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.
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.
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.
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.
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.
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.
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.
Myosin type II isoforms found in smooth muscle.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A specific pair of GROUP E CHROMOSOMES of the human chromosome classification.
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.
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.
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.
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.
The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
A specific pair of GROUP G CHROMOSOMES of the human chromosome classification.
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.
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Bone-forming cells which secrete an EXTRACELLULAR MATRIX. HYDROXYAPATITE crystals are then deposited into the matrix to form bone.
Cis-acting DNA sequences which can increase transcription of genes. Enhancers can usually function in either orientation and at various distances from a promoter.
A type of chromosome aberration characterized by CHROMOSOME BREAKAGE and transfer of the broken-off portion to another location, often to a different chromosome.
The process of bone formation. Histogenesis of bone including ossification.
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.
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.
An EPIDERMAL GROWTH FACTOR related protein that is found in a variety of tissues including EPITHELIUM, and maternal DECIDUA. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form which binds to the EGF RECEPTOR.
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.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
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.
Established cell cultures that have the potential to propagate indefinitely.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
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.
Factors that form a preinitiation complex at promoters that are specifically transcribed by RNA POLYMERASE I.
An enzyme that catalyzes the conversion of an orthophosphoric monoester and water to an alcohol and orthophosphate. EC 3.1.3.1.

Cbfa1 isoforms exert functional differences in osteoblast differentiation. (1/863)

Cbfa1 is an essential transcription factor for osteoblast differentiation and bone formation. We investigated functional differences among three isoforms of Cbfa1: Type I (originally reported as Pebp2alphaA by Ogawa et al. (Ogawa, E., Maruyama, M., Kagoshima, H., Inuzuka, M., Lu, J., Satake, M., Shigesada, K., and Ito, Y. (1993) Proc. Natl. Acad. Sci. U. S. A. 90, 6859-6863), Type II (originally reported as til-1 by Stewart et al. (Stewart, M., Terry, A., Hu, M., O'Hara, M., Blyth, K., Baxter, E., Cameron, E., Onions, D. E., and Neil, J. C. (1997) Proc. Natl. Acad. Sci. U. S. A. 94, 8646-8651), and Type III (originally reported as Osf2/Cbfa1 by Ducy et al. (Ducy, P., Zhang, R., Geoffroy, V., Ridall, A. L., and Karsenty, G. (1997) Cell 89, 747-754). A reverse transcriptase-polymerase chain reaction analysis demonstrated that these isoforms were expressed in adult mouse bones. The transient transfection of Type I or Type II Cbfa1 in a mouse fibroblastic cell line, C3H10T1/2, induced the expression of alkaline phosphatase (ALP) activity. This induction was synergistically enhanced by the co-introduction of Xenopus BMP-4 cDNA. In contrast, the transient transfection of Type III cDNA induced no ALP activity. In C3H10T1/2 cells stably transfected with each isoform of Cbfa1, the gene expression of ALP was also strongly induced in cells transfected with Type I and Type II Cbfa1 but not in cells with Type III Cbfa1. Osteocalcin, osteopontin,and type I collagen gene expressions were induced or up-regulated in all of the cells stably transfected with each isoform of Cbfa1, and Type II transfected cells exhibited the highest expression level of osteocalcin gene. A luciferase reporter gene assay using a 6XOSE2-SV40 promoter (6 tandem binding elements for Cbfa1 ligated in front of the SV40 promoter sequence), a mouse osteocalcin promoter, and a mouse osteopontin promoter revealed the differences in the transcriptional induction of target genes by each Cbfa1 isoform with or without its beta-subunit. These results suggest that all three of the Cbfa1 isoforms used in the present study are involved in the stimulatory action of osteoblast differentiation, but they exert different functions in the process of osteoblast differentiation.  (+info)

Regulation of chondrocyte differentiation by Cbfa1. (2/863)

Cbfa1, a developmentally expressed transcription factor of the runt family, was recently shown to be essential for osteoblast differentiation. We have investigated the role of Cbfa1 in endochondral bone formation using Cbfa1-deficient mice. Histology and in situ hybridization with probes for indian hedgehog (Ihh), collagen type X and osteopontin performed at E13.5, E14.5 and E17.5 demonstrated a lack of hypertrophic chondrocytes in the anlagen of the humerus and the phalanges and a delayed onset of hypertrophy in radius/ulna in Cbfa1-/- mice. Detailed analysis of Cbfa1 expression using whole mount in situ hybridization and a lacZ reporter gene reveled strong expression not only in osteoblasts but also in pre-hypertrophic and hypertrophic chondrocytes. Our studies identify Cbfa1 as a major positive regulator of chondrocyte differentiation.  (+info)

Maturational disturbance of chondrocytes in Cbfa1-deficient mice. (3/863)

Cbfa1, a transcription factor that belongs to the runt-domain gene family, plays an essential role in osteogenesis. Cbfa1-deficient mice completely lacked both intramembranous and endochondral ossification, owing to the maturational arrest of osteoblasts, indicating that Cbfa1 has a fundamental role in osteoblast differentiation. However, Cbfa1 was also expressed in chondrocytes, and its expression was increased according to the maturation of chondrocytes. Terminal hypertrophic chondrocytes expressed Cbfa1 extensively. The significant expression of Cbfa1 in hypertrophic chondrocytes was first detected at embryonic day 13.5 (E13.5), and its expression in hypertrophic chondrocytes was most prominent at E14.5-16.5. In Cbfa1-deficient mice, whose entire skeleton was composed of cartilage, the chondrocyte differentiation was disturbed. Calcification of cartilage occurred in the restricted parts of skeletons, including tibia, fibula, radius, and ulna. Type X collagen, BMP6, and Indian hedgehog were expressed in their hypertrophic chondrocytes. However, osteopontin, bone sialoprotein, and collagenase 3 were not expressed at all, indicating that they are directly regulated by Cbfa1 in the terminal hypertrophic chondrocytes. Chondrocyte differentiation was severely disturbed in the rest of the skeleton. The expression of PTH/PTHrP receptor, Indian hedgehog, type X collagen, and BMP6 was not detected in humerus and femur, indicating that chondrocyte differentiation was blocked before prehypertrophic chondrocytes. These findings demonstrate that Cbfa1 is an important factor for chondrocyte differentiation.  (+info)

A Cbfa1-dependent genetic pathway controls bone formation beyond embryonic development. (4/863)

The molecular mechanisms controlling bone extracellular matrix (ECM) deposition by differentiated osteoblasts in postnatal life, called hereafter bone formation, are unknown. This contrasts with the growing knowledge about the genetic control of osteoblast differentiation during embryonic development. Cbfa1, a transcriptional activator of osteoblast differentiation during embryonic development, is also expressed in differentiated osteoblasts postnatally. The perinatal lethality occurring in Cbfa1-deficient mice has prevented so far the study of its function after birth. To determine if Cbfa1 plays a role during bone formation we generated transgenic mice overexpressing Cbfa1 DNA-binding domain (DeltaCbfa1) in differentiated osteoblasts only postnatally. DeltaCbfa1 has a higher affinity for DNA than Cbfa1 itself, has no transcriptional activity on its own, and can act in a dominant-negative manner in DNA cotransfection assays. DeltaCbfa1-expressing mice have a normal skeleton at birth but develop an osteopenic phenotype thereafter. Dynamic histomorphometric studies show that this phenotype is caused by a major decrease in the bone formation rate in the face of a normal number of osteoblasts thus indicating that once osteoblasts are differentiated Cbfa1 regulates their function. Molecular analyses reveal that the expression of the genes expressed in osteoblasts and encoding bone ECM proteins is nearly abolished in transgenic mice, and ex vivo assays demonstrated that DeltaCbfa1-expressing osteoblasts were less active than wild-type osteoblasts. We also show that Cbfa1 regulates positively the activity of its own promoter, which has the highest affinity Cbfa1-binding sites characterized. This study demonstrates that beyond its differentiation function Cbfa1 is the first transcriptional activator of bone formation identified to date and illustrates that developmentally important genes control physiological processes postnatally.  (+info)

Collagenase 3 is a target of Cbfa1, a transcription factor of the runt gene family involved in bone formation. (5/863)

