Core Binding Factors: Heterodimeric transcription factors containing a DNA-binding alpha subunits, (CORE BINDING FACTOR ALPHA SUBUNITS), along with a non-DNA-binding beta subunits, CORE BINDING FACTOR BETA SUBUNIT. Core Binding Factor regulates GENETIC TRANSCRIPTION of a variety of GENES involved primarily in CELL DIFFERENTIATION and CELL CYCLE progression.Core Binding Factor beta Subunit: A non-DNA binding transcription factor that is a subunit of core binding factor. It forms heterodimeric complexes with CORE BINDING FACTOR ALPHA SUBUNITS, and regulates GENETIC TRANSCRIPTION of a variety of GENES involved primarily in CELL DIFFERENTIATION and CELL CYCLE progression.Core Binding Factor alpha Subunits: A family of transcription factors that bind to the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. Family members contain a highly conserved DNA-binding domain known as the runt domain. They can act as both activators and repressors of expression of GENES involved in CELL DIFFERENTIATION and CELL CYCLE progression.Core Binding Factor Alpha 2 Subunit: A transcription factor that dimerizes with the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly conserved DNA-binding domain known as the runt domain. Runx1 is frequently mutated in human LEUKEMIAS.Core Binding Factor Alpha 1 Subunit: A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly conserved DNA-binding domain known as the runt domain and is involved in genetic regulation of skeletal development and CELL DIFFERENTIATION.Transcription Factor AP-2: A family of DNA binding proteins that regulate expression of a variety of GENES during CELL DIFFERENTIATION and APOPTOSIS. Family members contain a highly conserved carboxy-terminal basic HELIX-TURN-HELIX MOTIF involved in dimerization and sequence-specific DNA binding.Smooth Muscle Myosins: Myosin type II isoforms found in smooth muscle.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Chromosomes, Human, Pair 16: A specific pair of GROUP E CHROMOSOMES of the human chromosome classification.Chromosome Inversion: An aberration in which a chromosomal segment is deleted and reinserted in the same place but turned 180 degrees from its original orientation, so that the gene sequence for the segment is reversed with respect to that of the rest of the chromosome.DNA-Binding Proteins: Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.Leukemia, Myeloid, Acute: Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.Oncogene Proteins, Fusion: The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.Chromosomes, Human, Pair 21: A specific pair of GROUP G CHROMOSOMES of the human chromosome classification.Neoplasm Proteins: Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Osteoblasts: Bone-forming cells which secrete an EXTRACELLULAR MATRIX. HYDROXYAPATITE crystals are then deposited into the matrix to form bone.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Enhancer Elements, Genetic: Cis-acting DNA sequences which can increase transcription of genes. Enhancers can usually function in either orientation and at various distances from a promoter.Protein Binding: The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.Translocation, Genetic: A type of chromosome aberration characterized by CHROMOSOME BREAKAGE and transfer of the broken-off portion to another location, often to a different chromosome.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Osteogenesis: The process of bone formation. Histogenesis of bone including ossification.Osteocalcin: Vitamin K-dependent calcium-binding protein synthesized by OSTEOBLASTS and found primarily in BONES. Serum osteocalcin measurements provide a noninvasive specific marker of bone metabolism. The protein contains three residues of the amino acid gamma-carboxyglutamic acid (Gla), which, in the presence of CALCIUM, promotes binding to HYDROXYAPATITE and subsequent accumulation in BONE MATRIX.Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.Leukemia, Myeloid: Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.Pol1 Transcription Initiation Complex Proteins: Factors that form a preinitiation complex at promoters that are specifically transcribed by RNA POLYMERASE I.Alkaline Phosphatase: An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.Promoter Regions, Genetic: DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Core Binding Factor Alpha 3 Subunit: A transcription factor that dimerizes with the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly conserved DNA-binding domain known as the runt domain.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.Telomeric Repeat Binding Protein 1: A ubiquitously expressed telomere-binding protein that is present at TELOMERES throughout the CELL CYCLE. It is a suppressor of telomere elongation and may be involved in stabilization of telomere length. It is structurally different from TELOMERIC REPEAT BINDING PROTEIN 2 in that it contains acidic N-terminal amino acid residues.G-Box Binding Factors: A family of transcription factors found primarily in PLANTS that bind to the G-box DNA sequence CACGTG or to a consensus sequence CANNTG.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Access to Information: Individual's rights to obtain and use information collected or generated by others.Stem Cells: Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.Journal Impact Factor: A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.Saccharomyces cerevisiae: A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.Saccharomyces cerevisiae Proteins: Proteins obtained from the species SACCHAROMYCES CEREVISIAE. The function of specific proteins from this organism are the subject of intense scientific interest and have been used to derive basic understanding of the functioning similar proteins in higher eukaryotes.Sodium Fluoride: A source of inorganic fluoride which is used topically to prevent dental caries.Fluorides: Inorganic salts of hydrofluoric acid, HF, in which the fluorine atom is in the -1 oxidation state. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed) Sodium and stannous salts are commonly used in dentifrices.Fluoride PoisoningDepsipeptides: Compounds consisting of chains of AMINO ACIDS alternating with CARBOXYLIC ACIDS via ester and amide linkages. They are commonly cyclized.Leukemia, Lymphocytic, Chronic, B-Cell: A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.Histone Deacetylase Inhibitors: Compounds that inhibit HISTONE DEACETYLASES. This class of drugs may influence gene expression by increasing the level of acetylated HISTONES in specific CHROMATIN domains.Cytarabine: A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472)Dictionaries, MedicalLeukemia Virus, Murine: Species of GAMMARETROVIRUS, containing many well-defined strains, producing leukemia in mice. Disease is commonly induced by injecting filtrates of propagable tumors into newborn mice.

FIRE3 in the promoter of the rat fatty acid synthase (FAS) gene binds the ubiquitous transcription factors CBF and USF but does not mediate an insulin response in a rat hepatoma cell line. (1/96)

Several putative insulin-responsive elements (IRE) in the fatty acid synthase (FAS) promoter have been identified and shown to be functional in adipocytes and hepatocytes. Here we report on the insulin-responsiveness in the rat hepatoma cell line H4IIE of four cis-elements in the FAS promoter: the FAS insulin-responsive elements, FIRE2 and FIRE3; the inverted CCAAT element, ICE; and the insulin/glucose-binding element, designated hepatic FIRE element, hFIRE, originally identified in rat hepatocytes. Using electrophoretic mobility shift assay (EMSA) competition experiments together with supershifts and in vitro transcription/translation we show that FIRE3 (-68/-58) binds not only the upstream stimulatory factors USF-1/USF-2 but also the CCAAT-binding factor CBF, also known as the nuclear factor Y, NF-Y. The putative IRE FIRE2, which shows sequence similarity to FIRE3, is located between -267 and -249. Gel retardation experiments indicate that USF-1 and USF-2 also bind to this element, which contains an imperfect E-box motif. Using the same approach we have shown that hFIRE binds the stimulatory proteins Sp1 and Sp3 in addition to CBF. Transient transfection experiments using FAS promoter constructs deleted for FIRE2 and FIRE3 demonstrate that neither of these elements mediates the insulin response of the FAS promoter in the rat hepatoma cell line H4IIE, however, ICE at -103/-87 is responsible for mediating the effect of the insulin antagonist cAMP. The hFIRE element located at -57/-34, in spite of its role in the glucose/insulin response in primary rat hepatocytes, is apparently not involved in the insulin regulation of the rat FAS promoter in H4IIE cells. The fact that the topology of the promoters of the FAS genes in rat, human, goose and chicken is conserved regarding CBF-binding sites and USF-binding sites implies an important role for these ubiquitously expressed transcription factors in the regulation of the FAS promoter.  (+info)

Collagenase 3 is a target of Cbfa1, a transcription factor of the runt gene family involved in bone formation. (2/96)

