaling, probably facilitates the phosphorylation of CTNNB1 and APC by GSK3B. Likely to function as a tumor suppressor. Facilitates the phosphorylation of TP53 by HIPK2 upon ultraviolet irradiation. Enhances TGF-beta signaling by recruiting the RNF111 E3 ubiquitin ligase and promoting the degradation of inhibitory SMAD7 (By similarity). Also component of the AXIN1-HIPK2-TP53 complex which controls cell growth, apoptosis and development.
Cadherins play an important role in morphogenesis and have recently been implicated in the regulation of cell proliferation, however the mechanisms by which they function are poorly understood. In the vertebrate CNS, loss of ,italic,N-cadherin (N-cad),,/, results in impaired neuroepithelial integrity. Zebrafish ,italic,N-cad,,/, null mutants also exhibit a transient increase in neurons and in cell proliferation in the neural tube. Here, we investigate the cellular and molecular basis for this phenotype, using multiple ,italic,N-cad,,/, alleles with distinct molecular properties. We confirm that cell proliferation is enhanced in ,italic,N-cad,,/, mutants, but contrary to previous findings, we observe that the increase is sustained over multiple stages of development. At the cellular level, loss of ,italic,N-cad,,/, results in a shorter cell cycle. Furthermore, we demonstrate that hyperproliferation is not linked to abnormal beta-catenin localization, suggesting that Wnt signaling is not ...
Cadherins play an important role in morphogenesis and have recently been implicated in the regulation of cell proliferation, however the mechanisms by which they function are poorly understood. In the vertebrate CNS, loss of ,italic,N-cadherin (N-cad),,/, results in impaired neuroepithelial integrity. Zebrafish ,italic,N-cad,,/, null mutants also exhibit a transient increase in neurons and in cell proliferation in the neural tube. Here, we investigate the cellular and molecular basis for this phenotype, using multiple ,italic,N-cad,,/, alleles with distinct molecular properties. We confirm that cell proliferation is enhanced in ,italic,N-cad,,/, mutants, but contrary to previous findings, we observe that the increase is sustained over multiple stages of development. At the cellular level, loss of ,italic,N-cad,,/, results in a shorter cell cycle. Furthermore, we demonstrate that hyperproliferation is not linked to abnormal beta-catenin localization, suggesting that Wnt signaling is not ...
CG-001 is a selective Wnt/β-catenin signalling inhibitor with an IC50 of 3μM. ICG 001, a small molecule that down-regulates beta-catenin/T cell factor signaling by specifically binding to cyclic AMP response element-binding protein. ICG001 selectively ind
Calcium-dependent homotypic cell-cell adhesion, mediated by molecules such as E-cadherin, guides the establishment of classical epithelial cell polarity and contributes to the control of migration, growth, and differentiation. These actions involve additional proteins, including alpha- and beta-catenin (or plakoglobin) and p120, as well as linkage to the cortical actin cytoskeleton. The molecular basis for these interactions and their hierarchy of interaction remain controversial. We demonstrate a direct interaction between F-actin and alpha (E)-catenin, an activity not shared by either the cytoplasmic domain of E-cadherin or beta-catenin. Sedimentation assays and direct visualization by transmission electron microscopy reveal that alpha 1(E)-catenin binds and bundles F-actin in vitro with micromolar affinity at a catenin/G-actin monomer ratio of approximately 1:7 (mol/mol). Recombinant human beta-catenin can simultaneously bind to the alpha-catenin/actin complex but does not bind actin ...
The farnesoid X receptor (FXR) controls the synthesis and transport of bile acids (BAs). Mice lacking expression of FXR, designated Fxr-null, have elevated levels of serum and hepatic BAs and an increase in BA pool size. Surprisingly, at 12 months of age, male and female Fxr-null mice had a high incidence of degenerative hepatic lesions, altered cell foci and liver tumors including hepatocellular adenoma, carcinoma and hepatocholangiocellular carcinoma, the latter of which is rarely observed in mice. At 3 months, Fxr-null mice had increased expression of the proinflammatory cytokine IL-1beta mRNA and elevated beta-catenin and its target gene c-myc. They also had increased cell proliferation as revealed by increased PCNA mRNA and BrdU incorporation. These studies reveal a potential role for FXR and BAs in hepatocarcinogenesis.
The study, published online in the September 2011 edition of The Journal of Neuroscience, identified Sox17 as the gene that helps regulate the Wnt/beta-catenin signaling pathway during the transition of oligodendrocyte progenitor cells, or immature brain cells, to a more mature, differentiated state where they generate myelin.. "This is the first time the Sox17 gene has been identified as a regulator of the Wnt/beta-catenin pathway during myelination," said Li-Jin Chew, PhD, lead author of the study. "Our findings indicate that loss of Sox17 over-stimulates the Wnt/beta-catenin pathway and keeps oligodendrocyte progenitor cells from maturing and producing myelin, potentially causing developmental disabilities in developing babies and children.". Myelin is the protective material around the axons of neurons; in mass these types of ensheathed neurons are collectively called white matter. White matter serves as the primary messaging "network" that conducts signals rapidly between gray matter areas. ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Negative regulator of the canonical Wnt signaling pathway involved in neuroectodermal patterning. Acts by specifically binding phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), translocating to the cell membrane and interacting with key regulators of the canonical Wnt signaling pathway, such as components of the beta-catenin destruction complex ...
Background: The Wnt/beta-catenin signaling pathway plays a key role in stem cell maintenance in the colorectum. Rare high penetrance genetic mutations in components of this pathway result in familial colorectal cancer, yet the impact of common, germline variants remains unknown. Methods: We assessed 172 variants in 26 genes from the Wnt/beta-catenin pathway in 809 CRC cases and 814 healthy controls, followed by replication of the top findings in another 691 cases and 775 controls. In silico informatic tools were used to predict functional effects of variants. Results: Eighteen SNPs in the pathway were significantly associated with CRC risk (P ,0.05) in the discovery phase. We observed a significant dose-response increase in CRC risk by number of risk genotypes carried (P = 4.19 x 10-8). Gene-based analysis implicated CSNK1D (P = 0.014), FZD3 (P = 0.023), and APC (P = 0.027) as significant for CRC risk. In the replication phase, FZD3:rs11775139 remained significantly associated with reduced risk ...
(a) Nuclear suprabasal beta-catenin (β-catenin) staining expression in all layers of epidermis except the parakeratotic and cornified layers of a psoriasis les
LEF1 antibody [1C3.1D10] (lymphoid enhancer-binding factor 1) for WB. Anti-LEF1 mAb (GTX12033) is tested in Human samples. 100% Ab-Assurance.
1I7X: The structure of the beta-catenin/E-cadherin complex and the molecular basis of diverse ligand recognition by beta-catenin.
ORoak and other (2012) sequenced the exomes, that is the DNA regions that code for the protein product of genes, of children with sporadic autism as well as of their parents and unaffected siblings. Sixhundredseventyseven exomes of 209 families were examined. Eighty percent of the discovered gene mutations were of paternal origin, increasing with age. Roughly 40 percent of the new protein-altering mutations were associated with a molecular signaling pathway regulating gene transcription through beta-catenin/chromatin remodeling. Recurrent mutations were found in genes CHD8 and NTNG1. The product of CHD8 is a protein involved in chromatin remodeling. This finding points at a specific molecular mechanism that may explain impaired transcription of the genetic code, representing the most disruptive genetic modification identified in this study according to the authors. NTNG1s product Netrin-G1 is a protein that serves as cue in nerve cell axon guidance and has been associated with schizophrenia. ...