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)

Cbfa1 is required for epithelial-mesenchymal interactions regulating tooth development in mice. (6/863)

Osteoblasts and odontoblasts, cells that are responsible for the formation of bone and dentin matrices respectively, share several molecular characteristics. Recently, Cbfa1 was shown to be a critical transcriptional regulator of osteoblast differentiation. Mutations in this gene cause cleidocranial dysplasia (CCD), an autosomal dominant disorder in humans and mice characterized by defective bone formation. CCD also results in dental defects that include supernumerary teeth and delayed eruption of permanent dentition. The dental abnormalities in CCD suggest an important role for this molecule in the formation of dentition. Here we describe results of studies aimed at understanding the functions of Cbfa1 in tooth formation. RT-PCR and in situ hybridization analyses show that Cbfa1 has a unique expression pattern in dental mesenchyme from the bud to early bell stages during active epithelial morphogenesis. Unlike that observed in osteoblast differentiation, Cbfa1 is downregulated in fully differentiated odontoblasts and is surprisingly expressed in ectodermally derived ameloblasts during the maturation phase of enamel formation. The role of Cbfa1 in tooth morphogenesis is further illustrated by the misshapen and severely hypoplastic tooth organs in Cbfa1-/- mice. These tooth organs lacked overt odontoblast and ameloblast differentiation and normal dentin and enamel matrices. Epithelial-mesenchymal recombinants demonstrate that dental epithelium regulates mesenchymal Cbfa1 expression during the bud and cap stages and that these effects are mimicked by the FGFs but not by the BMPs as shown by our bead implantation assays. We propose that Cbfa1 regulates the expression of molecules in mesenchyme that act reciprocally on dental epithelium to control its growth and differentiation. Taken together, our data indicate a non-redundant role for Cbfa1 in tooth development that may be distinct from that in bone formation. In odontogenesis, Cbfa1 is not involved in the early signaling networks regulating tooth initiation and early morphogenesis but regulates key epithelial-mesenchymal interactions that control advancing morphogenesis and histodifferentiation of the epithelial enamel organ.  (+info)

Dexamethasone enhances In vitro vascular calcification by promoting osteoblastic differentiation of vascular smooth muscle cells. (7/863)

Vascular calcification is often associated with atherosclerotic lesions. Moreover, the process of atherosclerotic calcification has several features similar to the mineralization of skeletal tissue. Therefore, we hypothesized that vascular smooth muscle cells might acquire osteoblastic characteristics during the development of atherosclerotic lesions. In the present study, we investigated the effect of dexamethasone (Dex), which is well known to be a potent stimulator of osteoblastic differentiation in vitro, on vascular calcification by using an in vitro calcification model. We demonstrated that Dex increased bovine vascular smooth muscle cell (BVSMC) calcification in a dose- and time-dependent manner. Dex also enhanced several phenotypic markers of osteoblasts, such as alkaline phosphatase activity, procollagen type I carboxy-terminal peptide production, and cAMP responses to parathyroid hormone in BVSMCs. We also examined the effects of Dex on human osteoblast-like (Saos-2) cells and compared its effects on BVSMCs and Saos-2 cells. The effects of Dex on alkaline phosphatase activity and the cAMP response to parathyroid hormone in BVSMCs were less prominent than those in Saos-2 cells. Interestingly, we detected that Osf2/Cbfa1, a key transcription factor in osteoblastic differentiation, was expressed in both BVSMCs and Saos-2 cells and that Dex increased the gene expression of both transcription factors. These findings suggest that Dex may enhance osteoblastic differentiation of BVSMCs in vitro.  (+info)

Does adult fracture repair recapitulate embryonic skeletal formation? (8/863)

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)

Core binding factors (CBFs) are a group of proteins that play critical roles in the development and differentiation of hematopoietic cells, which are the cells responsible for the formation of blood and immune systems. The term "core binding factor" refers to the ability of these proteins to bind to specific DNA sequences, known as core binding sites, and regulate gene transcription.

The two main CBFs are:

1. Core Binding Factor Alpha (CBF-α): Also known as RUNX1 or AML1, this protein forms a complex with Core Binding Factor Beta (CBF-β) to regulate the expression of genes involved in hematopoiesis. Mutations in CBF-α have been associated with various types of leukemia and myelodysplastic syndromes.
2. Core Binding Factor Beta (CBF-β): Also known as PEBP2B, this protein partners with CBF-α to form the active transcription factor complex. CBF-β enhances the DNA binding affinity and stability of the CBF-α/CBF-β heterodimer.

In certain types of leukemia, chromosomal abnormalities can lead to the formation of fusion proteins involving CBF-α or CBF-β. These fusion proteins disrupt normal hematopoiesis and contribute to the development of cancer. Examples include the t(8;21) translocation that creates the AML1/ETO fusion protein in acute myeloid leukemia (AML) and the inv(16) inversion that forms the CBFB-MYH11 fusion protein in AML.

Core Binding Factor (CBF) is a transcription factor that plays a crucial role in the development and differentiation of various tissues, including hematopoietic cells. It is composed of two subunits: alpha (CBFA or AML1) and beta (CBFB or PEBP2b).

The CBFA subunit, also known as RUNX1, is a transcription factor that binds to DNA and regulates the expression of target genes involved in hematopoiesis, neurogenesis, and other developmental processes. It contains a highly conserved DNA-binding domain called the runt homology domain (RHD) that recognizes specific DNA sequences.

Mutations in CBFA have been associated with various hematological disorders, including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and familial platelet disorder with predisposition to AML (FDPA). These mutations can lead to altered gene expression, impaired differentiation, and increased proliferation of hematopoietic cells, contributing to the development of these diseases.

Core Binding Factor Alpha 1 Subunit, also known as CBF-A1 or RUNX1, is a protein that plays a crucial role in hematopoiesis, which is the process of blood cell development. It is a member of the core binding factor (CBF) complex, which regulates gene transcription and is essential for the differentiation and maturation of hematopoietic stem cells into mature blood cells.

The CBF complex consists of three subunits: CBF-A, CBF-B, and a histone deacetylase (HDAC). The CBF-A subunit can have several isoforms, including CBF-A1, which is encoded by the RUNX1 gene. Mutations in the RUNX1 gene have been associated with various hematological disorders, such as acute myeloid leukemia (AML), familial platelet disorder with propensity to develop AML, and thrombocytopenia with absent radii syndrome.

CBF-A1/RUNX1 functions as a transcription factor that binds to DNA at specific sequences called core binding factors, thereby regulating the expression of target genes involved in hematopoiesis. Proper regulation of these genes is essential for normal blood cell development and homeostasis.

Core Binding Factor-beta (CBF-β) is a subunit of the Core Binding Factor (CBF), which is a heterodimeric transcription factor composed of a DNA-binding alpha subunit and a non-DNA binding beta subunit. The CBF plays a crucial role in hematopoiesis, the process of blood cell development, by regulating the expression of various genes involved in this process.

The CBF-β subunit is a 36 kDa protein that is encoded by the CBFB gene in humans. It does not bind to DNA directly but instead forms a complex with the DNA-binding alpha subunit, which is either RUNX1 (also known as AML1), RUNX2, or RUNX3. The CBF-β subunit stabilizes the interaction between the alpha subunit and DNA, enhances its DNA-binding affinity, and increases the transcriptional activity of the complex.

Mutations in the CBFB gene have been associated with several hematological disorders, including acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and familial platelet disorder with predisposition to AML (FPD/AML). These mutations can lead to aberrant transcriptional regulation of hematopoietic genes, resulting in the development of these disorders.

Core Binding Factor Alpha 2 Subunit, also known as CBF-A2 or CEBP-α, is a protein that forms a complex with other proteins to act as a transcription factor. Transcription factors are proteins that help regulate the expression of genes by binding to specific DNA sequences and controlling the rate of transcription of genetic information from DNA to RNA.

CBF-A2 is a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors, which are important in regulating various biological processes such as cell growth, development, and inflammation. CBF-A2 forms a heterodimer with Core Binding Factor Beta (CBF-β) to form the active transcription factor complex known as the core binding factor (CBF).