Collagenase 3 (MMP-13) is a recently identified member of the matrix metalloproteinase (MMP) gene family that is expressed at high levels in diverse human carcinomas and in articular cartilage from arthritic patients. In addition to its expression in pathological conditions, collagenase 3 has been detected in osteoblasts and hypertrophic chondrocytes during fetal ossification. In this work, we have evaluated the possibility that Cbfa1 (core binding factor 1), a transcription factor playing a major role in the expression of osteoblastic specific genes, is involved in the expression of collagenase 3 during bone formation. We have functionally characterized a Cbfa motif present in the promoter region of collagenase 3 gene and demonstrated, by cotransfection experiments and gel mobility shift assays, that this element is involved in the inducibility of the collagenase 3 promoter by Cbfa1 in osteoblastic and chondrocytic cells. Furthermore, overexpression of Cbfa1 in osteoblastic cells unable to produce collagenase 3 leads to the expression of this gene after stimulation with transforming growth factor beta. Finally, we show that mutant mice deficient in Cbfa1, lacking mature osteoblasts but containing hypertrophic chondrocytes which are also a major source of collagenase 3, do not express this protease during fetal development. These results provide in vivo evidence that collagenase 3 is a target of the transcriptional activator Cbfa1 in these cells. On the basis of these transcriptional regulation studies, together with the potent proteolytic activity of collagenase 3 on diverse collagenous and noncollagenous bone and cartilage components, we proposed that this enzyme may play a key role in the process of bone formation and remodeling.  (+info)

Does adult fracture repair recapitulate embryonic skeletal formation? (3/96)

Bone formation is a continuous process that begins during fetal development and persists throughout life as a remodeling process. In the event of injury, bones heal by generating new bone rather than scar tissue; thus, it can accurately be described as a regenerative process. To elucidate the extent to which fetal skeletal development and skeletal regeneration are similar, we performed a series of detailed expression analyses using a number of genes that regulate key stages of endochondral ossification. They included genes in the indian hedgehog (ihh) and core binding factor 1 (cbfa1) pathways, and genes associated with extracellular matrix remodeling and vascular invasion including vascular endothelial growth factor (VEGF) and matrix metalloproteinase 13 (mmp13). Our analyses suggested that even at the earliest stages of mesenchymal cell condensation, chondrocyte (ihh, cbfa1 and collagen type II-positive) and perichondrial (gli1 and osteocalcin-positive) cell populations were already specified. As chondrocytes matured, they continued to express cbfa1 and ihh whereas cbfa1, osteocalcin and gli1 persisted in presumptive periosteal cells. Later, VEGF and mmp13 transcripts were abundant in chondrocytes as they underwent hypertrophy and terminal differentiation. Based on these expression patterns and available genetic data, we propose a model where Ihh and Cbfa1, together with Gli1 and Osteocalcin participate in establishing reciprocal signal site of injury. The persistence of cbfa1 and ihh, and their targets osteocalcin and gli1, in the callus suggests comparable processes of chondrocyte maturation and specification of a neo-perichondrium occur following injury. VEGF and mmp13 are expressed during the later stages of healing, coincident with the onset of vascularization of the callus and subsequent ossification. Taken together, these data suggest the genetic mechanisms regulating fetal skeletogenesis also regulate adult skeletal regeneration, and point to important regulators of angiogenesis and ossification in bone regeneration.  (+info)

Mutation analysis of core binding factor A1 in patients with cleidocranial dysplasia. (4/96)

Cleidocranial dysplasia (CCD) is a dominantly inherited disorder characterized by patent fontanelles, wide cranial sutures, hypoplasia of clavicles, short stature, supernumerary teeth, and other skeletal anomalies. We recently demonstrated that mutations in the transcription factor CBFA1, on chromosome 6p21, are associated with CCD. We have now analyzed the CBFA1 gene in 42 unrelated patients with CCD. In 18 patients, mutations were detected in the coding region of the CBFA1 gene, including 8 frameshift, 2 nonsense, and 9 missense mutations, as well as 2 novel polymorphisms. A cluster of missense mutations at arginine 225 (R225) identifies this residue as crucial for CBFA1 function. In vitro green fluorescent protein fusion studies show that R225 mutations interfere with nuclear accumulation of CBFA1 protein. There is no phenotypic difference between patients with deletions or frameshifts and those with other intragenic mutations, suggesting that CCD is generally caused by haploinsufficiency. However, we were able to extend the CCD phenotypic spectrum. A missense mutation identified in one family with supernumerary teeth and a radiologically normal skeleton indicates that mutations in CBFA1 can be associated exclusively with a dental phenotype. In addition, one patient with severe CCD and a frameshift mutation in codon 402 had osteoporosis leading to recurrent bone fractures and scoliosis, providing first evidence that CBFA1 may help maintain adult bone, in addition to its function in bone development.  (+info)

A full-length Cbfa1 gene product perturbs T-cell development and promotes lymphomagenesis in synergy with myc. (5/96)

The Cbfa1/PEBP2 alpha A/AML3 gene plays an essential role in osteogenesis but is also expressed in the T-cell lineage where it has been implicated in lymphoma development as a target for retroviral insertional mutagenesis. As lymphoma cells with til-1 insertion express at least five distinct Cbfa1 isoforms, it is important to establish which, if any, have intrinsic oncogenic potential. We have generated transgenic mice in which the most abundant lymphoma isoform (G1/p57) is expressed under the control of the CD2 locus control region. Co-precipitation analysis of transgenic thymus revealed high levels of Cbfa1 protein in an abundant complex containing the binding cofactor Cbfb. CD2-Cbfa1-G1 mice displayed abnormal T-cell development, with a pronounced skew towards CD8 SP cells in the thymus and developed a low incidence of spontaneous lymphomas (6% at 12 months) with cells of similar phenotype. Strongly synergistic tumour development was seen when CD2-Cbfa1-G1 mice were crossed with lines carrying myc transgenes (CD2-myc or tamoxifen-regulatable CD2-mycER) and Cbfa1 was found to rescue expression of the CD2-myc transgene in pre-leukaemic mice. However, synergy did not appear to be due to a dominant block of myc-induced apoptosis by Cbfa1 as explanted primary tumours and cell lines from CD2-Cbfa1-G1/CD2-mycER mice showed accelerated death on induction with tamoxifen at similar rates to CD2-mycER controls. Moreover, thymocytes from preleukaemic CD2-Cbfa1-G1 mice showed reduced survival in vitro and increased sensitivity to the inhibitory effects of TGF-beta. This study demonstrates that a full-length Cbf alpha-chain gene can act as an oncogene without fusion to a heterologous protein.  (+info)

Parathyroid hormone regulation of the rat collagenase-3 promoter by protein kinase A-dependent transactivation of core binding factor alpha1. (6/96)

Previously we showed that the activator protein-1 site and the runt domain binding site in the collagenase-3 promoter act cooperatively in response to parathyroid hormone (PTH) in the rat osteoblastic osteosarcoma cell line, UMR 106-01. Our results of the expression pattern of core binding factor alpha1 (Cbfa1), which binds to the runt domain site, indicated that there is no change in the levels of Cbfa1 protein or RNA under either control conditions or after PTH treatment. The importance of posttranslational modification of Cbfa1 in the signaling pathway for PTH-induced collagenase-3 promoter activity was analyzed. PTH stimulation of collagenase-3 promoter activity was completely abrogated by protein kinase A (PKA) inhibition. To determine the role of PKA activity with respect to Cbfa1 activation (in addition to its known activity of phosphorylating cAMP-response element-binding protein to enhance c-fos promoter activity), we utilized the heterologous Gal4 transcription system. PTH stimulated the transactivation of activation domain-3 in Cbfa1 through the PKA site. In vitro phosphorylation studies indicated that the PKA site in the wild type activation domain-3 is a substrate for phosphorylation by PKA. Thus, we demonstrate that PTH induces a PKA-dependent transactivation of Cbfa1, and this transactivation is required for collagenase-3 promoter activity in UMR cells.  (+info)

An osteogenesis-related transcription factor, core-binding factor A1, is constitutively expressed in the chondrocytic cell line TC6, and its expression is upregulated by bone morphogenetic protein-2. (7/96)