TGF-β is a key profibrotic factor, but targeting TGF-β to prevent fibrosis also abolishes its protective anti-inflammatory effects. Here, we investigated the hypothesis that we can redirect TGF-β signaling by preventing downstream profibrotic interaction of β-catenin with T cell factor (TCF), thereby enhancing the interaction of β-catenin with Foxo, a transcription factor that controls differentiation of TGF-β induced regulatory T cells (iTregs), and thus, enhance anti-inflammatory effects of TGF-β In iTregs derived from EL4 T cells treated with recombinant human TGF-β1 (rhTGF-β1) in vitro, inhibition of β-catenin/TCF transcription with ICG-001 increased Foxp3 expression, interaction of β-catenin and Foxo1, binding of Foxo1 to the Foxp3 promoter, and Foxo transcriptional activity ...
CTNNB1 - CTNNB1 - Human, 4 unique 29mer shRNA constructs in retroviral untagged vector shRNA available for purchase from OriGene - Your Gene Company.
Human tongue surface with bacteria. Coloured scanning electron micrograph (SEM) of bacteria (yellow) amongst epithelial cells on the surface of a human tongue. Epithelial cells are flat, scale-like squamous cells that are constantly shed and replaced. The epithelium covers the sensory papillae (small projections, not seen) on the tongue, which are sensitive to several different sensory stimuli, including taste. Bacteria on the tongue surface is normal, but can cause halitosis (bad breath). Magnification: x1700 when printed 10 centimetres wide. - Stock Image C002/6112
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 ...
Developmentally, the pancreas and liver are closely related and pathological conditions − including elevated glucocorticoid levels − result in the appearance of hepatocytes in the pancreas. The role of the WNT signalling pathway in this process has been examined in the model transdifferentiating pancreatic acinar AR42J-B-13 (B-13) cell. Glucocorticoid treatment resulted in a transient loss of constitutive WNT3a expression, phosphorylation and depletion of β-catenin, loss of β-catenin nuclear localisation, and significant reductions in T-cell factor/lymphoid enhancer factor (Tcf/Lef) transcriptional activity before overt changes in phenotype into hepatocyte-like (B-13/H) cells. A return to higher Tcf/Lef transcriptional activity correlated with the re-expression of WNT3a in B-13/H cells. β-catenin knock down alone substituted for and enhanced glucocorticoid-dependent transdifferentiation. Overexpression of a mutant β-catenin (pt-Xβ-cat) protein that blocked glucocorticoid-dependent ...
Glycogen synthase kinase 3 (GSK3) was discovered as a metabolic enzyme, that regulates the response of glycogen synthase to insulin; however, it is now known to be active in a wide range of cellular processes, ranging from apoptosis to embryonic development (Cohen and Frame, 2001; Frame and Cohen, 2001; Harwood, 2001). In animal development, it is best known for its activity in Wnt signalling, where it regulates cellular differentiation, migration and growth (Miller, 2002). In the canonical Wnt/β-catenin pathway, cell stimulation by Wnt protein ligands leads to the accumulation and nuclear translocation of β-catenin, which acts as a transactivator for genes regulated by T-cell factor/lymphoid enhancer factor (TCF/LEF) (reviewed by Brantjes et al., 2002).. Dictyostelium has a single GSK3 homologue, GskA, that has 78% amino acid identity to mammalian GSK3β (Harwood et al., 1995). Upon starvation, neighbouring Dictyostelium amoebae aggregate, using cAMP as chemoattractant. The cells then ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
Cell-cell adherens junctions (AJs), the most common type of intercellular adhesions, are important for maintaining tissue architecture and cell polarity and can limit cell movement and proliferation. At AJs, E-cadherin serves as an essential cell adhesion molecules (CAMs). The cytoplasmic tail binds beta-catenin, which in turn binds alpha-catenin. Alpha-catenin is associated with F-actin bundles directly and indirectly. The integrity of the cadherin-catenin complex is negatively regulated by phosphorylation of beta-catenin by receptor tyrosine kinases (RTKs) and cytoplasmic tyrosine kinases (Fer, Fyn, Yes, and Src), which leads to dissociation of the cadherin-catenin complex. Integrity of this complex is positively regulated by beta -catenin phosphorylation by casein kinase II, and dephosphorylation by protein tyrosine phosphatases. Changes in the phosphorylation state of beta-catenin affect cell-cell adhesion, cell migration and the level of signaling beta-catenin. Wnt signaling acts as a ...
Wnt signaling controls diverse developmental processes such as axis formation, anteroposterior patterning and the development of the neural crest (Moon et al., 1997; Raible and Ragland, 2005; Wodarz and Nusse, 1998). Precise regulation is necessary for many developmental processes and misregulation of several components of the canonical Wnt signaling pathway has been implicated in cancer formation (Polakis, 2007). Conversely, reduction or loss of function of Wnt signaling leads to general developmental defects or loss of organs, demonstrating the need for a tight regulation of the levels of Wnt signaling (Logan and Nusse, 2004).. The Wnt signaling pathway is highly conserved among all metazoans. Wnt ligands bind to frizzled (fz) transmembrane receptors leading to accumulation and nuclear localization of β-catenin, which serves as a transcriptional co-activator for TCF/Lef transcription factors (Logan and Nusse, 2004; Wodarz and Nusse, 1998). In addition to this so called `canonical Wnt ...
By Ramis-Conde, Ignacio Drasdo, Dirk; Anderson, Alexander R A; Chaplain, Mark A J ABSTRACT In this article, we show, using a mathematical multiscale model, how cell adhesion may be regulated by interactions between E-cadherin and beta-catenin and how the control of cell adhesion may be related to cell migration, to the epithelial- mesenchymal transition and to invasion in populations of eukaryotic cells. E-cadherin mediates cell-cell adhesion and plays a critical role in the formation and maintenance of junctional contacts between cells. Loss of E-cadherin-mediated adhesion is a key feature of the epithelial-mesenchymal transition. beta-catenin is an intracellular protein associated with the actin cytoskeleton of a cell. E- cadherins bind to beta-catenin to form a complex which can interact both with neighboring cells to form bonds, and with the cytoskeleton of the cell. When cells detach from one another, beta-catenin is released into the cytoplasm, targeted for degradation, and downregulated. ...
When we examined solid pseudopapillary tumours of the pancreas, a tumour characterised by β‐catenin mutations within exon 3, these tumours showed a strong reduction in E‐cadherin:β‐catenin complexes. Moreover in HCC, a tumour type which has approximately 20% β‐catenin exon 3 mutations, there was a good correlation between reduction in E‐cadherin and activation of Wnt signalling targets. Thus, it may be that in these cancers, E‐cadherin limits the precise levels of Wnt signalling driven by β‐catenin mutation. Thus, downregulation of E‐cadherin in these tumours may drive tumour progression. It should also be noted that opposing patterns of Wnt signalling and E‐cadherin have been shown in murine liver, with β‐catenin higher in zone 3 of the liver and E‐cadherin in zone 1. Therefore, one might predict that β‐catenin mutations would yield a greater phenotype in hepatocytes from zone 3 of the liver versus zone 1 (Benhamouche et al, 2006). Hence, one could speculate ...
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 ...
Beginning at Leu 1029, the APC‐rA peptide adopts a conformation strikingly different from that of XTcf3 or E‐cadherin (Figure 3B). The C‐terminal half of the peptide, from Leu1029 to Glu1034, bulges out of the β‐catenin groove, away from the paths of XTcf3 and E‐cadherin (Figures 2B and 3B). This difference in conformation is probably due to the presence of a lysine residue at amino acid 1030 of APC‐rA. In XTcf3 and E‐cadherin this position is occupied by an acidic residue (Glu24 of XTcf3, Glu682 of E‐cadherin), which forms a salt bridge with β‐catenin Lys312 to form the second charged button of the extended region (Figure 3B). The lysine at this position in APC‐rA probably causes charge repulsion with β‐catenin Lys312, leading to a deviation from the conformations of the other two ligands. The conformation of the backbone at Lys1030 suggests that the side chain of this residue is in the vicinity of β‐catenin Glu462 and several other acidic residues. Although APC‐rA ...