The CBF complex binds to the CCAAT box, a specific DNA sequence found in the promoter regions of many genes. By binding to this sequence, the CBF complex can either activate or repress the transcription of target genes, depending on the context and the presence of other regulatory factors.

Mutations in the gene encoding CBF-A2 have been associated with several human diseases, including acute myeloid leukemia (AML) and multiple myeloma. In AML, mutations in the CBF-A2 gene can lead to the formation of abnormal CBF complexes that disrupt normal gene expression patterns and contribute to the development of leukemia.

Core Binding Factor Alpha 3 Subunit (also known as CBFA3 or AML1) is a protein that forms part of a complex responsible for the regulation of gene transcription, particularly those involved in hematopoiesis (the formation of blood cells). It is a member of the runt-domain family of transcription factors and plays a critical role in normal blood cell development.

Mutations in the CBFA3 gene have been associated with certain types of leukemia, such as acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). These mutations can lead to abnormal blood cell development and cancer.

Transcription Factor AP-2 is a specific protein involved in the process of gene transcription. It belongs to a family of transcription factors known as Activating Enhancer-Binding Proteins (AP-2). These proteins regulate gene expression by binding to specific DNA sequences called enhancers, which are located near the genes they control.

AP-2 is composed of four subunits that form a homo- or heterodimer, which then binds to the consensus sequence 5'-GCCNNNGGC-3'. This sequence is typically found in the promoter regions of target genes. Once bound, AP-2 can either activate or repress gene transcription, depending on the context and the presence of cofactors.

AP-2 plays crucial roles during embryonic development, particularly in the formation of the nervous system, limbs, and face. It is also involved in cell cycle regulation, differentiation, and apoptosis (programmed cell death). Dysregulation of AP-2 has been implicated in several diseases, including various types of cancer.

Smooth muscle myosin is a type of motor protein that is responsible for the contraction and relaxation of smooth muscles, which are found in various organs such as the bladder, blood vessels, and digestive tract. Smooth muscle myosin is composed of two heavy chains and four light chains, forming a hexameric structure. The heavy chains have an N-terminal head domain that contains the ATPase activity and a C-terminal tail domain that mediates filament assembly.

The smooth muscle myosin molecule has several unique features compared to other types of myosins, such as skeletal or cardiac myosin. For example, smooth muscle myosin has a longer lever arm, which allows for greater force generation during contraction. Additionally, the regulatory mechanism of smooth muscle myosin is different from that of skeletal or cardiac myosin. In smooth muscles, the contractile activity is regulated by phosphorylation of the light chains, which is mediated by a specific kinase called myosin light chain kinase (MLCK).

Overall, the proper regulation and function of smooth muscle myosin are critical for maintaining normal physiological functions in various organs. Dysregulation or mutations in smooth muscle myosin can lead to several diseases, such as hypertension, atherosclerosis, and gastrointestinal motility disorders.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

Human chromosome pair 16 consists of two rod-shaped structures present in the nucleus of each cell in the human body. Each chromosome is made up of DNA tightly coiled around histone proteins, forming a complex structure called a chromatin.

Chromosomes come in pairs, with one chromosome inherited from each parent. Chromosome pair 16 contains two homologous chromosomes, which are similar in size, shape, and genetic content but may have slight variations due to differences in the DNA sequences inherited from each parent.

Chromosome pair 16 is one of the 22 autosomal pairs, meaning it contains non-sex chromosomes that are present in both males and females. Chromosome 16 is a medium-sized chromosome, and it contains around 2,800 genes that provide instructions for making proteins and regulating various cellular processes.

Abnormalities in chromosome pair 16 can lead to genetic disorders such as chronic myeloid leukemia, some forms of mental retardation, and other developmental abnormalities.

DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.

The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.

DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.

A chromosome inversion is a genetic rearrangement where a segment of a chromosome has been reversed end to end, so that its order of genes is opposite to the original. This means that the gene sequence on the segment of the chromosome has been inverted.

In an inversion, the chromosome breaks in two places, and the segment between the breaks rotates 180 degrees before reattaching. This results in a portion of the chromosome being inverted, or turned upside down, relative to the rest of the chromosome.

Chromosome inversions can be either paracentric or pericentric. Paracentric inversions involve a segment that does not include the centromere (the central constriction point of the chromosome), while pericentric inversions involve a segment that includes the centromere.

Inversions can have various effects on an individual's phenotype, depending on whether the inversion involves genes and if so, how those genes are affected by the inversion. In some cases, inversions may have no noticeable effect, while in others they may cause genetic disorders or predispose an individual to certain health conditions.

Acute myeloid leukemia (AML) is a type of cancer that originates in the bone marrow, the soft inner part of certain bones where new blood cells are made. In AML, the immature cells, called blasts, in the bone marrow fail to mature into normal blood cells. Instead, these blasts accumulate and interfere with the production of normal blood cells, leading to a shortage of red blood cells (anemia), platelets (thrombocytopenia), and normal white blood cells (leukopenia).

AML is called "acute" because it can progress quickly and become severe within days or weeks without treatment. It is a type of myeloid leukemia, which means that it affects the myeloid cells in the bone marrow. Myeloid cells are a type of white blood cell that includes monocytes and granulocytes, which help fight infection and defend the body against foreign invaders.

In AML, the blasts can build up in the bone marrow and spread to other parts of the body, including the blood, lymph nodes, liver, spleen, and brain. This can cause a variety of symptoms, such as fatigue, fever, frequent infections, easy bruising or bleeding, and weight loss.

AML is typically treated with a combination of chemotherapy, radiation therapy, and/or stem cell transplantation. The specific treatment plan will depend on several factors, including the patient's age, overall health, and the type and stage of the leukemia.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

An oncogene protein fusion is a result of a genetic alteration in which parts of two different genes combine to create a hybrid gene that can contribute to the development of cancer. This fusion can lead to the production of an abnormal protein that promotes uncontrolled cell growth and division, ultimately resulting in a malignant tumor. Oncogene protein fusions are often caused by chromosomal rearrangements such as translocations, inversions, or deletions and are commonly found in various types of cancer, including leukemia and sarcoma. These genetic alterations can serve as potential targets for cancer diagnosis and therapy.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Human chromosome pair 21 consists of two rod-shaped structures present in the nucleus of each cell in the human body. Each member of the pair is a single chromosome, and they are identical to each other. Chromosomes are made up of DNA, which contains genetic information that determines many of an individual's traits and characteristics.

Chromosome pair 21 is one of the 23 pairs of human autosomal chromosomes, meaning they are not sex chromosomes (X or Y). Chromosome pair 21 is the smallest of the human chromosomes, and it contains approximately 48 million base pairs of DNA. It contains around 200-300 genes that provide instructions for making proteins and regulating various cellular processes.

Down syndrome, a genetic disorder characterized by intellectual disability, developmental delays, distinct facial features, and sometimes heart defects, is caused by an extra copy of chromosome pair 21 or a part of it. This additional genetic material can lead to abnormalities in brain development and function, resulting in the characteristic symptoms of Down syndrome.

Protein binding, in the context of medical and biological sciences, refers to the interaction between a protein and another molecule (known as the ligand) that results in a stable complex. This process is often reversible and can be influenced by various factors such as pH, temperature, and concentration of the involved molecules.

In clinical chemistry, protein binding is particularly important when it comes to drugs, as many of them bind to proteins (especially albumin) in the bloodstream. The degree of protein binding can affect a drug's distribution, metabolism, and excretion, which in turn influence its therapeutic effectiveness and potential side effects.

Protein-bound drugs may be less available for interaction with their target tissues, as only the unbound or "free" fraction of the drug is active. Therefore, understanding protein binding can help optimize dosing regimens and minimize adverse reactions.

A neoplasm is a tumor or growth that is formed by an abnormal and excessive proliferation of cells, which can be benign or malignant. Neoplasm proteins are therefore any proteins that are expressed or produced in these neoplastic cells. These proteins can play various roles in the development, progression, and maintenance of neoplasms.