Core-binding factor A1 (Cbfa1), also called Pebp2 alpha A/AML3, is a transcription factor that belongs to the runt-domain gene family. Cbfa1-deficient mice are completely incapable of both endochondral and intramembranous bone formation, indicating that Cbfa1 is indispensable for osteogenesis. Maturation of chondrocytes in these mice is also disorganized, suggesting that Cbfa1 may also play a role in chondrogenesis. The aim of this study was to examine the expression and regulation of Pebp2 alpha A/AML3/Cbfa1 expression in the chondrocyte-like cell line, TC6. Northern blot analysis indicated that Cbfa1 mRNA was constitutively expressed as a 6.3 kb message in TC6 cells and the level of Cbfa1 expression was enhanced by treatment with bone morphogenetic protein-2 (BMP2) in a time- and dose-dependent manner. This effect was blocked by an RNA polymerase inhibitor, 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole, but not by a protein synthesis inhibitor, cycloheximide. Western blot analysis of the cell lysates using polyclonal antibody raised against Cbfa1 indicated that BMP2 treatment increased the Cbfa1 protein level in TC6 cells. In TC6 cells, BMP2 treatment enhanced expression of alkaline phosphatase and type I collagen mRNAs but suppressed that of type II collagen mRNA. In addition to TC6 cells, Cbfa1 mRNA was also expressed in primary cultures of chondrocytes and BMP2 treatment enhanced Cbfa1 mRNA expression in these cells similarly to its effect on TC6 cells. These data indicate that the Pebp2 alpha A/AML3/Cbfa1 gene is expressed in a chondrocyte-like cell line, TC6, and its expression is enhanced by treatment with BMP.  (+info)

Exogenous cdk4 overcomes reduced cdk4 RNA and inhibition of G1 progression in hematopoietic cells expressing a dominant-negative CBF - a model for overcoming inhibition of proliferation by CBF oncoproteins. (8/96)

Core Binding Factor (CBF) is required for the development of definitive hematopoiesis, and the CBF oncoproteins AML1-ETO, TEL-AML1, and CBFbeta-SMMHC are commonly expressed in subsets of acute leukemia. CBFbeta-SMMHC slows the G1 to S cell cycle transition in hematopoietic cells, but the mechanism of this effect is uncertain. We have sought to determine whether inhibition of CBF-mediated trans-activation is sufficient to slow proliferation. We demonstrate that activation of KRAB-AML1-ER, a protein containing the AML1 DNA-binding domain, the KRAB repression domain, and the Estrogen receptor ligand binding domain, also slows G1, if its DNA-binding domain is intact. Also, exogenous AML1 overcame CBFbeta-SMMHC-induced inhibition of proliferation. Representational difference analysis (RDA) identified cdk4 RNA expression as an early target of KRAB-AML1 activation. Inhibition of CBF activities by KRAB-AML1-ER or CBFbeta-SMMHC rapidly reduced endogenous cdk4 mRNA levels, even in cells proliferating at or near control rates as a result of exogenous cdk4 expression. Over-expression of cdk4, especially a variant which cannot bind p16INK4a, overcame cell cycle inhibition resulting from activation of KRAB-AML1-ER, although cdk4 did not accelerate proliferation when expressed alone. These findings indicate that mutations which alter the expression of G1 regulatory proteins can overcome inhibition of proliferation by CBF oncoproteins. Oncogene (2000).  (+info)