Wnt-5a signaling may activate PKC and intracellular Ca2+ mobilization to trigger a series of downstream effects including activation of NF-AT and CaMKII (Kuhl et al., 2000a; Saneyoshi et al., 2002). During early Xenopus development, Wnt-5a activates calcineurin, which leads to NF-AT nuclear localization and increased β-catenin degradation (Saneyoshi et al., 2002). To address how Wnt-5a transduces its signal in mammalian cells, we checked whether Wnt-5a activates NF-AT transcriptional activity and whether such activation is required for Wnt-5a-induced β-catenin degradation. We found that NF-AT transcriptional activity was only weakly activated by Wnt-5a (∼50%), whereas it was strongly up-regulated by activated calcineurin (∼300%; Fig. 3 A). In addition, we found that although activated calcineurin was able to inhibit the TOPFLASH activity up-regulated by β-catenin S37A, Wnt-5a had an additive effect in its presence (Fig. 3 B). Moreover, specific inhibition of calcineurin by Cyclosporin A ...
Hyperactivation of the canonical Wnt/β-catenin pathway, caused by mutations in such components as β-catenin and APC, is one of the most frequent signaling abnormalities in several human cancers including colorectal carcinomas (15), melanomas (16), hepatoblastomas (17), medulloblastomas (18), prostatic carcinomas (19), and uterine and ovarian endometrioid adenocarcinomas (10, 20-22). In breast cancer, however, evidence of comparable mutations is surprisingly lacking (23). In contrast, there is strong evidence, based on immunohistochemical analyses, that the Wnt/β-catenin pathway is activated (23-25). Importantly, aberrant β-catenin expression in breast cancer is associated with poor clinical outcome (23-26). Metaplastic carcinomas have never been analyzed for Wnt pathway gene mutations.. Because breast carcinoma arises from glandular epithelium, it usually exhibits the features of an adenocarcinoma. However, in some cases, part or all of the neoplastic cells differentiate into a nonglandular ...
A variety of signals governing early extension, guidance, and connectivity of olfactory receptor neuron (ORN) axons has been identified; however, little is known about axon-mesoderm and forebrain (FB)-mesoderm signals. Using Wnt-ßcatenin reporter mice, we identify a novel Wnt-responsive resident cell population, located in a Frizzled7 expression domain at the surface of the embryonic FB, along the trajectory of incoming ORN axons. Organotypic slice cultures that recapitulate olfactory-associated Wnt-ßcatenin activation show that the ßcatenin response depends on a placode-derived signal(s). Likewise, in Dlx5-/- embryos, in which the primary connections fail to form, Wnt-ßcatenin response on the surface of the FB is strongly reduced. The olfactory placode expresses a number of ßcatenin-activating Wnt genes, and the Frizzled7 receptor transduces the canonical Wnt signal; using Wnt expression plasmids we show that Wnt5a and Wnt7b are sufficient to rescue ßcatenin activation in the absence of ...
Beta-catenin signaling is required for hair follicle development and regeneration which are involved in the resuscitation of hair follicle stem cells (HFSCs). To further characterize the role of beta-catenin in the regulation of proliferation of HFSCs, the beta-catenin expression was measured in the defined stages of hair follicle cycle and the proliferative potency was determined by using an in vitro cell growth assay. Our results showed that activation of beta-catenin correlated with HFSCs proliferation, which appeared to be mediated by the nuclear translocation of stabilized beta-catenin and the activation of responsible cell cycle genes (cyclin D1 and p21). In addition, PI3K/Akt pathway was also involved in the HFSCs proliferation, partly regulated by beta-catenin signaling pathway. These results demonstrate that beta-catenin is an essential factor in the regulation of HFSCs proliferation via PI3K/Akt pathway and might be a potential therapeutic target for the regulation of the yield of ...
Activity of the canonical Wnt signal pathway in kidney homogenates of sham and nephrectomized rats. The expression of active Wnt components in kidney homogenate
beta Catenin (phospho Thr41/Ser45) antibody (catenin (cadherin-associated protein), beta 1, 88kDa) for WB. Anti-beta Catenin (phospho Thr41/Ser45) pAb (GTX50180) is tested in Human samples. 100% Ab-Assurance.
Journal of Neurosurgery, Volume 0, Issue 0, Page 1-9, Ahead of Print.. Fengming Lan, M.S., Xiao Yue, M.S., Lei Han, Ph.D., Xubo Yuan, Ph.D., Zhendong Shi, M.S., Kai Huang, M.S., Yang Yang, M.S., Jian Zou, M.S., Junxia Zhang, Ph.D., Tao Jiang, M.D., Ph.D., Peiyu Pu, M.D., Ph.D., and Chunsheng Kang, M.D., Ph.D.. Object. The goal in this study was to investigate the antitumor effect of aspirin in glioblastoma cells and the molecular mechanism involved in its antineoplastic activities.. Methods. The authors used the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method, flow cytometry, the annexin V method, and Transwell cell invasion test to detect the proliferation and invasive activity of U87 and A172 glioma cells before and after being treated with aspirin. To determine the effects of aspirin on β-catenin/T-cell factor (TCF) transcription activity, reporter constructs containing 3 repeats of the wild-type (TOPflash) or mutant (FOPflash) TCF-binding sites were used. Reverse ...
1M1E: ICAT inhibits Beta-catenin binding to Tcf/Lef-family transcription factors and the general coactivator p300 using independent structural modules.
Beta-catenin/Tcf reporter mice. These mice express GFP gene under the control of the Tcf/Lef binding sites and a minimal thymidine kinase promoter from the TOPFLASH plasmid. Immunohistochemistry with a GFP antibody can be used to assess the Tg expression in the intestine. In other organs except for the intestine. In the splenocytes, expression of GFP was observed by FACS analysis, In other organs, the GFP expression patterns are not examined yet ...
Wnt-C59 (C59) is a PORCN inhibitor for Wnt3A-mediated activation of a multimerized TCF-binding site driving luciferase with IC50 of 74 pM in HEK293 cells.
Component of the Wnt-Fzd-LRP5-LRP6 complex that triggers beta-catenin signaling through inducing aggregation of receptor-ligand complexes into ribosome-sized signalsomes. Cell-surface coreceptor of Wnt/beta-catenin signaling, which plays a pivotal role in bone formation. The Wnt-induced Fzd/LRP6 coreceptor complex recruits DVL1 polymers to the plasma membrane which, in turn, recruits the AXIN1/GSK3B-complex to the cell surface promoting the formation of signalsomes and inhibiting AXIN1/GSK3-mediated phosphorylation and destruction of beta-catenin. Required for posterior patterning of the epiblast during gastrulation, By similarity. {ECO:0000250, ECO:0000269,PubMed:11357136, ECO:0000269,PubMed:11448771, ECO:0000269,PubMed:15778503, ECO:0000269,PubMed:16341017, ECO:0000269,PubMed:16513652, ECO:0000269,PubMed:17326769, ECO:0000269,PubMed:17400545, ECO:0000269,PubMed:19107203, ECO:0000269,PubMed:19293931, ECO:0000269,PubMed:19801552 ...
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The cadherin-catenin complex (CCC) is crucial for successful completion of morphogenesis during embryonic development, and for suppression of metastatic phenoty...
Polyclonal antibody for ALPHA 1 CATENIN/CTNNA1 detection. Host: Rabbit.Size: 100μg/vial. Tested applications: IHC-P. Reactive species: Human. ALPHA 1 CATENIN/CTNNA1 information: Molecular Weight: 100071 MW; Subcellular Localization: Isoform 1: Cytoplasm,
β-Catenin is essential for embryonic development and required for cell renewal/regeneration in adult life. Cellular β-catenin exists in three different pools: membranous, cytoplasmic and nuclear. In...
Mutations in the Wnt/-catenin pathway occur in most colorectal cancers (CRCs), and these mutations lead to increased nuclear accumulation of the -catenin transcriptional co-activator. element within the first intron of the gene to drive expression in CRC cells. As such, reducing -catenin expression in CRC cells using shRNAs leads to decreased mRNA and protein levels. …Read More. ...
One interesting contrast between the two studies is the haul of genes. The Vancouver group found ARID1A as a recurrently mutated gene; the Hopkins group not only bagged ARID1A but also KRAS, PIK3CA and PPP2R1A. KRAS and PIK3CA are well-known oncogenes in multiple tumor types and had previously been implicated in OCCC, but PP2R1A is a novel find. The Vancouver group did specifically search for KRAS and PIK3CA mutants in their cohorts by PCR assays and found one patient sample and one cell line with KRAS mutations. Again, it would be interesting to review the RNA-Seq data to generate hypotheses as to why these were not found in the Vancouver set. On the other hand, the RNA-Seq data did identify one case of a rearranged ARID1A. While it is possible to use hybridization capture to identify gene fusions, this cannot be practically done in a hypothesis-free manner. In other words, without advance interest in ARID1A that approach would not work. In addition, CTTNB1 (beta catenin) mutations had been ...