Some neoplasm proteins may contribute to the uncontrolled cell growth and division seen in cancer, such as oncogenic proteins that promote cell cycle progression or inhibit apoptosis (programmed cell death). Others may help the neoplastic cells evade the immune system, allowing them to proliferate undetected. Still others may be involved in angiogenesis, the formation of new blood vessels that supply the tumor with nutrients and oxygen.

Neoplasm proteins can also serve as biomarkers for cancer diagnosis, prognosis, or treatment response. For example, the presence or level of certain neoplasm proteins in biological samples such as blood or tissue may indicate the presence of a specific type of cancer, help predict the likelihood of cancer recurrence, or suggest whether a particular therapy will be effective.

Overall, understanding the roles and behaviors of neoplasm proteins can provide valuable insights into the biology of cancer and inform the development of new diagnostic and therapeutic strategies.

In the context of medical and biological sciences, a "binding site" refers to a specific location on a protein, molecule, or cell where another molecule can attach or bind. This binding interaction can lead to various functional changes in the original protein or molecule. The other molecule that binds to the binding site is often referred to as a ligand, which can be a small molecule, ion, or even another protein.

The binding between a ligand and its target binding site can be specific and selective, meaning that only certain ligands can bind to particular binding sites with high affinity. This specificity plays a crucial role in various biological processes, such as signal transduction, enzyme catalysis, or drug action.

In the case of drug development, understanding the location and properties of binding sites on target proteins is essential for designing drugs that can selectively bind to these sites and modulate protein function. This knowledge can help create more effective and safer therapeutic options for various diseases.

Osteoblasts are specialized bone-forming cells that are derived from mesenchymal stem cells. They play a crucial role in the process of bone formation and remodeling. Osteoblasts synthesize, secrete, and mineralize the organic matrix of bones, which is mainly composed of type I collagen.

These cells have receptors for various hormones and growth factors that regulate their activity, such as parathyroid hormone, vitamin D, and transforming growth factor-beta. When osteoblasts are not actively producing bone matrix, they can become trapped within the matrix they produce, where they differentiate into osteocytes, which are mature bone cells that play a role in maintaining bone structure and responding to mechanical stress.

Abnormalities in osteoblast function can lead to various bone diseases, such as osteoporosis, osteogenesis imperfecta, and Paget's disease of bone.

Genetic enhancer elements are DNA sequences that increase the transcription of specific genes. They work by binding to regulatory proteins called transcription factors, which in turn recruit RNA polymerase II, the enzyme responsible for transcribing DNA into messenger RNA (mRNA). This results in the activation of gene transcription and increased production of the protein encoded by that gene.

Enhancer elements can be located upstream, downstream, or even within introns of the genes they regulate, and they can act over long distances along the DNA molecule. They are an important mechanism for controlling gene expression in a tissue-specific and developmental stage-specific manner, allowing for the precise regulation of gene activity during embryonic development and throughout adult life.

It's worth noting that genetic enhancer elements are often referred to simply as "enhancers," and they are distinct from other types of regulatory DNA sequences such as promoters, silencers, and insulators.

Translocation, genetic, refers to a type of chromosomal abnormality in which a segment of a chromosome is transferred from one chromosome to another, resulting in an altered genome. This can occur between two non-homologous chromosomes (non-reciprocal translocation) or between two homologous chromosomes (reciprocal translocation). Genetic translocations can lead to various clinical consequences, depending on the genes involved and the location of the translocation. Some translocations may result in no apparent effects, while others can cause developmental abnormalities, cancer, or other genetic disorders. In some cases, translocations can also increase the risk of having offspring with genetic conditions.

Osteogenesis is the process of bone formation or development. It involves the differentiation and maturation of osteoblasts, which are bone-forming cells that synthesize and deposit the organic matrix of bone tissue, composed mainly of type I collagen. This organic matrix later mineralizes to form the inorganic crystalline component of bone, primarily hydroxyapatite.

There are two primary types of osteogenesis: intramembranous and endochondral. Intramembranous osteogenesis occurs directly within connective tissue, where mesenchymal stem cells differentiate into osteoblasts and form bone tissue without an intervening cartilage template. This process is responsible for the formation of flat bones like the skull and clavicles.

Endochondral osteogenesis, on the other hand, involves the initial development of a cartilaginous model or template, which is later replaced by bone tissue. This process forms long bones, such as those in the limbs, and occurs through several stages involving chondrocyte proliferation, hypertrophy, and calcification, followed by invasion of blood vessels and osteoblasts to replace the cartilage with bone tissue.

Abnormalities in osteogenesis can lead to various skeletal disorders and diseases, such as osteogenesis imperfecta (brittle bone disease), achondroplasia (a form of dwarfism), and cleidocranial dysplasia (a disorder affecting skull and collarbone development).

Osteocalcin is a protein that is produced by osteoblasts, which are the cells responsible for bone formation. It is one of the most abundant non-collagenous proteins found in bones and plays a crucial role in the regulation of bone metabolism. Osteocalcin contains a high affinity for calcium ions, making it essential for the mineralization of the bone matrix.

Once synthesized, osteocalcin is secreted into the extracellular matrix, where it binds to hydroxyapatite crystals, helping to regulate their growth and contributing to the overall strength and integrity of the bones. Osteocalcin also has been found to play a role in other physiological processes outside of bone metabolism, such as modulating insulin sensitivity, energy metabolism, and male fertility.

In summary, osteocalcin is a protein produced by osteoblasts that plays a critical role in bone formation, mineralization, and turnover, and has been implicated in various other physiological processes.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Transforming Growth Factor-alpha (TGF-α) is a type of growth factor, specifically a peptide growth factor, that plays a role in cell growth, proliferation, and differentiation. It belongs to the epidermal growth factor (EGF) family of growth factors. TGF-α binds to the EGF receptor (EGFR) on the surface of cells and activates intracellular signaling pathways that promote cellular growth and division.

TGF-α is involved in various biological processes, including embryonic development, wound healing, and tissue repair. However, abnormal regulation of TGF-α has been implicated in several diseases, such as cancer. Overexpression or hyperactivation of TGF-α can contribute to uncontrolled cell growth and tumor progression by stimulating the proliferation of cancer cells and inhibiting their differentiation and apoptosis (programmed cell death).

TGF-α is produced by various cell types, including epithelial cells, fibroblasts, and immune cells. It can be secreted in a membrane-bound form (pro-TGF-α) or as a soluble protein after proteolytic cleavage.

Promoter regions in genetics refer to specific DNA sequences located near the transcription start site of a gene. They serve as binding sites for RNA polymerase and various transcription factors that regulate the initiation of gene transcription. These regulatory elements help control the rate of transcription and, therefore, the level of gene expression. Promoter regions can be composed of different types of sequences, such as the TATA box and CAAT box, and their organization and composition can vary between different genes and species.

Tumor Necrosis Factor-alpha (TNF-α) is a cytokine, a type of small signaling protein involved in immune response and inflammation. It is primarily produced by activated macrophages, although other cell types such as T-cells, natural killer cells, and mast cells can also produce it.

TNF-α plays a crucial role in the body's defense against infection and tissue injury by mediating inflammatory responses, activating immune cells, and inducing apoptosis (programmed cell death) in certain types of cells. It does this by binding to its receptors, TNFR1 and TNFR2, which are found on the surface of many cell types.

In addition to its role in the immune response, TNF-α has been implicated in the pathogenesis of several diseases, including autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis, as well as cancer, where it can promote tumor growth and metastasis.

Therapeutic agents that target TNF-α, such as infliximab, adalimumab, and etanercept, have been developed to treat these conditions. However, these drugs can also increase the risk of infections and other side effects, so their use must be carefully monitored.

Proto-oncogene proteins are normal cellular proteins that play crucial roles in various cellular processes, such as signal transduction, cell cycle regulation, and apoptosis (programmed cell death). They are involved in the regulation of cell growth, differentiation, and survival under physiological conditions.

When proto-oncogene proteins undergo mutations or aberrations in their expression levels, they can transform into oncogenic forms, leading to uncontrolled cell growth and division. These altered proteins are then referred to as oncogene products or oncoproteins. Oncogenic mutations can occur due to various factors, including genetic predisposition, environmental exposures, and aging.