Approximately 40% of patients affected by core binding factor (CBF) acute myeloid leukemia (AML) ultimately die from the disease. Few prognostic markers have been identified. In this study we reviewed 192 patients with core binding factor acute myeloid leukemia (AML), treated with curative intent (age, 15-79 years) in 11 Italian institutions. Overall, 10-year overall survival (OS), disease-free survival (DFS), and event-free survival were 63.9%, 54.8%, and 49.9%, respectively; patients with the t(8;21) and inv(16) chromosomal rearrangements exhibited significant differences at diagnosis. Despite similarly high complete remission (CR) rate, patients with inv(16) experienced superior DFS and a high chance of achieving a second CR, often leading to prolonged OS also after relapse. We found that a complex karyotype (ie, ≥4 cytogenetic anomalies) affected survival; the KIT D816 mutation predicted worse prognosis only in patients with the t(8;21) rearrangement, whereas FLT3 mutations had no ...
Stem Cells International is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies in all areas of stem cell biology and applications. The journal will consider basic, translational, and clinical research, including animal models and clinical trials.
This study is examining the appropriate dose and side effects of dasatinib, when it is given with the standard of care chemotherapy for children and adolescents
KIT is a receptor tyrosine kinase that is functionally relevant for hematopoiesis, mast cell development and function, gametogenesis and melanogenesis. Normal KIT signaling requires binding to stem cell factor, and PI3K-Akt is one of the putative effector pathways. In humans, germline loss-of-function KIT mutations have been associated with piebaldism - an autosomal dominant condition characterized by depigmented patches of skin and hair. Gain-of-function KIT mutations are usually acquired and have been associated with myeloid malignancies including core binding factor acute myeloid leukemia and systemic mastocytosis (SM), germ cell tumors, gastrointestinal stromal tumors and sinonasal T cell lymphomas. KITD816V is the most prevalent KIT mutation in mast cell disease and occurs in more than 90% of the cases that fulfill the World Health Organization diagnostic criteria for SM. However, its precise pathogenetic contribution is not well understood. In clinical practice, SM is considered either indolent or
core binding factor alpha: core binding factor plays a key role in several development pathways and in human disease; has been sequenced
TY - JOUR. T1 - Selection of reversions and suppressors of a mutation in the CBF binding site of a lymphomagenic retrovirus. AU - Martiney, Marita J.. AU - Rulli, Karen. AU - Beaty, Robert. AU - Levy, Laura S.. AU - Lenz, Jack. PY - 1999/8/23. Y1 - 1999/8/23. N2 - The retrovirus SL3 induces T-cell lymphomas in mice. The transcriptional enhancer in the long terminal repeat (LTR) of SL3 contains two 72-bp repeats. Each repeat contains a binding site for the transcription factor CBF (also called AML1). The CBF binding sites are called core elements. SAA is a mutant that is identical to SL3 except for the presence of a single-base-pair substitution in each of the two core elements. This mutation significantly attenuates viral lymphomagenicity. Most lymphomas that occur in SAA-infected mice contain proviruses with reversions or second-site suppressor mutations within the core element. We examined the selective pressures that might account for the predominance of the reversions and suppressor ...
The purpose of the study is to determine whether Fludarabine in combination with cytarabine is more effective than high-dose cytarabine in post-remission
PRIMARY OBJECTIVES:. I. To assess the safety and tolerability of dasatinib with intensive induction therapy (daunorubicin hydrochloride and cytarabine), consolidation chemotherapy (high-dose cytarabine), and as single agent in maintenance therapy in patients with newly diagnosed core-binding factor acute myeloid leukemia (AML).. SECONDARY OBJECTIVES:. I. To assess clinical outcomes such as event-free survival (EFS), complete response (CR) rate, cumulative incidence of relapse (CIR), cumulative incidence of death (CID), disease-free survival (DFS), and overall survival (OS) of patients treated with these regimens.. II. To describe the frequency and severity of adverse events of patients treated on this study during induction, consolidation, and continuation therapy.. III. To describe the interaction of pretreatment disease and patient characteristics including morphology, cytogenetics, immunophenotype, molecular genetic features, white blood cell (WBC) count and hemogram, and performance status ...
The Runx1-CBFbeta transcription factor is required for the emergence of all definitive hematopoietic cells. It is the earliest specific marker of sites from whi...
Among patients with good prognosis core binding factor AML, there is an overall survival rate of only 44%. To understand the genetic factors contributing to poor outcomes within this subgroup, Dr Chew is analysing bone marrow samples collected from 18 patients before and during treatment.. According to Dr Chew, multiple genetic abnormalities acquired during therapy are probably responsible for good prognosis core binding AML developing resistance to chemotherapy.. "To help us predict who will respond poorly to therapy, were identifying the genetic mutations occurring in patients who relapse," he said. "This information will allow us to tailor patient treatment accordingly. Currently a stem cell transplant is considered the definitive treatment and our findings will help clinicians decide if their patients AML will develop resistance and if a stem cell transplant is recommended.". Dr Chew is testing the usefulness of the genetic variations he identifies through an international ...
Disease, Muscle, Muscle Cells, Smooth Muscle, Smooth Muscle Cells, Cells, Heme, Hydrogen, Alkaline Phosphatase, Kidney, Kidney Disease, Osteocalcin, Upregulation, Vascular Calcification, Calcium, Heme Oxygenase, Vascular Smooth Muscle, Atherosclerosis, Bone, Core Binding Factor
This phase II study of romidepsin in relapsed and refractory AML shows that this HDACI has a differential antileukemic activity in patients with CBF AML [predominantly t(8;21)] and that this was associated with an up-regulation of AML1 target genes. These findings are in keeping with observations in vitro that have established that t(8;21) AML is sensitive to therapy with various HDACIs including romidepsin (7, 16-19, 27). Despite the in vitro evidence suggesting an inherent sensitivity of this cytogenetic subset of AML to this class of agents, this is the first study to actually show antileukemic activity in vivo in a cohort of patients with t(8;21) AML and other translocations involving the AML1 gene.. Romidepsin has been investigated in a phase I trial (28) conducted at this dose and schedule in two groups of patients with chronic lymphocytic leukemia and AML, respectively. In that trial that involved 10 AML patients, there were no patients with CBF AML. There were no objective responses ...
Cells, Lead, Acute Myeloid Leukemia, Bone, Bone Marrow, Core-binding Factor, Cytogenetic, Cytogenetic Abnormalities, Disease, Leukemia, Marrow, Myeloid Leukemia, Patient, Patients, Protein Array, Proteins, Regression, Regression Analysis, Ability, Algorithm
Looking for online definition of core-binding factor, runt domain, alpha subunit 3 in the Medical Dictionary? core-binding factor, runt domain, alpha subunit 3 explanation free. What is core-binding factor, runt domain, alpha subunit 3? Meaning of core-binding factor, runt domain, alpha subunit 3 medical term. What does core-binding factor, runt domain, alpha subunit 3 mean?
As per available reports about 248 journals, 14 Conferences and workshops are presently dedicated exclusively to Acute Respiratory Failure and about 1
To study the effects and importance of fluoride on FBs in the development of extraperiosteal calcification and the ossification of skeletal fluorosis, the presence of the osteogenic phenotype, which is indicated by the expression of core-binding factor a1 (Cbfa1) and osteocalcin (OCN), in an FB cell line (L929) and in osteoblasts (OBs) exposed to fluoride was determined. Fibroblasts and osteoblasts were exposed to different concentrations of fluoride (0, 0.0001, 0.001, 0.1, 1.0, 10.0 and 20.0mg/L F-). By using RT-PCR and ELISA, the mRNA levels of Cbfa1 and OCN were measured at 48h, and the protein levels of Cbfa1 and OCN were measured at 2, 4, 24, 48 and 72h. The data demonstrated the following: (1) The Cbfa1 protein level in fluoride-treated fibroblasts clearly increased at 48h in the groups treated with 0.0001, 0.001, 0.1, 1.0 and 20.0mg/L F-. The Cbfa1 protein level of the group treated with 10mg/L F- at 72h was higher than that of the control group. The level of Cbfa1 mRNA in the fibroblasts ...
TY - JOUR. T1 - HDAC1 is a required cofactor of CBFb-SMMHC and a potential therapeutic target in inversion 16 acute myeloid leukemia. AU - Richter, Lisa E.. AU - Wang, Yiqian. AU - Becker, Michelle E.. AU - Coburn, Rachel A.. AU - Williams, Jacob T.. AU - Amador, Catalina. AU - Hyde, R. Katherine. PY - 2019/6/1. Y1 - 2019/6/1. N2 - Acute myeloid leukemia (AML) is a neoplastic disease characterized by the uncontrolled proliferation and accumulation of immature myeloid cells. A common mutation in AML is the inversion of chromosome 16 [inv (16)], which generates a fusion between the genes for core binding factor beta (CBFB) and smooth muscle myosin heavy chain gene (MYH11), forming the oncogene CBFB-MYH11. The expressed protein, CBFb-SMMHC, forms a heterodimer with the key hematopoietic transcription factor RUNX1. Although CBFb-SMMHC was previously thought to dominantly repress RUNX1, recent work suggests that CBFb-SMMHC functions together with RUNX1 to activate transcription of specific target ...