human AMER1 protein: regulates the distribution of the tumor suppressor APC between microtubules and the plasma membrane; amino acid sequence in first source
The canonical WNT-β-catenin pathway is essential for self-renewal, growth and survival of AML stem/blast progenitor cells (BPCs). Deregulated WNT signaling inhibits degradation of β-catenin, causing increased nuclear translocation and co-factor activity of β-catenin with the transcriptional regulator TCF4/LEF1 in AML BPCs. Here, we determined the pre-clinical anti-AML activity of the ...
negative regulator of transcriptional activity repressing expression of SPP1 and beta-catenin/TCF7L2 target genes, which are involved in myogenesis, muscle maintenance, and regeneration in a histone deacetylase dependent ...
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
GSK-3阻害剤(経路に合図することの標的を妨げる)がいろいろな分析のために使われて、いくつかは臨床試験に入りました。そして、それは新しいガン療法です。
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 ...
Research Grants, Research Topics, Publications, Genomes and Genes, Species, Scientific Experts about adenomatous polyposis coli protein
The sys-1 gene encodes a highly divergent β-catenin (6, 8). Several lines of evidence support the idea that SYS-1 is a functional β-catenin. First, transgenic SYS-1 can rescue a null mutant of bar-1, which encodes a typical β-catenin. Second, SYS-1 binds the β-catenin binding domain of POP-1/TCF. Third, SYS-1 acts as a transcriptional coactivator for POP-1 in a TOPFLASH reporter. Fourth, ceh-22 expression in distal SGP daughters depends on POP-1 binding sites in the ceh-22b promoter and also on SYS-1 and POP-1. Therefore, SYS-1 acts in many ways like a typical β-catenin.. Both SYS-1/β-catenin and POP-1/TCF control the SGP asymmetric cell division (7, 9). In pop-1 mutants, as in sys-1 mutants, the SGP daughters both adopt a proximal fate (Fig. 1B). Importantly, POP-1 is asymmetrically distributed to SGP daughters (10), a phenomenon that has been seen in many asymmetric cell divisions and has been dubbed "POP-1 asymmetry" (11). Although counterintuitive, nuclear POP-1 is reduced in distal ...
Wnt pathway deregulation is a common characteristic of many cancers. But only Colorectal Cancer predominantly harbours mutations in APC, whereas other cancer types (hepatocellular carcinoma, solid pseudopapillary tumours of pancreas) have activating mutations in β-catenin (CTNNB1). We have compared the dynamics and the potency of β-catenin mutations in vivo. Within the murine small intestine (SI), an activating mutation of β-catenin took much longer to achieve a Wnt deregulation and acquire a crypt-progenitor-cell (CPC) phenotype than Apc or Gsk3 loss. Within the colon, a single activating mutation of β-catenin was unable to drive Wnt deregulation or induce the CPC phenotype. This ability of β-catenin mutation to differentially transform the SI versus the colon correlated with significantly higher expression of the β-catenin binding partner E-cadherin. This increased expression is associated with a higher number of E-cadherin:β-catenin complexes at the membrane. Reduction of E-cadherin ...
Canonical Wnt signaling is mediated by a molecular "switch" that regulates the transcriptional properties of the T-cell factor (TCF) family of DNA-binding proteins. Members of the myeloid translocation gene (MTG) family of transcriptional corepressors are frequently disrupted by chromosomal translocations in acute myeloid leukemia, whereas MTG16 may be inactivated in up to 40% of breast cancer and MTG8 is a candidate cancer gene in colorectal carcinoma. Genetic studies imply that this corepressor family may function in stem cells. Given that mice lacking Myeloid Translocation Gene Related-1 (Mtgr1) fail to maintain the secretory lineage in the small intestine, we surveyed transcription factors that might recruit Mtgr1 in intestinal stem cells or progenitor cells and found that MTG family members associate specifically with TCF4. Coexpression of beta-catenin disrupted the association between these corepressors and TCF4. Furthermore, when expressed in Xenopus embryos, MTG family members inhibited ...
Nasopharyngeal carcinoma has a high incidence in southern China. The Wnt/β-catenin signaling pathway plays a major role in cancer development and progression. Our current study aims to determine the clinical significance of the Wnt/β-catenin pathway components such as β-catenin, cyclooxygenase 2, cyclin D1, c-Myc, and E-cadherin in 148 nasopharyngeal carcinomas by immunohistochemistry. We found that nasopharyngeal carcinoma stage T3+T4 had significantly higher expression of β-catenin, cyclooxygenase 2, cyclin D1, and c-Myc and lower expression of E-cadherin than nasopharyngeal carcinoma stage T1+T2 (P | .001, P | .05, respectively).There was significantly higher expression of β-catenin (P = .001) and cyclooxygenase 2 (P = .003) and lower expression of E-cadherin (P = .001) in nasopharyngeal carcinoma with lymph node metastasis than in nasopharyngeal carcinoma without lymph node metastasis. The expression of β-catenin in nasopharyngeal carcinoma was positively correlated with cyclooxygenase 2 (r =
Next, α catenin links bound β catenin and γ catenin to the actin filaments of the cell cytoskeleton via interactions with various actin binding proteins or by binding actin itself.24-26 The p120 protein, however, binds at a unique site directly to E-cadherin that is bound to either β catenin or γ catenin without linking it to the actin cytoskeleton.24-26 The p120 protein has been reported to act as an inhibitor of cadherin mediated adhesion, although the actual mechanism of inhibition is unclear.27. The β catenin molecule interacts with the adenomatous polyposis coli (APC) tumour suppressor protein, glycogen synthase kinase β, and an adaptor protein axin (or a homologue, conductin) in a complex, which is responsible for its degradation.28 This destruction complex is essential to maintain appropriate concentrations of free cytoplasmic β catenin. APC and E-cadherin have been shown to compete for the same binding region on β catenin.29 It has been suggested that APC modulates the ...
Detachment of cell-cell adhesion is indispensable for the first step of invasion and metastasis of cancer. This mechanism is frequently associated with the impairment of either E-cadherin expression or function. However, mechanisms of such abnormalities have not been fully elucidated. In this study, we demonstrated that the function of E-cadherin was completely abolished in the human gastric cancer cell line HSC-39, despite the high expression of E-cadherin, because of mutations in one of the E-cadherin-associated cytoplasmic proteins, beta-catenin. Although immunofluorescence staining of HSC-39 cells by using an anti-E-cadherin antibody (HECD-1) revealed the strong and uniform expression of E-cadherin on the cell surface, cell compaction and cell aggregation were not observed in this cell. Western blotting (immunoblotting) using HECD-1 exhibited a 120-kDa band which is equivalent to normal E-cadherin. Northern (RNA) blotting demonstrated a 4.7-kb band, the same as mature E-cadherin mRNA. ...
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
Pancreatic β-cells are highly responsive to changes in glucose, but the mechanisms involved are only partially understood. There is increasing evidence that the β-catenin signalling pathway plays an important role in regulating β-cell function, but the mechanisms regulating β-catenin signalling in these cells is not well understood. In the present study we show that β-catenin levels and downstream signalling are regulated by changes in glucose levels in INS-1E and β-TC6-F7 β-cell models. We found a glucose-dependent increase in levels of β-catenin in the cytoplasm and nucleus of INS-1E cells. Expression of cyclin D1 also increased with glucose and required the presence of β-catenin. This was associated with an increase in phosphorylation of β-catenin on Ser552, which is known to stabilize the molecule and increase its transcriptional activity. In a search for possible signalling intermediates we found forskolin and cell-permeable cAMP analogues recapitulated the glucose effects, ...
|.. The individuals in isolated populations of small wnt size that over express in the brain the transcription factor beta-catenin selective GSK-3 inhibitor APC (adenomatous polyposis coli) binds to another protein, called β-catenin, and stimulates its phosphorylation. In cells with an APC mutation, induces the expression of genes that stimulate cell birth. One of these…