Examples of proto-oncogene proteins include:

1. Ras proteins: Involved in signal transduction pathways that regulate cell growth and differentiation. Activating mutations in Ras genes are found in various human cancers.
2. Myc proteins: Regulate gene expression related to cell cycle progression, apoptosis, and metabolism. Overexpression of Myc proteins is associated with several types of cancer.
3. EGFR (Epidermal Growth Factor Receptor): A transmembrane receptor tyrosine kinase that regulates cell proliferation, survival, and differentiation. Mutations or overexpression of EGFR are linked to various malignancies, such as lung cancer and glioblastoma.
4. Src family kinases: Intracellular tyrosine kinases that regulate signal transduction pathways involved in cell proliferation, survival, and migration. Dysregulation of Src family kinases is implicated in several types of cancer.
5. Abl kinases: Cytoplasmic tyrosine kinases that regulate various cellular processes, including cell growth, differentiation, and stress responses. Aberrant activation of Abl kinases, as seen in chronic myelogenous leukemia (CML), leads to uncontrolled cell proliferation.

Understanding the roles of proto-oncogene proteins and their dysregulation in cancer development is essential for developing targeted cancer therapies that aim to inhibit or modulate these aberrant signaling pathways.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

An amino acid sequence is the specific order of amino acids in a protein or peptide molecule, formed by the linking of the amino group (-NH2) of one amino acid to the carboxyl group (-COOH) of another amino acid through a peptide bond. The sequence is determined by the genetic code and is unique to each type of protein or peptide. It plays a crucial role in determining the three-dimensional structure and function of proteins.

Cell differentiation is the process by which a less specialized cell, or stem cell, becomes a more specialized cell type with specific functions and structures. This process involves changes in gene expression, which are regulated by various intracellular signaling pathways and transcription factors. Differentiation results in the development of distinct cell types that make up tissues and organs in multicellular organisms. It is a crucial aspect of embryonic development, tissue repair, and maintenance of homeostasis in the body.

Genetic transcription is the process by which the information in a strand of DNA is used to create a complementary RNA molecule. This process is the first step in gene expression, where the genetic code in DNA is converted into a form that can be used to produce proteins or functional RNAs.

During transcription, an enzyme called RNA polymerase binds to the DNA template strand and reads the sequence of nucleotide bases. As it moves along the template, it adds complementary RNA nucleotides to the growing RNA chain, creating a single-stranded RNA molecule that is complementary to the DNA template strand. Once transcription is complete, the RNA molecule may undergo further processing before it can be translated into protein or perform its functional role in the cell.

Transcription can be either "constitutive" or "regulated." Constitutive transcription occurs at a relatively constant rate and produces essential proteins that are required for basic cellular functions. Regulated transcription, on the other hand, is subject to control by various intracellular and extracellular signals, allowing cells to respond to changing environmental conditions or developmental cues.

Leukemia, myeloid is a type of cancer that originates in the bone marrow, where blood cells are produced. Myeloid leukemia affects the myeloid cells, which include red blood cells, platelets, and most types of white blood cells. In this condition, the bone marrow produces abnormal myeloid cells that do not mature properly and accumulate in the bone marrow and blood. These abnormal cells hinder the production of normal blood cells, leading to various symptoms such as anemia, fatigue, increased risk of infections, and easy bruising or bleeding.

There are several types of myeloid leukemias, including acute myeloid leukemia (AML) and chronic myeloid leukemia (CML). AML progresses rapidly and requires immediate treatment, while CML tends to progress more slowly. The exact causes of myeloid leukemia are not fully understood, but risk factors include exposure to radiation or certain chemicals, smoking, genetic disorders, and a history of chemotherapy or other cancer treatments.

POL1 (Polymerase 1) Transcription Initiation Complex Proteins are a set of proteins that come together to form the initiation complex for the transcription of ribosomal RNA (rRNA) genes in eukaryotic cells. The POL1 complex includes RNA polymerase I, select transcription factors, and other regulatory proteins. This complex is responsible for the transcription of rRNA genes located within the nucleolus, a specialized region within the cell nucleus. Proper assembly and functioning of this initiation complex are crucial for the production of ribosomes, which play a critical role in protein synthesis.

Alkaline phosphatase (ALP) is an enzyme found in various body tissues, including the liver, bile ducts, digestive system, bones, and kidneys. It plays a role in breaking down proteins and minerals, such as phosphate, in the body.

The medical definition of alkaline phosphatase refers to its function as a hydrolase enzyme that removes phosphate groups from molecules at an alkaline pH level. In clinical settings, ALP is often measured through blood tests as a biomarker for various health conditions.

Elevated levels of ALP in the blood may indicate liver or bone diseases, such as hepatitis, cirrhosis, bone fractures, or cancer. Therefore, physicians may order an alkaline phosphatase test to help diagnose and monitor these conditions. However, it is essential to interpret ALP results in conjunction with other diagnostic tests and clinical findings for accurate diagnosis and treatment.