The novel FMS-like tyrosine kinase 3 (FLT3)-N676K point mutation within the FLT3 kinase domain-1 was recently identified in 6 % of de novo acute myeloid leukemia (AML) patients with inv(16). Because FLT3-N676K was encountered almost exclusively in inv(16) AML, we investigated the transforming potential of FLT3-N676K, the cooperation between FLT3-N676K and core binding factor ß-smooth muscle myosin heavy chain (CBFß-SMMHC) (encoded by the inv(16) chimeric gene CBFB-MYH11) in inducing acute leukemia, and tested the sensitivity of FLT3-N676K-positive leukemic cells to FLT3 inhibitors. Retroviral expression of FLT3-N676K in myeloid 32D cells induced AML in syngeneic C3H/HeJ mice (n = 11/13, median latency 58 days), with a transforming activity similar to FLT3-internal tandem duplication (ITD) (n = 8/8), FLT3-TKD D835Y (n = 8/9), and FLT3-ITD-N676K (n = 9/9) mutations. Three out of 14 (21.4 %) C57BL/6J mice transplanted with FLT3-N676K-transduced primary hematopoietic progenitor cells developed ...
Core binding factor (CBF) is a heterodimeric transcription factor that is essential for a number of developmental process including hemotopoiesis and bone development. CBFs contain a DNA-binding CBFα. subunit and a non-DNA binding CBFß. subunit ...
The pathogenesis of PDAC involves genetic alterations, such as K-ras protooncogene mutations, mutations of the p53, p16, and Smad4 tumour suppressor genes, and other less common mutations.2 In addition, there are numerous epigenetic alterations, including altered expression of several growth factors and their receptors.3 For example, PDACs overexpress all TGFβ isoforms and their receptors, and overexpression of these ligands and receptors is often associated with shortened postoperative survival of patients with pancreatic cancer.14,15. The TGFβ pathway is carefully regulated, with Smad proteins as the key component in the signal transduction pathway. In addition, other regulators, such as transcription factors, which facilitate Smad binding to target promoters, may provide routes for feedback and crosstalk.16 For example, members of the CBFA (core binding factor A) family of transcription factors act both as targets and partners of activated Smads. This family, also termed the "Runx family", ...
According to Dr. Stone, MRD status in CBF-AML might also make a difference in treatment selection. A separate study of patients with CBF-AML found that those with an MRD level of at least 1% at one point following induction therapy experienced relapse 90% of the time, with a median remission duration of 10 months (P , .001).4 "This is one group of patients we could justify transplanting," Dr. Stone observed, "but that doesnt mean its going to make a difference.". MRD test results have also been shown to improve outcome prediction,5 albeit modestly, when included with more typical clinical data (ie, age, gender, performance status, white blood cell count, platelet count, bone marrow blast percentage, cytogenetic risk, and NPM1/FLT3-ITD status). Because predictive outcome was only improved by 3%, however, MRD testing is not worth the effort for that reason alone, according to Dr. Stone.. Testing Limitations. Whether performed with multiparameter flow cytometry or next-generation sequencing, MRD ...
Decreased Llgl1 expression has been previously shown to be associated with increased metastatic potential, malignant phenotype, or inferior survival in a variety of solid tumors (Ohali et al., 2004; Schimanski et al., 2005; Kuphal et al., 2006). Given that Llgl1 restrains self-renewal in HSCs and that leukemia is characterized by aberrant activation of self-renewal, we assessed for a role in human AML. First, we asked whether the gene expression signature revealed by genetic inactivation of Llgl1 (Llgl1−/− signature) in HSCs was associated with any genetic subtypes of primary AML. Indeed, clustering based on the Llgl1−/− signature (Fig. 4 B) grouped AML cases into subgroups significantly associated with cytogenetic abnormalities (Fig. 4, B and C). Especially core-binding factor leukemias (t(8;21) and inv(16)) or t(15;17) clustered into specific subgroups. Moreover, the Llgl1−/− signature was most strongly correlated with group 7 based on hierarchical clustering. This group contained ...
Core binding factors are heterodimeric transcription factors involved in diverse developmental processes. They consist of a DNA binding Runx subunit and a non-DNA binding CBFβ sub-unit. Runx proteins are encoded by three genes: Runx1, Runx2 , and ...
Complete information for CBFB gene (Protein Coding), Core-Binding Factor Beta Subunit, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
A series of studies of f-electron systems based on density functional theory methods have been performed. The focus of the studies has been on magnetic and structural properties, as well as investigating ways to handle strong electron correlation in these systems.. A version of the self-interaction correction (SIC) method has been developed for a full-potential linear muffin-tin orbital method. The method is demonstrated to have the strong capabilities of previous SIC implementations, to study energetics and phase stabilities of d- and f-electron systems with localisation-delocalisation transitions, but with no geometrical constraints from the underlying band structure method. The method is applied to the high-TC superconductor CeOFeAs, in which the f-shell of the Ce atoms is argued to undergo a Mott transition to a delocalised state under pressure.. The non-collinear magnetic structures of two rare earth compounds, TbNi5 and CeRhIn5 have been studied, and in both cases the complex magnetic ...
Saturday, October 17, 1953 ld Blinds The Daily Register-Mail, Galesburg, Til- Saturday, October 17, 1953 , 8 GALVA-Meeting of duck hunters of Lake Calhoun Association was held Thursday night at the clubhouse. Plans were made for those Interested to meet at 8 oclock Sunday morning at the clubhouse to build blinds for the hu. Edition of Galesburg Register-Mail
PHP & Kejuruteraan Perisian Projects for $250 - $750. Prescription Pad Writing Software contrive by CompuRx Infotech Pvt. Ltd. is having the ability to check for drug safety at individual disease level like in case of G6PD(40 drugs contraindicated), POR...
The protein encoded by this gene is the beta subunit of a heterodimeric core-binding transcription factor belonging to the PEBP2/CBF transcription factor family which master-regulates a host of genes specific to hematopoiesis (e.g., RUNX1) and osteogenesis (e.g., RUNX2). The beta subunit is a non-DNA binding regulatory subunit; it allosterically enhances DNA binding by alpha subunit as the complex binds to the core site of various enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers and GM-CSF promoters. Alternative splicing generates two mRNA variants, each encoding a distinct carboxyl terminus. In some cases, a pericentric inversion of chromosome 16 [inv(16)(p13q22)] produces a chimeric transcript consisting of the N terminus of core-binding factor beta in a fusion with the C-terminal portion of the smooth muscle myosin heavy chain 11. This chromosomal rearrangement is associated with acute myeloid leukemia of the M4Eo subtype. Two ...
Autor: Otto, Florian et al.; Genre: Zeitschriftenartikel; Im Druck veröffentlicht: 2002-02-13; Keywords: cleidocranial dysplasia; CCD; transcription factor; core binding factor; runt domain; RUNX2; CBFA1; differentiation; osteoblast; Titel: Mutations in the RUNX2 gene in patients with cleidocranial dysplasia
TY - JOUR. T1 - Runx1 expression marks long-term repopulating hematopoietic stem cells in the midgestation mouse embryo. AU - North, Trista E.. AU - De Bruijn, Marella F T R. AU - Stacy, Terryl. AU - Talebian, Laleh. AU - Lind, Evan. AU - Robin, Catherine. AU - Binder, Michael. AU - Dzierzak, Elaine. AU - Speck, Nancy A.. PY - 2002. Y1 - 2002. N2 - Hematopoietic stem cells (HSCs) are first found in the aorta-gonad-mesonephros region and vitelline and umbilical arteries of the midgestation mouse embryo. Runx1 (AML1), the DNA binding subunit of a core binding factor, is required for the emergence and/or subsequent function of HSCs. We show that all HSCs in the embryo express Runx1. Furthermore, HSCs in Runx1+/- embryos are heterogeneous and include CD45+ cells, endothelial cells, and mesenchymal cells. Comparison with wild-type embryos showed that the distribution of HSCs among these various cell populations is sensitive to Runx1 dosage. These data provide the first morphological description of ...
Only the PBM motif is a classic HLH motif. Three different ChIP-chip-derived motifs are all diverse, but all score highly on ChIP-chip data! Are they motifs of other TFs? Check. 602: GCN4; 1095, TEC1; 1096: resembles 602, but is a closer match to CUP9/TOS8. Also hits GCN4. According to the literature (PMID: 9032238) the core binding site for the Rtg1p-Rtg3p heterodimer is 5-GGTCAC-3; the only motif that resembles this is 1446. Vague resemblance to 602 and 1096. I am going to retain 1446, which represents the literature site; PBM motif 870, which resembles an E-box, and ChIP-chip motif 1445, which scores highest on ChIP-chip data. But give all low confidence ...