Aqeilan, R. I., et al. (2005). WW domain-containing proteins, WWOX and YAP, compete for interaction with ErbB-4 and modulate its transcriptional function. Cancer Res. 65(15): 6764-72. 16061658 Alarcon, C., et al.. (2009). Nuclear CDKs drive Smad transcriptional activation and turnover in BMP and TGF-beta pathways. Cell 139(4): 757-69. PubMed Citation: 19914168 Aragón, E., et al. (2011). A Smad action turnover switch operated by WW domain readers of a phosphoserine code. Genes Dev. 25(12): 1275-88. PubMed Citation: 21685363 Azzolin, L., Panciera, T., Soligo, S., Enzo, E., Bicciato, S., Dupont, S., Bresolin, S., Frasson, C., Basso, G., Guzzardo, V., Fassina, A., Cordenonsi, M. and Piccolo, S. (2014). YAP/TAZ incorporation in the beta-Catenin destruction complex orchestrates the Wnt response. Cell 158: 157-170. PubMed ID: 24976009 Badouel, C., et al. (2009). The FERM-domain protein Expanded regulates Hippo pathway activity via direct interactions with the transcriptional activator Yorkie. Dev. ...
Our study unveils a TREM2/β-catenin pathway that regulates bone mass by regulating the rate of OC generation. Mechanistically, TREM2 and β-catenin augment the M-CSF-induced proliferation of OcP, retarding their differentiation into mature OC. Ablation of either TREM2 or β-catenin inhibits the proliferation of OcP, accelerating their differentiation into bone-resorbing OC, which ultimately cause osteoporosis. The possibility that TREM2 and β-catenin act along the same pathway is supported not only by the similar osteoporotic phenotypes of TREM2−/− and βcatΔ/Δ mice, but also by genetic evidence that simultaneous heterozygosity for TREM2- and β-catenin-null alleles results in osteoporosis, whereas no phenotype is observed in mice heterozygous for either of these alleles.. TREM2 may enhance M-CSF-induced activation of β-catenin by facilitating the recruitment of DAP12 to the receptor for M-CSF. In turn, DAP12 may activate Syk and Pyk2, which promote phosphorylation and nuclear ...
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]. This complex is then able to bind β-catenins in the cytoplasm, that have dissociated from adherens contacts between cells. With the help of casein kinase 1 (CK1), which carries out an initial phosphorylation of β-catenin, GSK-3β is able to phosphorylate β-catenin a second time. This targets β-catenin for ubiquitination and degradation by cellular proteasomes. This prevents it from translocating into the nucleus, where it acts as a transcription factor for proliferation genes. APC is also thought to be targeted to microtubules via the PDZ binding domain, stabilizing them[citation needed]. 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 ...
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. ...
β-Catenin expression was observed in the membrane and/or cytoplasm without any significant nuclear expression. HER-2/neu and EGFR were observed on the membrane in 21% and 6% of tumors, respectively, and Met stained in a membrane/cytoplasm distribution in 28% of cases. Cyclin D1 was expressed in the nucleus and MMP7 was expressed in the cytoplasm in 26% and 75% of tumors, respectively. Nuclear expression of p53 was noted in 31% of tumors. When each marker was analyzed separately, only p53 and Met demonstrated a significant correlation with survival. However, patients who had tumors that coexpressed high levels of β-catenin and p53 had markedly worse overall survival (P = 0.0026). In multivariate analysis, only tumor size, Met, and the coexpression of β-catenin and p53 retained statistical significance. ...
Sigma-Aldrich offers abstracts and full-text articles by [Jessica Svedlund, Maria Aurén, Magnus Sundström, Henning Dralle, Göran Akerström, Peyman Björklund, Gunnar Westin].
Kirschenbaum F, Hsu SC, Cordell B, McCarthy JV. Substitution of a glycogen synthase kinase-3beta phosphorylation site in presenilin 1 separates presenilin function from beta-catenin signaling ...
Adenomatous Polyposis Coli Protein: A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.
TY - JOUR. T1 - Abnormal expression and function of the E-cadherin-catenin complex in gastric carcinoma cell lines. AU - Jawhari, A. U.. AU - Noda, M.. AU - Farthing, M. J.G.. AU - Pignatelli, M.. PY - 1999/1/1. Y1 - 1999/1/1. N2 - Dysfunction of the cadherin-catenin complex, a key component of adherens junctions, is thought to confer invasive potential to cells. The aim of this study is to examine the expression and function of the E-cadherin/catenin complex in gastric carcinoma cell lines. Expression of E-cadherin, α, β and γ-catenin and p120(ctn), and of the adenomatous polyposis coil protein (APC), together with function of the cadherin-catenin complex was examined in a panel of gastric carcinoma cell lines, using immunocytochemistry, Western blotting and a cell-cell aggregation assay. Protein interactions were examined by sequential immunoprecipitation and immunoblotting with antibodies to E-cadherin, α, β and γ-catenin, p120(ctn) and APC. Abnormalities of E-cadherin, α- and ...
We have shown that LEF1 played critical and nonredundant roles in iNKT cell expansion and iNKT2 effector fate differentiation. We showed that in the absence of LEF1, iNKT cell expansion at ST0 and ST1 failed to occur and that LEF1 directly regulated expression of the CD127 component of the IL-7 receptor and the transcription factor c-myc, both of which are required for this phase of expansion (Dose et al., 2009; Mycko et al., 2009; Tani-ichi et al., 2013). LEF1 was also required for the development of iNKT2 cells, which include both IL-4 only and IL-4 plus IFNγ-producing iNKT cells, and LEF1 directly regulated the expression of the iNKT2 signature transcription factor GATA3. Our findings are particularly striking given that LEF1 deficiency has only subtle effects on conventional T cells during their differentiation and in the periphery during their activation and acquisition of the memory phenotype as the result of redundancy with the related transcription factor TCF1 (Okamura et al., 1998; Yu ...
TY - JOUR. T1 - Ras farnesylation inhibitor FTI-277 restores the E-cadherin/catenin cell adhesion system in human cancer cells and reduces cancer metastasis. AU - Nam, Jeong Seok. AU - Ino, Yoshinori. AU - Sakamoto, Michiie. AU - Hirohashi, Setsuo. PY - 2002/9/1. Y1 - 2002/9/1. N2 - The E-cadherin/catenin cell adhesion system is often down-regulated in epithelial tumors. This is thought to play an important role in cancer invasion and metastasis, and restoration of this system may suppress metastatic spread of cancer. In this study, the effects of a Ras farnesylation inhibitor (FTI-277) on E-cadherin-mediated cell-cell adhesion and metastatic potential were examined. In cell aggregation assays, FTI-277 stimulated aggregation of colon, liver and breast cancer cells. In vitro cultures of cancer cells showed that FTI-277 induced strong cell-cell contact. Immunoblotting analysis showed that FTI-277 increased E-cadherin/catenin (α, β and γ) expression and strongly stabilized E-cadherin/catenin ...
Role of Wnt/beta-catenin signaling in hepatocellular carcinoma, pathogenesis, and clinical significance Ahmed M Khalaf,1 David Fuentes,1 Ali I Morshid,2 Mata R Burke,3 Ahmed O Kaseb,4 Manal Hassan,4 John D Hazle,1 Khaled M Elsayes2 1Department of Imaging Physics, University of Texas MD Anderson Cancer Center, Houston, TX, USA; 2Department of Diagnostic Radiology, University of Texas MD Anderson Cancer Center, Houston, TX, USA; 3Department of Medicine, University of Alabama at Birmingham (UAB), Birmingham, AL, USA; 4Department of Gastrointestinal Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, USA Abstract: Hepatocellular carcinoma (HCC) is one of the most common primary hepatic malignancies and one of the fastest-growing causes of cancer-related mortality in the United States. The molecular basis of HCC carcinogenesis has not been clearly identified. Among the molecular signaling pathways implicated in the pathogenesis of HCC, the Wnt/β-catenin signaling pathway is one of the most
Canonical Wnt signaling triggering β-catenin-dependent gene expression contributes to cell cycle progression, in particular at the G1/S transition. Recently, however, it became clear that the cell cycle can also feed back on Wnt signaling at the G2/M transition. This is illustrated by the fact that mitosis-specific cyclin-dependent kinases can phosphorylate the Wnt co-receptor LRP6 to prime the pathway for incoming Wnt signals when cells enter mitosis. In addition, there is accumulating evidence that various Wnt pathway components might exert additional, Wnt-independent functions that are important for proper regulation of mitosis. The importance of Wnt pathways during mitosis was most recently enforced by the discovery of Wnt signaling contributing to the stabilization of proteins other than β-catenin, specifically at G2/M and during mitosis. This Wnt-mediated stabilization of proteins, now referred to as Wnt/STOP, might on one hand contribute to maintaining a critical cell size required for ...