Runt-related transcription factor 2 (RUNX2) also known as core-binding factor subunit alpha-1 (CBF-alpha-1) is a protein that ... The protein can bind DNA both as a monomer or, with more affinity, as a subunit of a heterodimeric complex. Transcript variants ... This protein is a member of the RUNX family of transcription factors and has a Runt DNA-binding domain. It is essential for ... Zinc finger protein 521 (ZFP521) and activating transcription factor 4 (ATF4) are cofactors of Runx2. Binding of the ...
... core-binding factor (CBF), alpha-B subunit, etc.) binds to the core site, 5'-pygpyggt-3', of a number of enhancers and ... The protein is a heterodimer of alpha- and beta-subunits. The alpha-subunit binds DNA as a monomer, and appears to have a role ... highly similar to the Drosophila melanogaster segmentation gene runt and to the mouse transcription factor PEBP2 alpha subunit ... The region of shared similarity, known as the Runt domain, is responsible for DNA-binding and protein-protein interaction. In ...
... or core-binding factor subunit alpha-2 (CBFA2) is a protein that in humans is encoded by the RUNX1 gene. RUNX1 is a ... a DNA binding CBFα chain (RUNX1 or RUNX2) and a non-DNA-binding subunit called core binding factor β (CBFβ); the binding ... Wang, S, Speck, NA (January 1992). "Purification of core-binding factor, a protein that binds the conserved core site in murine ... It belongs to the Runt-related transcription factor (RUNX) family of genes which are also called core binding factor-α (CBFα). ...
Due to the higher expression, the factor will bind with a high probability to the polymerase-core-enzyme. Doing so, other ... subunits) binds a sigma factor to form a complex called the RNA polymerase holoenzyme. It was previously believed that the RNA ... The core RNA polymerase (consisting of 2 alpha (α), 1 beta (β), 1 beta-prime (β'), and 1 omega (ω) ... Instead, it changes its binding with the core during initiation and elongation. Therefore, the sigma factor cycles between a ...
This gene encodes one of the smaller subunits of TFIID that binds to the basal transcription factor GTF2B as well as to several ... The protein complex that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to ... "Induced alpha helix in the VP16 activation domain upon binding to a human TAF". Science. 277 (5330): 1310-3. doi:10.1126/ ... TAF9 RNA polymerase II, TATA box binding protein (TBP)-associated factor, 32kDa, also known as TAF9, is a protein that in ...
... it allosterically enhances DNA binding by the alpha subunit as the complex binds to the core site of various enhancers and ... Core-binding factor subunit beta is a protein that in humans is encoded by the CBFB gene. The protein encoded by this gene is ... "Entrez Gene: CBFB core-binding factor, beta subunit". The Cancer Genome Atlas Network (2012). "Comprehensive molecular ... the beta subunit of a heterodimeric core-binding transcription factor belonging to the PEBP2/CBF transcription factor family ...
... subunit of 150 kDa, a beta prime subunit (β′) of 155 kDa, and a small omega (ω) subunit. A sigma (σ) factor binds to the core, ... RNA polymerase "core" from E. coli consists of five subunits: two alpha (α) subunits of 36 kDa, a beta (β) ... The core enzyme has five subunits (~400 kDa): β′ The β′ subunit is the largest subunit, and is encoded by the rpoC gene. The β ... The ω subunit facilitates assembly of RNAP and stabilizes assembled RNAP. In order to bind promoters, RNAP core associates with ...
The protein that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to position ... Transcription initiation factor TFIID subunit 11 also known as TAFII28, is a protein that in humans is encoded by the TAF11 ... The conserved region contains four alpha helices and three loops arranged as in histone H3. TAF11 has been shown to interact ... In molecular biology, TAFII28 refers to the TATA box binding protein associated factor. Together with the TATA-binding protein ...
Chen Y; Le Cahérec F; Chuck SL (1998). "Calnexin and other factors that alter translocation affect the rapid binding of ... This gene encodes an alpha subunit of the heteromeric SEC61 complex, which also contains beta and gamma subunits. GRCh38: ... Knight BC; High S (1998). "Membrane integration of Sec61alpha: a core component of the endoplasmic reticulum translocation ... Protein transport protein Sec61 subunit alpha isoform 1 is a protein that in humans is encoded by the SEC61A1 gene. The protein ...
TATA box-binding protein-associated factor) subunits (TAF1A, TAF1B, and TAF1C). These TAFs do not have a histone-like fold ... It contains two short alpha helices and a long central alpha helix. TAF1 (TAFII250) TAF2 (CIF150) TAF3 (TAFII140) TAF4 ( ... for example the downstream promoter element or gene-specific core promoter sequence Due to such interactions, they contribute ... The TBP-associated factors (TAF) are proteins that associate with the TATA-binding protein in transcription initiation. It is a ...
... which include two alphas, a beta, and a beta prime (α, α, β, and β'). A fifth subunit, sigma (called the σ-factor), is only ... The binding of the σ-factor to the promoter is the first step in initiation. Once the σ-factor releases from the polymerase, ... When the σ-factor detaches, it is in core polymerase form. The σ-factor recognizes promoter sequences at -35 and -10 regions ... Bacteria have a σ-factor that detects and binds to promoter sites but eukaryotes do not need a σ-factor. Instead, eukaryotes ...
"The alpha-like RNA polymerase II core subunit 3 (RPB3) is involved in tissue-specific transcription and muscle differentiation ... cooperation with promoter-bound activator domains and binding to TFIIB". J. Mol. Biol. 261 (5): 599-606. doi:10.1006/jmbi. ... POLR2J has been shown to interact with: Apoptosis antagonizing transcription factor, POLR2C, and SATB1. GRCh38: Ensembl release ... The product of this gene exists as a heterodimer with another polymerase subunit; together they form a core subassembly unit of ...
This complex consists of three membrane proteins- alpha, beta, and gamma. This gene encodes the beta-subunit protein. The Sec61 ... Chen Y, Le Cahérec F, Chuck SL (1998). "Calnexin and other factors that alter translocation affect the rapid binding of ... Knight BC, High S (1998). "Membrane integration of Sec61alpha: a core component of the endoplasmic reticulum translocation ... 1999). "A novel ADP-ribosylation like factor (ARL-6), interacts with the protein-conducting channel SEC61beta subunit". FEBS ...
The protein that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to position ... "Structure-function analysis of the estrogen receptor alpha corepressor scaffold attachment factor-B1: identification of a ... This gene encodes a subunit of TFIID present in a subset of TFIID complexes. Translocations involving chromosome 17 and ... TATA-binding protein-associated factor 2N is a protein that in humans is encoded by the TAF15 gene. Initiation of transcription ...
"Core-binding factor β and Runx transcription factors promote adaptive natural killer cell responses". Science Immunology. 2 (18 ... Binding of IL-12 to IL-12R, which is composed of two different subunits (IL12Rβ1 and IL12Rβ2), leads to the interaction of ... "Increased sensitivity to interferon-alpha in psoriatic T cells". The Journal of Investigative Dermatology. 125 (5): 936-44. doi ... association with regulatory factors; 3. central DNA-binding domain - binding to the enhancer region of IFN-γ activated sequence ...
In normoxia, HIF alpha subunits are marked for the ubiquitin-proteasome degradation pathway through hydroxylation of proline- ... "Structural basis for binding of hypoxia-inducible factor to the oxygen-sensing prolyl hydroxylases". Structure. 17 (7): 981-9. ... The catalytic domain consists of a double-stranded β-helix core that is stabilized by three α-helices packed along the major β- ... X-ray crystallography and NMR spectroscopy showed that both peptides bind to the same binding site on PHD2, in a cleft on the ...
The 20S core is composed of 4 rings of 28 non-identical subunits; 2 rings are composed of 7 alpha subunits and 2 rings are ... It also binds closely to the E3 ubiquitin ligase MDM2, which is a regulator of the degradation of p53 and retinoblastoma ... Accordingly, gene expression by degradation of transcription factors, such as p53, c-jun, c-Fos, NF-κB, c-Myc, HIF-1α, MATα2, ... which contains 6 ATPase subunits and 2 non-ATPase subunits, and a lid, which contains up to 10 non-ATPase subunits. Proteasomes ...
"Multidomain organization of eukaryotic guanine nucleotide exchange translation initiation factor eIF-2B subunits revealed by ... The structure can be divided into a structural C-terminal core onto which the two N-terminal helices are attached. The core ... The W2 domain has a globular fold and is exclusively composed out of alpha-helices. ... the eIF-W2 domain functions as the binding site for Mnk eIF4E kinase, an enzyme that phosphorylates eukaryotic initiation ...