Runx1 mediates the development of the granular convoluted tubules in the submandibular glands[1] "The mouse granular convoluted tubules (GCTs), which are only located in the submandibular gland (SMG) are known to develop and maintain their structure in an androgen-dependent manner. We previously demonstrated that the GCTs are involuted by the epithelial deletion of core binding factor β (CBFβ), a transcription factor that physically interacts with any of the Runt-related transcription factor (RUNX) proteins (RUNX1, 2 and 3). This result clearly demonstrates that the Runx /Cbfb signaling pathway is indispensable in the development of the GCTs. However, it is not clear which of the RUNX proteins plays useful role in the development of the GCTs by activating the Runx /Cbfb signaling pathway. Past studies have revealed that the Runx /Cbfb signaling pathway plays important roles in various aspects of development and homeostatic events. Moreover, the Runx genes have different temporospatial ...
View mouse Terf2ip Chr8:112011398-112020528 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
Translokacje chromosomalne modyfikujące Core-Binding Factor[edytuj , edytuj kod]. Ostra białaczka mielobastyczna z cechami ... Core-binding factor acute myeloid leukemia.. „Arch Pathol Lab Med". 135 (11), s. 1504-9, Nov 2011. DOI: 10.5858/arpa.2010-0482- ... Core binding factor genes and human leukemia. „Haematologica". 87 (12), s. 1307-23, Dec 2002. PMID: 12495904. ... Core-binding factor acute myeloid leukemia: can we improve on HiDAC consolidation?. „Hematology Am Soc Hematol Educ Program". ...
RNA polymerase II core promoter proximal region sequence-specific DNA binding. • chromatin binding. • transcription factor ... transcription factor activity, sequence-specific DNA binding. • mitogen-activated protein kinase p38 binding. • FK506 binding. ... DNA binding. • RNA polymerase II regulatory region sequence-specific DNA binding. • RNA polymerase II transcription factor ... protein binding. • transcription factor activity, RNA polymerase II distal enhancer sequence-specific binding. • RNA polymerase ...
Core-binding factor subunit beta is a protein that in humans is encoded by the CBFB gene. The protein encoded by this gene is ... Core binding factor acute myeloid leukaemia is a cancer related to genetic changes in the CBF gene. It is most commonly caused ... "Entrez Gene: CBFB core-binding factor, beta subunit". The Cancer Genome Atlas Network (2012). "Comprehensive molecular ... Hart SM, Foroni L (2003). "Core binding factor genes and human leukemia". Haematologica. 87 (12): 1307-23. PMID 12495904. Bae ...
Runt-related transcription factor 1 (RUNX1) also known as acute myeloid leukemia 1 protein (AML1) or core-binding factor ... It belongs to the Runt-related transcription factor (RUNX) family of genes which are also called core binding factor-α (CBFα). ... but its DNA binding affinity is enhanced by 10 fold if it heterodimerises with the core binding factor β (CBFβ), also via the ... RUNX can behave as heterodimeric transcription factors collectively called the core binding factors (CBFs). The consensus ...
Bernués J, Espel E, Querol E (1986). "Identification of the core-histone-binding domains of HMG1 and HMG2". Biochim. Biophys. ... In the nucleus HMGB1 interacts with nucleosomes, transcription factors, and histones. This nuclear protein organizes the DNA ... After binding, HMGB1 bends DNA, which facilitates the binding of other proteins. HMGB1 supports transcription of many genes in ... Contact with core histones changes the structure of nucleosomes. The presence of HMGB1 in the nucleus depends on ...
Binding to HS stabilizes fibroblast growth factors (FGFs) and vascular endothelial growth factors (VEGFs) and prevents them ... The basic HSPG structure consists of a protein core to which several linear heparin sulfate (HS) chains are covalently O-linked ... Growth factors such as epidermal growth factor (EGF), fibroblast growth factor (FGF) and transforming growth factor beta (TGF-β ... heparin-binding growth factors, chemokines and lipoproteins. HSPGs are prominent components of blood vessels. ...
... core protein binds to the growth factors BMP-4 and influences its bioactivity. It has also been reported that the ... There is also evidence that biglycan binds to TGF-beta 1. Biglycan interacts with collagen, both via the core protein and GAG ... Bidanset DJ, Guidry C, Rosenberg LC, Choi HU, Timpl R, Hook M (March 1992). "Binding of the proteoglycan decorin to collagen ... The structure of biglycan core protein is highly conserved across species; over 90% homology has been reported for rat, mouse, ...
"Entrez Gene: CBFA2T2 core-binding factor, runt domain, alpha subunit 2; translocated to, 2". Rual JF, Venkatesan K, Hao T, ... The protein encoded by this gene binds to the AML1-MTG8 complex and may be important in promoting leukemogenesis. Several ...
"Entrez Gene: CBFA2T3 core-binding factor, runt domain, alpha subunit 2; translocated to, 3". Hoogeveen AT, Rossetti S, ... makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain". Mol. Cell. ...
"New core promoter element in RNA polymerase II-dependent transcription: sequence-specific DNA binding by transcription factor ... In the case of a transcription factor binding site, there may be a single sequence that binds the protein most strongly under ... An example is the E-box (sequence CACGTG), which binds transcription factors in the basic helix-loop-helix (bHLH) family (e.g. ... The process is more complicated, and at least seven different factors are necessary for the binding of an RNA polymerase II to ...
Proneural proteins specifically bind DNA sequences that contain a core hexanucleotide motif, CANNTG, known as an E-box. The ... Because heterodimerization is a prerequisite for DNA binding, factors that interfere with dimerization effectively act as ... they express a membrane bound ligand, called ''Delta'', which binds and activate Notch receptors expressed in neighboring cells ... contacts between bHLH residues and DNA are responsible for the common ability of neural bHLH proteins to bind to the core E- ...
Makde R, England J, Yennawar H, Tan S (2010). "Structure of the RCC1 chromatin factor bound to the nucleosome core particle". ... is attached to nucleosomes via core histones H2A and H2B. Thus, a gradient of GTP-bound Ran is generated around the vicinity of ... which directly binds the growing ends of microtubules and coordinates the binding of other +TIPs. Opposing the action of these ... Once they bind a kinetochore, they are stabilized and their dynamics are reduced. The newly mono-oriented chromosome oscillates ...
They are composed of a C-terminal ligand-binding region, a core DNA-binding domain (DBD) and an N-terminal domain that contains ... The N terminus interacts with other cellular transcription factors in a ligand-independent manner; and, depending on these ... Binding and activation[edit]. Ligand binding is an equilibrium process. Ligands bind to receptors and dissociate from them ... Allosteric modulators: They do not bind to the agonist-binding site of the receptor but instead on specific allosteric binding ...
WRKY transcription factors have been a significant area of plant research for the past 20 years. The WRKY DNA-binding domain ... Eighteen amino acids are highly conserved in the WRKY protein domain, including the core motif, zinc-finger binding cysteines ... The WRKY domain is found in the WRKY transcription factor family, a class of transcription factors. The WRKY domain is found ... the evolutionary conserved DNA-binding specificities of WRKY transcription factors by molecular dynamics and in vitro binding ...
The TFs binding sites are physical DNA sites recognized by transcription factors within a genome. Note: Historically, binding ... Notes: Promoter sequences are specific to the different sigma factors associated to the RNA polymerase core. A promoter is ... An operon with several promoters located near each other may also have dual binding sites, indicating that such a site can ... The graphic display of a TU will always contain only one promoter -when known- with the binding sites that regulate its ...
"Fibroblast growth factor-binding protein is a novel partner for perlecan protein core". J. Biol. Chem. 276 (13): 10263-71. doi: ... The heparan sulfate chains of perlecan bind growth factors in the ECM, and serve as co-ligands or ligand enhancers when bound ... Transcriptional activation by transforming growth factor-beta via a nuclear factor 1-binding element". J. Biol. Chem. 272 (8): ... "The protein core of the proteoglycan perlecan binds specifically to fibroblast growth factor-7". J. Biol. Chem. 275 (10): 7095- ...
"Fibroblast growth factor-binding protein is a novel partner for perlecan protein core". J Biol Chem. 276 (13): 10263-71. doi: ... Fibroblast growth factor-binding protein 1 is a protein that in humans is encoded by the FGFBP1 gene. FGFBP1, or HBP17, binds ... 2000). "Induction of the angiogenic modulator fibroblast growth factor-binding protein by epidermal growth factor is mediated ... "Characterization and molecular cloning of a putative binding protein for heparin-binding growth factors". J Biol Chem. 266 (25 ...
... factor binds to the core, forming the holoenzyme. After transcription starts, the factor can unbind and let the core enzyme ... In order to bind promoters, RNAP core associates with the transcription initiation factor sigma (σ) to form RNA polymerase ... RNA polymerase binding in bacteria involves the sigma factor recognizing the core promoter region containing the −35 and −10 ... A transcription factor and its associated transcription mediator complex must be attached to a DNA binding site called a ...