Beta-Catenin | SpringerLinkBeta-Catenin | SpringerLink

... beta 1 (88kD); Catenin beta; Catnb; Ctnnb; CTNNB1 Beta-catenin (β-catenin) (Armadillo in Drosophila) is a multifunctional ... Catenin (cadherin-associated protein), beta 1 (88kD); Catenin beta; Catnb; Ctnnb; CTNNB1 ... Beta-catenin (β-catenin) (Armadillo in Drosophila) is a multifunctional protein involved in two essential cellular events: cell ... Clevers H. Wnt/beta-catenin signaling in development and disease. Cell. 2006;127:469-80.PubMedPubMedCentralCrossRefGoogle ...
more infohttps://link.springer.com/referenceworkentry/10.1007%2F978-3-319-67199-4_528

Beta-catenin (IPR013284) | InterPro | EMBL-EBIBeta-catenin (IPR013284) | InterPro | EMBL-EBI

Beta-catenin (IPR013284). Short name: Beta-catenin Family relationships *Beta-catenin (IPR013284) *Junction plakoglobin/protein ... Beta-catenin forms a cadherin/beta-catenin/alphaE-catenin complex that can tether the tripartite adhesion complex and regulate ... The beta-catenin structure has been determined [PMID: 9298899, PMID: 11136974]. Beta catenin family proteins contain several ... The armadillo homologs beta-catenin and plakoglobin are differentially expressed during early development of Xenopus laevis.. ...
more infohttp://www.ebi.ac.uk/interpro/entry/IPR013284

Catenin beta-1 (Q02248) | InterPro | EMBL-EBICatenin beta-1 (Q02248) | InterPro | EMBL-EBI

InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
more infohttp://www.ebi.ac.uk/interpro/protein/Q02248

Beta-Catenin | ALZFORUMBeta-Catenin | ALZFORUM

If you know of any papers that use this antibody, please contact us at antibodies [at] alzforum [dot] org for consideration in the References section.. ...
more infohttps://www.alzforum.org/antibodies/beta-catenin-22

Phospho-regulation of Beta-catenin adhesion and signaling functions.  - PubMed - NCBIPhospho-regulation of Beta-catenin adhesion and signaling functions. - PubMed - NCBI

The degree to which beta-catenin participates in these two functions is dictated by the availability of beta-catenin binding ... Beta-catenin plays a critical structural role in cadherin-based adhesions and is also an essential co-activator of Wnt-mediated ... Phospho-regulation of Beta-catenin adhesion and signaling functions.. Daugherty RL1, Gottardi CJ. ... Inputs from various cell-signaling events can therefore impact beta-catenin function, which may be necessary for the finely ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/17928543?dopt=Abstract

Genomic organization of the human beta-catenin gene (CTNNB1).  - PubMed - NCBIGenomic organization of the human beta-catenin gene (CTNNB1). - PubMed - NCBI

Genomic organization of the human beta-catenin gene (CTNNB1).. Nollet F1, Berx G, Molemans F, van Roy F. ... The cytoplasmic beta-catenin protein is implicated in signal transduction and associates with both the cell-cell adhesion ... We determined the primary structure of the human beta-catenin gene (CTNNB1) by analysis of cDNA and genomic clones. The size of ... The intron-exon boundaries did not coincide either with conserved sites in the 12 armadillo repeat sequences of beta-catenin or ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/8838805?dopt=Abstract

A single mutation in the beta-catenin gene can lead to infertilityA single mutation in the beta-catenin gene can lead to infertility

... have discovered that a single mutation in the beta-catenin gene, which codes a protein known to be deeply involved in a number ... Beta-catenin is an essential protein in the Wnt/beta-catenin signaling pathway, which has been shown in mice to be involved in ... developed a mouse with single mutation to the beta-catenin gene, with the goal to discover so far unrevealed functions of beta- ... "A single mutation in the beta-catenin gene can lead to infertility." Medical News Today. MediLexicon, Intl., 10 Nov. 2014. Web. ...
more infohttps://www.medicalnewstoday.com/releases/285136.php

Beta-Catenin Antibody (Dako Omnis) | AgilentBeta-Catenin Antibody (Dako Omnis) | Agilent

Beta-catenin is also involved in the regulation of gene expression as a mediator of the Wnt signaling pathway. The expression ... and intracellular localization of beta-catenin is altered in many types of cancers. ... Beta-catenin is an 88 kDa multifunctional protein playing an essential role in cell-cell adhesion by binding to the ... Clone β-Catenin-1 Beta-catenin is an 88 kDa multifunctional protein playing an essential role in cell-cell adhesion by binding ...
more infohttps://www.agilent.com/en/product/immunohistochemistry/antibodies-controls/primary-antibodies/beta-catenin-

RCSB PDB 









- 1I7X: BETA-CATENIN/E-CADHERIN COMPLEX Literature Report PageRCSB PDB - 1I7X: BETA-CATENIN/E-CADHERIN COMPLEX Literature Report Page

The structure of the beta-catenin/E-cadherin complex and the molecular basis of diverse ligand recognition by beta-catenin. ... BETA-CATENIN A, C 538 Mus musculus Fragment: ARMADILLO DOMAIN Gene Name(s): Ctnnb1 Catnb ...
more infohttp://www.rcsb.org/pdb/explore/litView.do?structureId=1I7X

CTNNB1 - Beta-catenin - Sus scrofa (Pig) - CTNNB1 gene & proteinCTNNB1 - Beta-catenin - Sus scrofa (Pig) - CTNNB1 gene & protein

... beta-catenin-TCF7L2 complex, catenin complex, cell cortex, cell junction, cell periphery, cell-cell adherens junction, cell- ... R-SSC-195253. Degradation of beta-catenin by the destruction complex. R-SSC-196299. Beta-catenin phosphorylation cascade. R-SSC ... R-SSC-195253. Degradation of beta-catenin by the destruction complex. R-SSC-196299. Beta-catenin phosphorylation cascade. R-SSC ... Beta-cateninImported. ,p>Information which has been imported from another database using automatic procedures.,/p> ,p>,a href ...
more infohttp://www.uniprot.org/uniprot/Q8WNW4

Ctnnb1 - Catenin beta-1 - Mus musculus (Mouse) - Ctnnb1 gene & proteinCtnnb1 - Catenin beta-1 - Mus musculus (Mouse) - Ctnnb1 gene & protein

Catenin beta-1Imported. ,p>Information which has been imported from another database using automatic procedures.,/p> ,p>,a href ... tr,D3YUH4,D3YUH4_MOUSE Catenin beta-1 (Fragment) OS=Mus musculus GN=Ctnnb1 PE=1 SV=1 ...
more infohttp://www.uniprot.org/uniprot/D3YUH4

Beta-catenin - WikipediaBeta-catenin - Wikipedia

Catenin-associated Fer and Fyn tyrosine kinases regulate beta-catenin Tyr-142 phosphorylation and beta-catenin-alpha-catenin ... Catenin beta-1, also known as β-catenin, is a protein that in humans is encoded by the CTNNB1 gene. β-catenin is a dual ... Beta-catenin is widely expressed in many tissues. In cardiac muscle, beta-catenin localizes to adherens junctions in ... On the other hand, BCL9 and BCL9L must compete with α-catenin to access β-catenin molecules. The cellular level of beta-catenin ...
more infohttps://en.wikipedia.org/wiki/Beta-catenin

Anti-beta Catenin antibody [E247] Review (43313) | AbcamAnti-beta Catenin antibody [E247] Review (43313) | Abcam

... for Anti-beta Catenin antibody [E247] used in Immunocytochemistry/ Immunofluorescence. Abcam provides excellent in-house ...
more infohttps://www.abcam.com/beta-catenin-antibody-e247-ab32572/reviews/43313

Phospho Anti-beta Catenin (S45) antibody (ab18824) | AbcamPhospho Anti-beta Catenin (S45) antibody (ab18824) | Abcam

Rabbit polyclonal beta Catenin (phospho S45) antibody. Validated in WB. Cited in 1 publication(s). Immunogen corresponding to ... Anti-beta Catenin (phospho S45) antibody. See all beta Catenin primary antibodies. ... The majority of beta-catenin is localized to the cell membrane and is part of E-cadherin/catenin adhesion complexes which are ... Synthetic phospho-peptide corresponding to residues surrounding Ser45 of human Beta Catenin. ...
more infohttps://www.abcam.com/beta-catenin-phospho-s45-antibody-ab18824.html

beta Catenin Antibody
                
                
		        
	beta Catenin Antibody

beta Catenin Polyclonal Antibody from Invitrogen for Western Blot, Immunofluorescence, Immunocytochemistry, ... Protein Aliases: beta catenin; Beta-catenin; catenin; catenin (cadherin associated protein), beta 1, 88kDa; catenin (cadherin- ... Catenin beta; Catenin beta-1; CATNB; CTNB1; CTNNB Gene Aliases: armadillo; B-catenin; beta-catenin; Bfc; Catnb; CHBCAT; CTNNB; ... Cite beta Catenin Polyclonal Antibody. The following antibody was used in this experiment: beta Catenin Polyclonal Antibody ...
more infohttps://www.thermofisher.com/antibody/product/beta-Catenin-Antibody-Polyclonal/PA5-16762