It belongs to the thioredoxin superfamily fold which is defined by a beta-sheet core surrounded by alpha-helices. The active ... This two-subunit enzyme produces resistance to arsenite and antimonite. Arsenate, however, must first be reduced to arsenite ... Li S, Rosen BP, Borges-Walmsley MI, Walmsley AR (July 2002). "Evidence for cooperativity between the four binding sites of ... The arsC family also comprises the Spx proteins which are Gram-positive bacterial transcription factors that regulate the ...
This contains a core of two compact domains with each having five alpha helices. The first five-helix bundle is a conserved ... Viral cyclin D binds human Cdk6 and inhibits Rb by phosphorylating it, resulting in free transcription factors which result in ... A simplification in yeast is that all cyclins bind to the same Cdc subunit, the Cdc28. Cyclins in yeast are controlled by ... A role for cAMP response element-binding protein and activating transcription factor-2 in pp60(v-src) signaling in breast ...
Ruediger R, Fields K, Walter G (1999). "Binding specificity of protein phosphatase 2A core enzyme for regulatory B subunits and ... 1990). "alpha- and beta-forms of the 65-kDa subunit of protein phosphatase 2A have a similar 39 amino acid repeating structure ... Hong Y, Sarge KD (1999). "Regulation of protein phosphatase 2A activity by heat shock transcription factor 2". J. Biol. Chem. ... It consists of a common heteromeric core enzyme, which is composed of a catalytic subunit and a constant regulatory subunit, ...
... core binding factor alpha 2 subunit MeSH D12.776.930.155.200.300 - core binding factor alpha 3 subunit MeSH D12.776.930.316. ... nf-e2 transcription factor, p45 subunit MeSH D12.776.930.155.200.100 - core binding factor alpha 1 subunit MeSH D12.776.930.155 ... CCAAT-binding factor MeSH D12.776.930.127.124.500 - CCAAT-enhancer-binding protein-alpha MeSH D12.776.930.127.124.750 - CCAAT- ... alpha subunit MeSH D12.776.930.125.750.590 - myod protein MeSH D12.776.930.125.750.595 - myogenic regulatory factor 5 MeSH ...
A highly conserved core, amino acid repeat regions, and homologies with translation elongation factors". J Biol Chem. 266 (3): ... 2002). "Interaction network of human aminoacyl-tRNA synthetases and subunits of elongation factor 1 complex". Biochem. Biophys ... 2004). "A physical and functional map of the human TNF-alpha/NF-kappa B signal transduction pathway". Nat. Cell Biol. 6 (2): 97 ... identification of RNA-binding residues and functional implications for tandem repeats". Biochemistry. 39 (51): 15775-82. doi: ...
This gene encodes a germ cell-specific counterpart of the large (alpha/beta) subunit of general transcription factor TFIIA that ... pre-initiation complex on a eukaryotic core promoter involve the effects of TFIIA on the interaction between TATA-binding ... TFIIA-alpha and beta-like factor is a protein that in humans is encoded by the GTF2A1L gene. The assembly and stability of the ... "Entrez Gene: ALF TFIIA-alpha/beta-like factor". Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace the cap ...
... general transcription factor 2H subunit 5) is also known as the TTD group A (TTDA) subunit (and as Tfb5). The TTDA subunit is ... and part of a six-subunit complex of Rad3, Tfb1, Tfb2, Tfb4, Tfb5, and Ssl1 (referred to as core) In humans, the function of ... TTDA is present both bound to TFIIH, and as a free fraction that shuffles between the cytoplasm and nucleus; induction of NER- ... These proteins have a structural motif consisting of a 2-layer sandwich structure with an alpha/beta plait topology. ...
... alpha), β (beta), and γ (gamma). In the inactive state, the three subunits associate together and the α-subunit binds GDP. G ... 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 ... GTP-binding to the α-subunit causes dissociation of the β- and γ-subunits. Furthermore, the three subunits, α, β, and γ have ...
"The XPB subunit of repair/transcription factor TFIIH directly interacts with SUG1, a subunit of the 26S proteasome and putative ... which interacts with the seven-membered alpha ring of 20S core particle and establishes an asymmetric interface between the 19S ... It also have subunits that can bind with nucleotides (e.g., ATPs) in order to facilitate the association between 19S and 20S ... These subunits can be categorized into two classes based on the ATP dependence of subunits, ATP-dependent subunits and ATP- ...
A heterodimer of this protein and a beta subunit forms a complex that binds to the core DNA sequence 5'-YGYGGT-3' found in a ... Core binding factor RUNX1 RUNX2 GRCh38: Ensembl release 89: ENSG00000020633 - Ensembl, May 2017 GRCm38: Ensembl release 89: ... "Isolation of PEBP2 alpha B cDNA representing the mouse homolog of human acute myeloid leukemia gene, AML1". Oncogene. 8 (3): ... Runt-related transcription factor 3 is a protein that in humans is encoded by the RUNX3 gene. This gene encodes a member of the ...
... being bound by several eukaryotic initiation factors, including eIF1, eIF1A, and eIF3. The 40S ribosomal subunit is also ... This rRNA core is decorated with dozens of proteins. In the figure "Crystal Structure of the Eukaryotic 40S Ribosomal Subunit ... Eukaryote-specific extensions of conserved proteins, ranging from a few residues or loops to very long alpha helices and ... Crystal structure of the eukaryotic 40S ribosomal subunit from T. thermophila 40S subunit viewed from the subunit interface ...
... and RACK1 binding to Na+/H+ exchange regulatory factor". The Journal of Biological Chemistry. 277 (25): 22925-33. doi:10.1074/ ... also known as guanine nucleotide-binding protein subunit beta-2-like 1 (GNB2L1), is a 35 kDa protein that in humans is encoded ... Later studies established RACK1, and its yeast homolog Asc1, as a core ribosomal protein of the eukaryotic small (40S) ... "Crystal structure of the eukaryotic 40S ribosomal subunit in complex with initiation factor 1". Science. 331 (6018): 730-6. ...
A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... Core Binding Factor Alpha 2 Subunit. *Core Binding Factor Alpha 3 Subunit ... "Core Binding Factor Alpha 1 Subunit" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, ... This graph shows the total number of publications written about "Core Binding Factor Alpha 1 Subunit" by people in this website ...
SL3/AKV core-binding factor alpha A subunit. Additional Information & Resources. Tests Listed in the Genetic Testing Registry. ... The RUNX2 protein is a transcription factor, which means it attaches (binds) to specific regions of DNA and helps control the ... 2013 Jan;24(1):130-3. doi: 10.1097/SCS.0b013e3182636b7e. Citation on PubMed ...
Although numerous transcription factors involved in chondrocyte and osteoblast differentiation have been identified, lit … ... Core Binding Factor Alpha 1 Subunit Actions. * Search in PubMed * Search in MeSH ... Regulation of osteoblast differentiation by transcription factors. Komori T. Komori T. J Cell Biochem. 2006 Dec 1;99(5):1233-9 ... Although numerous transcription factors involved in chondrocyte and osteoblast differentiation have been identified, little is ...
Core Binding Factor Alpha 1 Subunit/metabolism; Extracellular Matrix/metabolism; Female; Humans; Mechanotransduction, Cellular ... The maintenance of mechanical conditioning is regulated by RUNX2, an osteogenic transcription factor, established driver of ...
The differentiation of neural crest cells into odontoblasts is orchestrated by transcription factors regulating the expression ... Core Binding Factor Alpha 1 Subunit / genetics Actions. * Search in PubMed * Search in MeSH ... Yuxiu Lin 1 , Yao Xiao 1 , ChuJiao Lin 1 , Qian Zhang 1 , Shu Zhang 1 , Fei Pei 1 , Huan Liu 1 2 , Zhi Chen 1 ... Yuxiu Lin 1 , Yao Xiao 1 , ChuJiao Lin 1 , Qian Zhang 1 , Shu Zhang 1 , Fei Pei 1 , Huan Liu 1 2 , Zhi Chen 1 ...
... caused by mutation in the transcription factor gene (CBFA1) encoding core-binding factor, runt domain, alpha-subunit 1 on 6p. ... Applying to factors that have a detrimental effect upon hereditary qualities, physical or mental. dysgerminoma (dis-jer-mi-no′ ... primary d. d. due to a functional disturbance and not due to inflammation, new growths, or anatomic factors. SYN: functional d ... caused by mutation in the transforming growth factor, beta-induced, gene (TGFB1) encoding keratoepithelin on 5q. Leyden-Möbius ...
Runt-related transcription factor 2 (RUNX2) also known as core-binding factor subunit alpha-1 (CBF-alpha-1) is a protein that ... The protein can bind DNA both as a monomer or, with more affinity, as a subunit of a heterodimeric complex. Transcript variants ... This protein is a member of the RUNX family of transcription factors and has a Runt DNA-binding domain. It is essential for ... Zinc finger protein 521 (ZFP521) and activating transcription factor 4 (ATF4) are cofactors of Runx2. Binding of the ...
SL3/AKV core-binding factor alpha C subunit. Description. RUNX3 is a member of the runt domain-containing family of ... transcription factors. A heterodimer of this protein and a beta subunit forms a complex that binds to the core DNA sequence 5- ... It also interacts with other transcription factors. It functions as a tumor suppressor, and the gene is frequently deleted or ... we will perform a multi-center study of FISH and hypermethylation markers as possible prognostic factors in BE. The centers ...