The degree to which the ETS1 transcription factor can bind to its binding sites on the PARP1 promoter depends on the ... helix DNA binding motif known as the Ets domain that specifically recognizes DNA sequences that contain a GGAA/T core element. ... Bi FF, Li D, Yang Q (2013). "Hypomethylation of ETS transcription factor binding sites and upregulation of PARP1 expression in ... The later suggests that several other transcription factors may facilitate Ets1 binding to unfavorable DNA sequences. Ets1 ...
The dimeric eukaryotic upstream binding factor (UBF) binds the UCE and the core element. UBF recruits and binds a protein ... allowing the UCE and the core elements to come into contact. RRN3/TIF-IA is phosphorylated and binds Pol I. Pol I binds to the ... When rRNA synthesis is stimulated, SL1 (selectivity factor 1) will bind to the promoters of rDNA genes that were previously ... Clos, Joachim; Buttgereit, Detlev; Grummt, Ingrid (February 1986). "A purified transcription factor (TIF-IB) binds to essential ...
FFAR2 transcription is regulated by the XBP1 transcription factor which binds to the core promoter. Mouse studies utilizing ... Brown AJ, Jupe S, Briscoe CP (2005). "A family of fatty acid binding receptors". DNA Cell Biol. 24 (1): 54-61. doi:10.1089/dna. ...
The protein encoded by this gene is an RNA binding protein and possible splicing factor. The encoded protein is found in the ... nucleus, where it colocalizes with core spliceosomal proteins. Studies of a mouse protein with high sequence similarity to this ... RNA-binding protein 39 is a protein that in humans is encoded by the RBM39 gene. ... "Entrez Gene: RBM39 RNA binding motif protein 39". Jung DJ, Na SY, Na DS, Lee JW (Jan 2002). "Molecular cloning and ...
In E. coli, a repressor binds the DNA operon and dislodges RNAP due to the loosely bound beta clamp, whereas in Synechocystis, ... Synechocystis possesses the 70S sigma factor (σ70), which can be divided into three groups. Group 1 sigma factors are critical ... Eubacterial RNAP holoenzymes consist of a core with four major subunits α2 ββ'. In cyanobacteria, β' is formed from two smaller ... the beta clamp binds tightly at initial binding. The effect of this difference is that synthetic repressible promoters do not ...
The core recommendations of this group took account of all psychological theory and spiritual factors in the human condition. " ... Service users who feel rejected are bound to escalate their behaviour in order to be heard and in order to "hit back" at those ... "Psychological mindedness" was the concept and the phrase that seemed to bind everything together. This work has led to the ... Conte HR, Ratto R, Karusa T (1996). "The Psychological Mindedness Scale: Factor structure and relationship to outcome of ...
They are composed of a C-terminal ligand-binding region, a core DNA-binding domain (DBD) and an N-terminal domain that contains ... The N terminus interacts with other cellular transcription factors in a ligand-independent manner; and, depending on these ... They do not bind to the agonist-binding site of the receptor but instead on specific allosteric binding sites, through which ... Ligand binding is an equilibrium process. Ligands bind to receptors and dissociate from them according to the law of mass ...
This model was said to be found in EU core countries such as Belgium, France, Germany, the Netherlands and Italy, and it is ... Trade unionism in the United Kingdom was a major factor in some of the economic crises during the 1960s and the 1970s, ... The agreements negotiated by a union are binding on the rank and file members and the employer and in some cases on other non- ... Ireland and the UK belong to this category, and in contrast to the EU core countries above, these countries first joined the EU ...
Core Binding Factor (CBF) Acute Myeloid Leukemia (AML) is cytogenetically characterized by either the t(8;21) or the inv(16)/t( ... Stem Cell Modeling of Core Binding Factor Acute Myeloid Leukemia. Federico Mosna and Michele Gottardi ...
In this study we reviewed 192 patients with core binding factor acute myeloid leukemia (AML), treated with curative intent (age ... In this study we reviewed 192 patients with core binding factor acute myeloid leukemia (AML), treated with curative intent (age ... Complex karyotype, older age, and reduced first-line dose intensity determine poor survival in core binding factor acute ... Approximately 40% of patients affected by core binding factor (CBF) acute myeloid leukemia (AML) ultimately die from the ...
Dasatinib in Combination With Chemotherapy for Relapsed or Refractory Core Binding Factor Acute Myeloid Leukemia: A Phase I ... Dasatinib in Combination With Chemotherapy for Relapsed or Refractory Core Binding Factor Acute Myeloid Leukemia: A Phase I ...
SL3-3 enhancer factor 1 subunit beta. SL3/AKV core-binding factor beta subunit. core-binding factor beta subunit. polyomavirus ... CBFB core-binding factor subunit beta [Homo sapiens] CBFB core-binding factor subunit beta [Homo sapiens]. Gene ID:865 ... core-binding factor subunit beta. Names. CBF-beta. PEA2-beta. PEBP2-beta. SL3-3 enhancer factor 1 beta subunit. ... core-binding factor subunit betaprovided by HGNC. Primary source. HGNC:HGNC:1539 See related. Ensembl:ENSG00000067955 MIM: ...
OUTCOME OF CORE BINDING FACTOR ACUTE MYELOID LEUKEMIA IN ADULT PATIENTS. PB1727. El Gammal, M.1; Mahmoud, A.2; Samra, M.1; ... Home , June 2019 - Volume 3 - Issue , OUTCOME OF CORE BINDING FACTOR ACUTE MYELOID LEUKEMIA IN ADU... ... Core binding factor acute myeloid leukemia (CBF AML) encodes two recurrent cytogentic abnormalities, t(8;21) and inv (16) and ... OUTCOME OF CORE BINDING FACTOR ACUTE MYELOID LEUKEMIA IN ADULT PATIENTS: PB1727 ...
The Core binding factor (CBF) is a group of heterodimeric transcription factors. Core binding factors are composed of: a non- ... DNA-binding CBFβ chain (CBFB) a DNA-binding CBFα chain (RUNX1, RUNX2, RUNX3) de Bruijn M, Speck N (2004). "Core-binding factors ... Core Binding Factors at the US National Library of Medicine Medical Subject Headings (MeSH) AI-10-49. ...
... core-binding factors (CBFs). CBFs consist of a DNA-binding CBFα subunit and a non-DNA-binding CBFβ subunit. The t(8;21), ... Core-Binding Factor: A Central Player in Hematopoiesis and Leukemia. Nancy A. Speck, Terry Stacy, Qing Wang, Trista North, Ting ... Core-Binding Factor: A Central Player in Hematopoiesis and Leukemia. Nancy A. Speck, Terry Stacy, Qing Wang, Trista North, Ting ... Core-Binding Factor: A Central Player in Hematopoiesis and Leukemia. Nancy A. Speck, Terry Stacy, Qing Wang, Trista North, Ting ...
Core-binding factor acute myeloid leukemia (CBF-AML) data in Asian countries has been rarely reported. We analyzed 392 patients ... Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of ... Identification of molecular and cytogenetic risk factors for unfavorable core-binding factor-positive adult AML with post- ... Paschka P (2008) Core binding factor acute myeloid leukemia. Semin Oncol 35(4):410-417CrossRefGoogle Scholar ...
Eukaryotic transcriptional regulation is complex. Typically, it takes place by cooperative regulation. A number of studies have characterized this aspect i
... core binding factor plays a key role in several development pathways and in human disease; has been sequenced ... Transcription Factors: 20597*Core Binding Factors: 223*Core Binding Factor alpha Subunits: 18*core binding factor alpha: 16 ... Subscribe to New Research on core binding factor alpha core binding factor plays a key role in several development pathways and ... 11/07/2000 - "Binding of CBFalpha/AML/PEBP2alpha (core binding factor alpha/acute myelogenous leukemia/polyoma enhancer binding ...
Not all patients with core binding factor acute myeloid leukemia (CBF-AML) display a good outcome. Modern risk factors include ... Prospective evaluation of gene mutations and minimal residual disease in patients with core binding factor acute myeloid ... but MRD remained the sole prognostic factor in multivariate analysis. At 36 months, cumulative incidence of relapse and RFS ...
Expression of core-binding factor a1 and osteocalcin in fluoride-treated fibroblasts and osteoblasts. Author: Duan X, Xu H, ... which is indicated by the expression of core-binding factor a1 (Cbfa1) and osteocalcin (OCN), in an FB cell line (L929) and in ... Tea Intake Is a Risk Factor for Skeletal Fluorosis. A number of recent studies have found that heavy tea drinkers can develop ...
Dasatinib (Sprycel™) in Patients With Newly Diagnosed Core Binding Factor (CBF) Acute Myeloid Leukemia (AML). The safety and ... Core binding factor (CBF) AML with molecular diagnosis of RUNX1-RUNX1T1 fusion transcript resulting from t(8;21)(q22;q22) (or a ... Genetics Home Reference related topics: Core binding factor acute myeloid leukemia Cytogenetically normal acute myeloid ... Adding dasatinib to intensive treatment in core-binding factor acute myeloid leukemia-results of the AMLSG 11-08 trial. ...
Description: Core binding factor A1 (CBFA1/RUNX2) is a runt-like transcription factor essential for osteoblast differentiation. ... This protein is a member of the RUNX family of transcription factors and has a Runt DNA-binding domain. It is essential for ... osteoblastic differentiation and skeletal morphogenesis and acts as a scaffold for nucleic acids and regulatory factors ...