RCSB PDB 









- 1M1E: Beta-catenin armadillo repeat domain bound to ICAT Structure Summary PageRCSB PDB - 1M1E: Beta-catenin armadillo repeat domain bound to ICAT Structure Summary Page

ICAT inhibits Beta-catenin binding to Tcf/Lef-family transcription factors and the general coactivator p300 using independent ... Beta-catenin A 538 Mus musculus Fragment: Armadillo Repeat Region (RESIDUES 134-671) Gene Name(s): Ctnnb1 Catnb ... Beta-catenin armadillo repeat domain bound to ICAT. *DOI: 10.2210/pdb1m1e/pdb ...
more infohttp://www.rcsb.org/pdb/explore/explore.do?structureId=1m1e

Phospho-beta Catenin (Tyr489) Antibody
		        
	Phospho-beta Catenin (Tyr489) Antibody

Phospho-beta Catenin (Tyr489) Polyclonal Antibody from Invitrogen for Western Blot and Immunohistochemistry (Paraffin) ... catenin (cadherin-associated protein), beta 1; catenin (cadherin-associated protein), beta 1, 88kDa; Catenin beta; Catenin beta ... This phosphorylation event primes beta-catenin for subsequent phosphorylation by GSK-3 beta. GSK-3 beta destabilizes beta- ... Protein Aliases: Beta-catenin; catenin (cadherin associated protein), beta 1, 88kDa; ...
more infohttps://www.thermofisher.com/antibody/product/Phospho-beta-Catenin-Tyr489-Antibody-Polyclonal/PA5-39715

Ctnnb1 MGI Mouse Gene Detail - MGI:88276 - catenin (cadherin associated protein), beta 1Ctnnb1 MGI Mouse Gene Detail - MGI:88276 - catenin (cadherin associated protein), beta 1

View mouse Ctnnb1 Chr9:120933400-120960507 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
more infohttp://www.informatics.jax.org/marker/key/778

Polyclonal Antibody Immunofluorescence Immunocytochemistry Beta-Catenin Binding from Cell Signaling TechnologyPolyclonal Antibody Immunofluorescence Immunocytochemistry Beta-Catenin Binding from Cell Signaling Technology

... and p120 catenin. β-catenin and γ-catenin associate with α-catenin, which links the cadherin-catenin complex to the actin ... and α-catenin. α-E-catenin is ubiquitously expressed, α-N-catenin is expressed in neuronal tissue, and α-T-catenin is primarily ... Polyclonal Antibody Immunofluorescence Immunocytochemistry Beta-Catenin Binding. Polyclonal Antibody - α-E-Catenin Antibody, ... α-catenin binds to β-catenin in the nucleus, preventing it from regulating transcription, and levels of both proteins appear to ...
more infohttps://www.cellsignal.com/1/3/polyclonal-antibody-immunofluorescence-immunocytochemistry-beta-catenin-binding

Modeling the Influence of the E-Cadherin-[Beta]-Catenin Pathway in Cancer Cell Invasion: A Multiscale Approach - RedorbitModeling the Influence of the E-Cadherin-[Beta]-Catenin Pathway in Cancer Cell Invasion: A Multiscale Approach - Redorbit

... p120-catenin, beta-catenin, and beta-catenin. The alpha- catenin and beta-catenin then form a complex to link the actin ... THE beta-CATENIN KINETICS We first present our model of the intracellular beta-catenin dynamics and show the importance of this ... We include soluble beta-catenin and the E-cadherin- beta-catenin complex as the main variables of our model. Upregulation of ... beta-catenin is an intracellular protein associated with the actin cytoskeleton of a cell. E- cadherins bind to beta-catenin to ...
more infohttp://www.redorbit.com/news/science/1529674/modeling_the_influence_of_the_ecadherinbetacatenin_pathway_in_cancer_cell/

PRI-724 | ≥99%(HPLC) | Selleck | Wnt/beta-catenin inhibitor
		
		
			
				
			
			
				
			
		
		
			
			
				
			
		
		
			
		...PRI-724 | ≥99%(HPLC) | Selleck | Wnt/beta-catenin inhibitor ...

Related Wnt/beta-catenin Products. * XAV-939 XAV-939 selectively inhibits Wnt/β-catenin-mediated transcription through ... PRI-724 specifically inhibits the recruiting of beta-catenin with its coactivator CBP.. ... PRI-724 specifically inhibits the recruiting of beta-catenin with its coactivator CBP. ... IWR-1-endo (IC50=180nM) inhibits Wnt-induced stabilization of β-catenin by acting on the target of β-catenin destruction ...
more infohttps://www.selleckchem.com/products/pri-724.html

MCC inhibits beta-catenin transcriptional activity by sequestering DBC1 in the cytoplasm. | Sigma-AldrichMCC inhibits beta-catenin transcriptional activity by sequestering DBC1 in the cytoplasm. | Sigma-Aldrich

MCC inhibits beta-catenin transcriptional activity by sequestering DBC1 in the cytoplasm.. [Laurent Pangon, Dessislava ... In particular, the MCC protein is known to regulate beta-catenin (β-cat) signaling, but the mechanism is poorly understood. ...
more infohttps://www.sigmaaldrich.com/catalog/papers/24824780

Isoquercitrin | Wnt/beta-catenin inhibitor | Read Reviews & Product Use Citations
		
	Isoquercitrin | Wnt/beta-catenin inhibitor | Read Reviews & Product Use Citations

Related Wnt/beta-catenin Products0. * XAV-939 XAV-939 selectively inhibits Wnt/β-catenin-mediated transcription through ... is an inhibitor of Wnt/β-catenin that acts downstream of the β-catenin nuclear translocation.. ... is an inhibitor of Wnt/β-catenin that acts downstream of the β-catenin nuclear translocation. ... ICG-001 antagonizes Wnt/β-catenin/TCF-mediated transcription and specifically binds to CREB-binding protein (CBP) with IC50 of ...
more infohttps://www.selleckchem.com/products/isoquercitrin.html

Dishevelled binding antagonist of beta catenin 2 - WikipediaDishevelled binding antagonist of beta catenin 2 - Wikipedia

Dishevelled binding antagonist of beta catenin 2 is a protein that in humans is encoded by the DACT2 gene. GRCh38: Ensembl ... Dishevelled binding antagonist of beta catenin 2". Retrieved 2017-09-10. Koga Y, Yao T, Hirahashi M, Kumashiro Y, Ohji Y, ... "Flat adenoma-carcinoma sequence with high-malignancy potential as demonstrated by CD10 and beta-catenin expression: a different ... "DACT2 is a functional tumor suppressor through inhibiting Wnt/β-catenin pathway and associated with poor survival in colon ...
more infohttps://en.wikipedia.org/wiki/Dishevelled_binding_antagonist_of_beta_catenin_2

beta-Catenin is not necessary for maintenance or repair of the bronchiolar epithelium.beta-Catenin is not necessary for maintenance or repair of the bronchiolar epithelium.