SL3/AKV core binding factor alpha A subunit. *SL3/AKV core-binding factor alpha A subunit ... CBF binds to the core site, 5-PYGPYGGT-3, of a number of enhancers and promoters, including murine leukemia virus, ... Transcription factor involved in osteoblastic differentiation and skeletal morphogenesis. Essential for the maturation of ... alpha 1(I) collagen, LCK, IL-3 and GM-CSF promoters (By similarity). Inhibits MYST4-dependent transcriptional activation. ...
Core Binding Factors [D12.776.930.155] * Core Binding Factor alpha Subunits [D12.776.930.155.200] * Core Binding Factor Alpha 1 ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... Core Binding Factor Alpha 1 Subunit Preferred Term Term UI T623663. Date12/13/2004. LexicalTag NON. ThesaurusID NLM (2006). ...
Core Binding Factors [D12.776.930.155] * Core Binding Factor alpha Subunits [D12.776.930.155.200] * Core Binding Factor Alpha 1 ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... Core Binding Factor Alpha 1 Subunit Preferred Term Term UI T623663. Date12/13/2004. LexicalTag NON. ThesaurusID NLM (2006). ...
Core Binding Factor Alpha 2 Subunit [D12.776.930.155.200.200] Core Binding Factor Alpha 2 Subunit ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ... Core Binding Factor Alpha 1 Subunit Descriptor Spanish: Subunidad alfa 1 del Factor de Unión al Sitio Principal Spanish from ...
Absorptiometry, Photon; Adolescent; Adult; Aging; Bone Density; Core Binding Factor Alpha 1 Subunit; Female; Gene Expression; ... Heredity factors are important for BMD, and Runx-2 is accepted as a regulator of osteoblasts and bone formation. The aim of our ... Heredity factors are important for BMD, and Runx-2 is accepted as a regulator of osteoblasts and bone formation. The aim of our ... of bone densitometry improved the possibility of studying BMD and the influence of genetic and environmental factors on bone. ...
PEBP2-alpha C; PEA2-alpha C; Oncogene AML-2; Core-binding factor subunit alpha-3; CBFA3; CBF-alpha-3; Acute myeloid leukemia 2 ... SL3/AKV core-binding factor alpha C subunit; SL3-3 enhancer factor 1 alpha C subunit; Polyomavirus enhancer-binding protein 2 ... CBF complexes repress ZBTB7B transcription factor during cytotoxic (CD8+) T cell development. They bind to RUNX-binding ... while CBFB is a non-DNA-binding regulatory subunit that allosterically enhances the sequence-specific DNA-binding capacity of ...
... level interferon and TNF signaling were deregulated in primary RUNX1mut CML cells and stem cell and B-lymphoid factors ... also known as core binding factor subunit alpha (CBFA2), is a transcription factor (TF) and an essential component of the core ... d GSEA of TNF, IFN-alpha, IFN-gamma, and CBF-AML pathways upregulated in RUNX1mut compared with RUNX1wt patients. e GSEA of ... binding factor complex that plays a key role in hematopoiesis [1]. Somatic and germline alterations involving RUNX1 gene are ...
Core Binding Factor Alpha 2 Subunit. *Gene Expression Regulation, Neoplastic. *Cell Differentiation ... Core Binding Factor Alpha 1 Subunit. * ... Secreted frizzled related protein 1 is a target to improve ...
CORE BINDING FACTOR ALPHA SUBUNITS), along with a non-DNA-binding beta subunits, CORE BINDING FACTOR BETA SUBUNIT. Core Binding ... A family of transcription factors that bind to the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. ... HN - 2006(1987) BX - Core Binding Factor alpha Proteins MH - Core Binding Factor beta Subunit UI - D050658 MN - D12.776.930.155 ... A transcription factor that dimerizes with CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. It contains a highly ...
Msx2 and Runx2 in mouse embryonic stem cells were monitored over a 48 hour period after exposure to the growth factors BMP2 and ... Animals, Base Sequence, Bone Morphogenetic Protein 2, Cell Differentiation, Cell Line, Core Binding Factor Alpha 1 Subunit, ... If you click Reject all non-essential cookies only necessary cookies providing core functionality such as security, network ... Msx2 and Runx2 in mouse embryonic stem cells were monitored over a 48 hour period after exposure to the growth factors BMP2 and ...
... the beta subunit does not bind the DNA directly but increases the affinity and stabilizes the binding of the alpha subunit to ... Cite this: Core Binding Factor (CBF) Primary Acute Myeloid Leukemia: Biology and Clinical Implications - Medscape - Mar 22, ... An alternative scenario could be that the CBFbeta/MYH11 protein binds to the CBF-alpha subunit to form a complex that in turn ... Core Binding Factor (CBF) Primary Acute Myeloid Leukemia: Biology and Clinical Implications. MedGenMed 2(2), 2000 [formerly ...
Core Binding Factor beta Subunit 67% * Lymphoma 60% * Ventricular Myosins 50% * Chromosomes, Human, Pair 16 50% ... proliferation of T-cells simulating non-Hodgkin lymphoma in a patient with psoriasis treated with tumor necrosis factor alpha ... Transcription factor MIST1 in terminal differentiation of mouse and human plasma cells. Capoccia, B. J., Lennerz, J. K. M., ... Combined core needle biopsy and fine-needle aspiration with ancillary studies correlate highly with traditional techniques in ...
Core Binding Factor alpha Subunits; DNA Primers; Gene Expression Regulation; Genes, Regulator; Neoplasm Proteins; Osteocalcin; ... Animals; Base Sequence; Cell Line; Chromatin; Core Binding Factor Alpha 1 Subunit; ... Together our results support a stepwise model for chromatin remodeling of the OC promoter and show that binding of the liganded ... These findings indicate that binding of liganded VDR in the distal promoter directly impacts the chromatin structure of the ...
The entire sequence was 83% similar to centaurin alpha, another PtdIns(3,4,5)P3-binding protein. The protein bound PtdIns(3,4,5 ... The core of the molecule is an antiparallel beta-sheet consisting of seven strands. The C terminus is folded into a long alpha- ... The PH domain in beta-adrenergic receptor kinase may be involved in binding to the beta gamma subunits of a trimeric G-protein ... A family of NMR solution structures of the growth factor receptor-bound protein 2 (Grb2) SH2 domain has been determined by ...
An ANY-box core was used, which contained a light-gray base and an adjustable perpendicular stick holding a camera and an ... S)-lacosamide binding to collapsin response mediator protein 2 (CRMP2) regulates CaV2.2 activity by subverting its ... 1a), the mitochondrial indicators ATP synthase-subunit c (SCMAS) and heat-shock protein-60 (HSP60) co-localized with the ... governed by the neuron-specific22 calcium/calmodulin-dependent protein kinase II alpha (CaMKIIa) promoter (CaMKIIaCre-mCATLoxP ...
Adolescent , Female , Humans , Cell Nucleus , Metabolism , Cleidocranial Dysplasia , Genetics , Core Binding Factor Alpha 1 ... Female , Humans , DNA-Binding Proteins , Genetics , Fingers , Congenital Abnormalities , Frameshift Mutation , Hair Diseases , ... Novel Mutation of Cleidocranial Dysplasia-related Frameshift Runt-related Transcription Factor 2 in a Sporadic Chinese Case / 中 ... Previous studies reported a connection between CCD and the haploinsufficiency of runt-related transcription factor 2 (RUNX2). ...
SETBP1 is a SET-binding protein regulating self-renewal potential through HOXA-protein activation. Somatic SETBP1 mutations ... Core Binding Factor Alpha 2 Subunit / genetics * Core Binding Factor Alpha 2 Subunit / metabolism ... In general, somatic SETBP1 mutations have a significant clinical impact on the outcome as poor prognostic factor, due to ... SETBP1 is a SET-binding protein regulating self-renewal potential through HOXA-protein activation. Somatic SETBP1 mutations ...
Core Binding Factor Alpha 3 Subunit / metabolism Actions. * Search in PubMed * Search in MeSH ... Mechanistically, Thpok- bound genes encoding the transcription factors Blimp1 and Runx3 and acted by antagonizing their ... The Emergence and Functional Fitness of Memory CD4+ T Cells Require the Transcription Factor Thpok Thomas Ciucci 1 , Melanie S ... The Emergence and Functional Fitness of Memory CD4+ T Cells Require the Transcription Factor Thpok Thomas Ciucci et al. ...
Core Binding Factor Alpha 2 Subunit N0000169997 Core Binding Factor Alpha 3 Subunit N0000169995 Core Binding Factor alpha ... Subunits N0000169994 Core Binding Factor beta Subunit N0000169993 Core Binding Factors N0000005782 Corn Oil N0000011299 Corpus ... Gi2 N0000170554 GTP-Binding Protein alpha Subunits N0000170556 GTP-Binding Protein alpha Subunits, G12-G13 N0000170558 GTP- ... Binding Protein alpha Subunits, Gi-Go N0000170557 GTP-Binding Protein alpha Subunits, Gq-G11 N0000170555 GTP-Binding Protein ...
PI3K catalytic subunit alpha (PIK3CA), and silencing information regulator 2 related enzyme 1 (SIRT1) may the core targets of ... nuclear factor erythroid 2-related factor (NFE2L2), nitric oxide synthase 3 (NOS3), nuclear receptor subfamily 3 group C member ... Radioligand binding assays demonstrated that the EDG-1 receptors expressed in Pichia pastoris have specific and saturation ... HIF1A, NFE2L2, NOS3, NR3C1, PIK3CA, and SIRT1 might be core targets of metformin for the treatment of NAFLD. ...

No FAQ available that match "core binding factor alpha 1 subunit"