Researchers Reveal Genomic Landscape of Core-Binding Factor Acute Myeloid Leukemia. By The ASCO Post. Posted: 11/4/2016 11:21: ... These genes encode for proteins that are part of the core-binding factor (CBF) complex, a transcriptional complex essential for ... University Pediatric Cancer Genome Project has completed a detailed map of the genomic landscape for core-binding factor acute ... the Pediatric Cancer Genome Project identified several mutations that may contribute to the development of core-binding factor ...
Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of ... For example, the fusion proteins AML1-ETO and core binding factor β (CBFβ)-MYH11 resulting from the t(8;21)(q22;q22) and (inv ... Histone Deacetylase Inhibitor Romidepsin Has Differential Activity in Core Binding Factor Acute Myeloid Leukemia. Olatoyosi M. ... Histone Deacetylase Inhibitor Romidepsin Has Differential Activity in Core Binding Factor Acute Myeloid Leukemia ...
Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor.. S Wang ... 4:233-242, 1990). We previously reported the purification of core-binding factors (CBF) from calf thymus nuclei (S. Wang and N. ... Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor. ... Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor. ...
Exon 8 splice site mutations in the gene encoding the E3-ligase CBL are associated with core binding factor acute myeloid ... CBL Exon 8/9 Mutants Activate the FLT3 Pathway and Cluster in Core Binding Factor/11q Deletion Acute Myeloid Leukemia/ ... All AML/MDS patients with identified CBL mutants belonged to the core binding factor and 11q deletion AML subtypes. ... Among 43 cases of core binding factor leukemias [t(8;21) and inv(16)] two patients expressing aberrant CBL transcripts were ...
Old and new prognostic factors in acute myeloid leukemia with deranged core-binding factor beta. Am J Hematol. 2013;88(7):594- ... Prognostic factors and outcome of core binding factor acute myeloid leukemia patients with t(8;21) differ from those of ... Identification of molecular and cytogenetic risk factors for unfavorable core-binding factor-positive adult AML with post- ... Core-binding factor acute myeloid leukemia: heterogeneity, monitoring and therapy. Am J Hematol. 2014;89(12):1121-1131. ...
RNA-sequencing Analysis of Core Binding Factor AML Identifies Recurrent ZBTB7A Mutations and Defines RUNX1-CBFA2T3 Fusion ... RNA-sequencing Analysis of Core Binding Factor AML Identifies Recurrent ZBTB7A Mutations and Defines RUNX1-CBFA2T3 Fusion ... RNA-sequencing Analysis of Core Binding Factor AML Identifies Recurrent ZBTB7A Mutations and Defines RUNX1-CBFA2T3 Fusion ... Targeting an RNA-Binding Protein Network in Acute Myeloid Leukemia. Wang E, Lu SX, Pastore A, Chen X, Imig J, Chun-Wei Lee S, ...
What is core-binding factor, runt domain, alpha subunit 3? Meaning of core-binding factor, runt domain, alpha subunit 3 medical ... What does core-binding factor, runt domain, alpha subunit 3 mean? ... core-binding factor, runt domain, alpha subunit 3 explanation ... Looking for online definition of core-binding factor, runt domain, alpha subunit 3 in the Medical Dictionary? ... Core-binding factor, runt domain, alpha subunit 3 , definition of core-binding factor, runt domain, alpha subunit 3 by Medical ...
Core binding factor a1 (CBFA1) is a key regulator of osteoblast differentiation. This study was designed to investigate the ... Functional analysis of core binding factor a1 and its relationship with related genes expressed by human periodontal ligament ... and receptor activator nuclear factor kappa B ligand (RANKL) were detected before and after RNA interference (RNAi) of CBFA1. ...
What is SL3/AKV core-binding factor alpha B subunit? Meaning of SL3/AKV core-binding factor alpha B subunit medical term. What ... SL3/AKV core-binding factor alpha B subunit explanation free. ... does SL3/AKV core-binding factor alpha B subunit mean? ... Looking for online definition of SL3/AKV core-binding factor alpha B subunit in the Medical Dictionary? ... SL3/AKV core-binding factor alpha B subunit , definition of SL3/AKV core-binding factor alpha B subunit by Medical dictionary ...
Mouse core-binding factor, runt domain, alpha subunit 2, translocated to, 3 (human) (Cbfa2t3), transcript variant 2, (10ug), 10 ... Home » cDNA » Mouse cDNA » Cbfa2t3 (untagged) - Mouse core-binding factor, runt domain, alpha subunit 2, translocated to, 3 ( ... MC219266 Cbfa2t3 (untagged) - Mouse core-binding factor, runt domain, alpha subunit 2, translocated to, 3 (human) (Cbfa2t3), ... Properties for Cbfa2t3 (untagged) - Mouse core-binding factor, runt domain, alpha subunit 2, translocated to, 3 (human) ( ...
Rna Polymerase Ii Core Promoter Proximal Region Sequence-Specific Dna Binding Transcription Factor Activity Involved In ... Rna Polymerase Ii Core Promoter Proximal Region Sequence-Specific Dna Binding Transcription Factor Activity Involved In ... Rna Polymerase Ii Core Promoter Proximal Region Sequence-Specific Dna Binding Transcription Factor Activity Involved In ... RNA polymerase II core promoter proximal region sequence-specific DNA binding transcription factor activity involved in ...
  • Core Binding Factor (CBF) Acute Myeloid Leukemia (AML) is cytogenetically characterized by either the t(8;21) or the inv(16)/t(16;16) chromosomal abnormalities, which, although being pathognomonic, are not sufficient per se to induce overt leukemia but rather determine a preclinical phase of disease when preleukemic subclones compete until the acquisition of clonal dominance by one of them. (hindawi.com)
  • The RNA polymerase transcribes the DNA (the beta subunit initiates the synthesis), but produces about 10 abortive (short, non-productive) transcripts which are unable to leave the RNA polymerase because the exit channel is blocked by the σ-factor. (wikipedia.org)
  • ITC analysis of ligand binding to preQ? (rochester.edu)
  • Single transcriptional and translational preQ1 riboswitches adopt similar pre-folded ensembles that follow distinct folding pathways into the same ligand-bound structure. (rochester.edu)
  • Although MTX includes a lower Significantly affinity, its make use of being a ligand continues to be effective for Significantly concentrating on if a multivalent style AST-1306 strategy [28,29,is certainly applied that may offer very tight binding in comparison to a weak monovalent binding interaction. (healthandwellnesssource.org)
  • 1NNP: X-ray structure of the GluR2 ligand-binding core (S1S2J) in complex with (S)-ATPA at 1.9 A resolution. (rcsb.org)
  • Domain II comprises four repeats homologous to the ligand-binding portion of the LDL receptor with six conserved cysteine residues and a pentapeptide, DGSDE, which mediates ligand binding by the LDL receptor. (wikipedia.org)
  • A molecule that binds to a receptor is called a ligand, and can be a protein or peptide (short protein), or another small molecule such as a neurotransmitter, hormone, pharmaceutical drug, toxin, or parts of the outside of a virus or microbe. (wikipedia.org)
  • When a ligand binds to its corresponding receptor, it activates or inhibits the receptor's associated biochemical pathway. (wikipedia.org)
  • They have a heteromeric structure in that each subunit consists of the extracellular ligand-binding domain and a transmembrane domain where the transmembrane domain in turn includes four transmembrane alpha helices. (wikipedia.org)
  • Type 3: Kinase-linked and related receptors (see "Receptor tyrosine kinase", and "Enzyme-linked receptor") - They are composed of an extracellular domain containing the ligand binding site and an intracellular domain, often with enzymatic-function, linked by a single transmembrane alpha helix. (wikipedia.org)
  • They are composed of a C-terminal ligand-binding region, a core DNA-binding domain (DBD) and an N-terminal domain that contains the AF1(activation function 1) region. (wikipedia.org)
  • Ligand binding is an equilibrium process. (wikipedia.org)
  • All RTKs consists of an extracellular ligand binding region, a single transmembrane helix and a cytoplasmic region (the tyrosine kinase domain). (wikipedia.org)
  • Ligand binding to the extracellular domain induces dimerization. (wikipedia.org)
  • It is not involved directly in TGF-beta signal transduction but by binding to various member of the TGF-beta superfamily at the cell surface it acts as a reservoir of ligand for TGF-beta receptors. (wikipedia.org)
  • This idea is supported by direct contact in vitro between activators and GTFs, including TATA box-binding protein (TBP) ( 2 ), TFIIB ( 3 ), TFIIF ( 4 ), TFIIH ( 5 ), as well as the Rpb5 subunit of RNAPII ( 6 ), and TBP-associated factors ( 7 , 8 ). (pnas.org)
  • The presence of XPC-RAD23B is required for assembly of the other core NER factors and progression through the NER pathway both in vitro and in vivo. (wikipedia.org)
  • HMGB1-LPS complex activates TLR4, and causes the binding of adapter proteins (MyD88 and others), leading to signal transduction and the activation of various signaling cascades. (wikipedia.org)
  • This complex then activates flavocytochrome b, the membrane-integrated catalytic core of the enzyme system. (wikipedia.org)
  • Ets1 overexpression in stratified squamous epithelial cells causes pro-oncogenic changes, such as suspension of terminal differentiation, high secretion of matrix metalloproteases (Mmps), epidermal growth factor ligands, and inflammatory mediators. (wikipedia.org)