Signaling by Wnt/beta-catenin regulates self-renewal of tissue stem cells in the gut and, when activated in the embryonic ... Signaling by Wnt/beta-catenin regulates self-renewal of tissue stem cells in the gut and, when activated in the embryonic ... Necessity of beta-catenin signaling was tested through Cre-mediated deletion of Catnb exons 2-6 in airway epithelial cells. ... Functional knockout of beta-catenin had no impact on expression of Clara cell differentiation markers, mitotic index, or ...
more infohttp://www.biomedsearch.com/nih/beta-Catenin-Not-Necessary-Maintenance/19213872.html
  • Isoquercitrin, a flavonoid compound with anticancer activity isolated from Bidens bipinnata L, is an inhibitor of Wnt/β-catenin that acts downstream of the β-catenin nuclear translocation. (selleckchem.com)
  • Isoquercitrin inhibits the signaling downstream of β-catenin nuclear translocation as isoquercitrin reverses the effect of β-catenin S33A, which cannot be phosphorylated and avoids degradation . (selleckchem.com)
  • For the first time, we were able to visualize the subcellular localization and nuclear translocation of endogenous β-catenin in living cells using these chromobodies. (mcponline.org)
  • 5 Here, we further investigated the ability of AIEC to activate Wnt transcription and nuclear translocation of b-catenin. (bmj.com)
  • Nuclear translocation of b-catenin was assessed by immunofluorescence in CRC cell-lines SW480 and DLD1. (bmj.com)
  • Infection of SW480 and DLD1 showed significant increases in b -catenin nuclear translocation as per prostaglandin E2 treatment (1-10 μM). (bmj.com)
  • alanin substitution abrogated K48 polyubiquitination, β-catenin nuclear translocation and tumor xenograft growth. (uky.edu)
  • Synthetic phospho-peptide corresponding to residues surrounding Ser45 of human Beta Catenin. (abcam.com)
  • Synthetic phosphopeptide conjugated to KLH derived from around the Tyrosine 333 phosphorylation site (YTY p EK) of Human beta Catenin (NP_001091679.1). (abcam.co.jp)
  • Phospho beta Catenin (Tyr86) synthetic peptide (conjugated to KLH) corresponding to amino acid residues around tyrosine 86 of human beta Catenin. (abcam.co.jp)
  • Suppression of PDE5 with siRNA or known PDE5 inhibitors was sufficient to selectively induce apoptosis and attenuate beta-catenin mediated transcription in breast tumor cells with minimal effects on normal mammary epithelial cells. (aacrjournals.org)
  • These findings provide evidence that SS induces apoptosis of breast tumor cells through a mechanism involving inhibition of PDE5 and attenuation of oncogenic Wnt/beta-catenin mediated transcription. (aacrjournals.org)
  • Overexpressed in vitro double truncated β-catenin increased transcriptional activity, cell proliferation and growth of tumor xenografts compared to FS β-catenin. (uky.edu)
  • The disruption of E-cadherin/beta-catenin complex formation promotes EMT, thereby stimulating tumor progression. (ox.ac.uk)
  • We show that activation of Wnt/β-catenin in the bronchiolar epithelium of the adult lung does not promote tumor development by itself. (omictools.com)
  • However, activation of Wnt/β- catenin signaling leads to a dramatic increase in tumor formation both in overall tumor number and size compared to KrasG12D alone. (omictools.com)
  • We show that activation of Wnt/β- catenin signaling significantly alters the KrasG12D tumor phenotype resulting in a phenotypic switch from bronchiolar epithelium to the highly proliferative distal progenitors found in the embryonic lung. (omictools.com)
  • Lymphoid enhancer binding factor (Lef) 1 is a Wnt-responsive transcription factor that associates with β-catenin. (asbmr.org)
  • Unlike what has been reported in T cells and colon cancer cell lines, Lef1ΔN activated gene transcription in the absence of exogenous β-catenin and cooperated with constitutively active β-catenin to further stimulate gene transcription in mesenchymal and osteoblastic cells. (asbmr.org)
  • Beta-catenin/T-cell factor-mediated transcription is modulated by cell density in human bronchial epithelial cells. (nih.gov)
  • 1996 ) Functional interaction of B-catenin with the transcription factor LEF-1. (biologists.org)
  • ß-catenin is then free to translocate to the cell nucleus where it acts as a co-factor for the T-cell factor/lymphoid enhancing factor (TCF/LEF) transcription factors. (mycancergenome.org)
  • ß-catenin subsequently translocates to the nucleus, where it acts as a co-factor for the TCF/LEF family of transcription factors. (mycancergenome.org)
  • However, the broad distribution and phenotype of signaling cells precluded establishment of a clear role for beta-catenin in the normal or repairing state. (biomedsearch.com)
  • In zebrafish, previous loss-of-function studies have not identified an essential role for beta-catenin in dorsal axis formation, but the maternal-effect mutation ichabod disrupts beta-catenin accumulation in dorsal nuclei and leads to a reduction of dorsoanterior derivatives. (biomedsearch.com)
  • Furthermore, an analysis of beta-catenin deletion constructs demonstrates that the internal armadillo repeat region is both necessary and sufficient to induce axis duplication. (rupress.org)
  • The degree to which beta-catenin participates in these two functions is dictated by the availability of beta-catenin binding partners, and an emerging theme is that these binding interactions are regulated by phosphorylation. (nih.gov)
  • This phosphorylation event primes beta-catenin for subsequent phosphorylation by GSK-3 beta. (thermofisher.com)
  • The intron-exon boundaries did not coincide either with conserved sites in the 12 armadillo repeat sequences of beta-catenin or with intron-exon boundaries in the armadillo gene of Drosophila. (nih.gov)
  • Subcellular fractionation demonstrated that all of the beta-catenin constructs that contain the armadillo repeat domain were present in both the soluble cytosolic and the membrane fraction. (rupress.org)
  • LMW β-catenin lacks both termini, leaving residues in the armadillo repeat intact. (uky.edu)
  • Moreover, the chromobody signal allowed us to trace the accumulation of diffusible, hypo-phosphorylated β-catenin in response to compound treatment in real time using High Content Imaging. (mcponline.org)
  • Immunolabeling for β-catenin confirmed the presence of abnormal nuclear accumulation in SSAs, with 35/54 (67%) SSAs showing nuclear labeling compared to 0/12 hyperplastic polyps (HPs). (pubmedcentralcanada.ca)
  • While β- and γ-catenin play structural roles in the junctional complex, p120 regulates cadherin adhesive activity and trafficking (1-4). (cellsignal.com)
  • Signaling by Wnt/beta-catenin regulates self-renewal of tissue stem cells in the gut and, when activated in the embryonic bronchiolar epithelium, leads to stem cell expansion. (biomedsearch.com)
  • Crystal structure of a beta-catenin/Tcf complex. (ebi.ac.uk)
  • The GL treatment resulted in a significant reduction of β-Catenin /TCF-4 complex in both of the cancer cells. (biomedcentral.com)
  • The ß-catenin-TCF/LEF complex results in the activation of targets including c-MYC and Cyclin-D1 (for review, see Giles, van Es, and Clevers 2003 ). (mycancergenome.org)
  • In Drosophila, Notum, a secreted alpha/beta-hydrolase, antagonizes the signaling of the prototypical Wnt Wingless (Wg), by releasing glypicans from the cell surface. (luriechildrens.org)
  • Takuya Murata of RIKEN BRC, the first author of the paper, says, "Because the amino acid sequence of beta-catenin is 100% identical in humans and mice, the nucleotide change we saw could cause the same mutation in humans. (medicalnewstoday.com)
  • We have identified and characterized a second zebrafish beta-catenin gene, beta-catenin-2, located on a different linkage group from the previously studied beta-catenin-1, but situated close to the ichabod mutation on LG19. (biomedsearch.com)
  • Although the ichabod mutation does not functionally alter the beta-catenin-2 reading frame, the level of maternal beta-catenin-2, but not beta-catenin-1, transcript is substantially lower in ichabod, compared with wild-type, embryos. (biomedsearch.com)
  • Southern blotting of beta-catenin DNA disclosed mutation at the genomic level. (asm.org)
  • Takemaru K-I, Ohmitsu M, Li F-Q. An oncogenic hub: beta-catenin as a molecular target for cancer therapeutics. (springer.com)
  • Molecular cloning reveals alternative splice forms of human alpha(E)-catenin. (ebi.ac.uk)
  • Biochemical analysis of nuclear extracts from cancer biopsies revealed the existence of low molecular weight (LMW) pβ-Cat 552 , increased to the exclusion of full size (FS) forms of β-catenin. (uky.edu)
  • Isoquercitrin exerts inhibitory effect on Wnt/β-catenin signaling and no toxic effects on colon cancer cell lines. (selleckchem.com)
  • Furthermore, we isolated a strain of Fn (F01) from a CRC tissue and examined whether Fn (F01) infection of colon cancer cells activated β-catenin signaling via the TLR4/P-PAK1/P-β-catenin S675 cascade. (oncotarget.com)
  • These observations also identify STRAP as a new player in regulating β-catenin signaling in hepatocellular cancers. (eur.nl)
  • Wnt/β-catenin activation enhanced cell proliferation, particularly in normally non-odontogenic regions of the dental lamina, which widely expressed Lef1, restricting the Sox2 domain. (nih.gov)
  • Nuclear activation of Wnt/β-catenin signaling is required for cell proliferation in inflammation and cancer. (uky.edu)