Core Binding Factor beta Subunit
Core Binding Factors
Core Binding Factor alpha Subunits
Core Binding Factor Alpha 2 Subunit
Transcription Factor AP-2
Core Binding Factor Alpha 1 Subunit
Transforming Growth Factor beta
Transcription Factors
Chromosomes, Human, Pair 16
DNA-Binding Proteins
Molecular Sequence Data
Indispensable role of the transcription factor PEBP2/CBF in angiogenic activity of a murine endothelial cell MSS31. (1/86)
Mice lacking the AML1/PEBP2alphaB/CBFa2 gene or PEBP2beta/CBFb gene exhibit a defect in definitive hematopoiesis and die in utero because of hemorrhage in the central nervous system. Hematopoiesis in the embryo is considered to be tightly associated with vascular development. Here we examined whether PEBP2/CBF plays any role in angiogenesis besides that in definitive hematopoiesis. We found that AML1/PEBP2alphaB/CBFa2, PEBP2alphaA/CBFa1, and PEBP2beta/CBFb were expressed in a murine endothelial cell line MSS31. The expression of these molecules as well as the DNA binding activity of PEBP2/CBF were augmented by angiogenic growth factors such as bFGF and VEGF. Moreover, the expression of PEBP2 alpha/CBFa protein in endothelial cells was confirmed at the site of angiogenesis in vivo. To further clarify the role of PEBP2/CBF in angiogenesis, we established permanent transfectants of PEBP2 beta-MYH11 gene, one that interacts with the runt domain of the alpha subunit and deregulates PEBP2/CBF in a dominant interfering manner. Proliferation, migration, and tube formation of the PEBP2 beta-MYH11 transfectants were significantly reduced in comparison with those activities of the mock transfectants. These results suggest that transcription factor PEBP2/CBF plays an important role in angiogenesis. (+info)Zebrafish homolog of the leukemia gene CBFB: its expression during embryogenesis and its relationship to scl and gata-1 in hematopoiesis. (2/86)
Mammalian CBFB encodes a transcription factor (CBF beta) that in combination with CBF alpha 2 binds to specific DNA sequences and regulates expression of a number of hematopoietic genes. CBFB is associated with human leukemias through a chromosome 16 inversion and is essential for definitive hematopoiesis during mouse embryo development. We have isolated a zebrafish cbfb complementary DNA (cDNA) clone from a zebrafish kidney cDNA library. This cbfb is highly homologous to human and mouse CBFB/Cbfb genes at both the DNA and protein level. In biochemical analyses, cbfbeta binds to human CBF alpha 2 and enhances its DNA binding. During zebrafish development, cbfb is expressed in the lateral plate mesoderm at tail bud stage and in the intermediate cell mass (ICM, the location of embryonic hematopoiesis) between the 21- to 26-somite stages. The cbfb is also expressed in Rohon-Beard cells, cranial nerve ganglia, hindbrain, retina, branchial arches, jaw, and fin buds. Expression of cbfb is decreased or absent in the ICM and Rohon-Beard cells in some hematopoietic mutants and is unaffected in others. We have also analyzed the expression of scl and gata-1 in the same hematopoietic mutants to ascertain the relative order of these transcription factors to cbfb in zebrafish hematopoiesis. Our results indicate that cbfb is expressed in early hematopoietic progenitors and that its expression pattern in the hematopoietic mutants is similar to that of scl. (Blood. 2000;96:4178-4184) (+info)Core-binding factor beta (CBFbeta), but not CBFbeta-smooth muscle myosin heavy chain, rescues definitive hematopoiesis in CBFbeta-deficient embryonic stem cells. (3/86)
Core-binding factor beta (CBFbeta) is the non-DNA-binding subunit of the heterodimeric CBFs. Genes encoding CBFbeta (CBFB), and one of the DNA-binding CBFalpha subunits, Runx1 (also known as CBFalpha2, AML1, and PEBP2alphaB), are required for normal hematopoiesis and are also frequent targets of chromosomal translocations in acute leukemias in humans. Homozygous disruption of either the Runx1 or Cbfb gene in mice results in embryonic lethality at midgestation due to hemorrhaging in the central nervous system, and severely impairs fetal liver hematopoiesis. Results of this study show that Cbfb-deficient mouse embryonic stem (ES) cells can differentiate into primitive erythroid colonies in vitro, but are impaired in their ability to produce definitive erythroid and myeloid colonies, mimicking the in vivo defect. Definitive hematopoiesis is restored by ectopic expression of full-length Cbfb transgenes, as well as by a transgene encoding only the heterodimerization domain of CBFbeta. In contrast, the CBFbeta-smooth muscle myosin heavy chain (SMMHC) fusion protein generated by the inv(16) associated with acute myeloid leukemias (M4Eo) cannot rescue definitive hematopoiesis by Cbfb-deficient ES cells. Sequences responsible for the inability of CBFbeta-SMMHC to rescue definitive hematopoiesis reside in the SMMHC portion of the fusion protein. Results also show that the CBFbeta-SMMHC fusion protein transdominantly inhibits definitive hematopoiesis, but not to the same extent as homozygous loss of Runx1 or Cbfb. CBFbeta-SMMHC preferentially inhibits the differentiation of myeloid lineage cells, while increasing the number of blastlike cells in culture. (+info)Primary chromosomal rearrangements of leukemia are frequently accompanied by extensive submicroscopic deletions and may lead to altered prognosis. (4/86)
BCR/ABL fluorescent in situ hybridization study of chronic myeloid leukemia (CML) and Philadelphia(+) (Ph(+)) acute lymphoid leukemia (ALL) indicated that approximately 9% of patients exhibited an atypical hybridization pattern consistent with a submicroscopic deletion of the 5' region of ABL and the 3' region of the BCR genes on the 9q(+) chromosome. The CML patients with deletions had a shorter survival time and a high relapse rate following bone marrow transplant. Since deletions are associated with both Ph(+) CML and ALL, it seemed probable that other leukemia-associated genomic rearrangements may also have submicroscopic deletions. This hypothesis was confirmed by the detection of deletions of the 3' regions of the CBFB and the MLL genes in AML M4 patients with inv(16) and in patients with ALL and AML associated with MLL gene translocations, respectively. In contrast, analysis of the AML M3 group of patients and AML M2 showed that similar large deletions were not frequently associated with the t(15;17) or t(8;21) translocations. Analysis of sequence data from each of the breakpoint regions suggested that large submicroscopic deletions occur in regions with a high overall density of Alu sequence repeats. These findings are the first to show that the process of deletion formation is not disease specific in leukemia and also implicate that the presence of repetitive DNA in the vicinity of breakpoint regions may facilitate the generation of submicroscopic deletions. Such deletions could lead to the loss of one or more genes, and the associated haploinsufficiency may result in the observed differences in clinical behavior. (Blood. 2001;97:3581-3588) (+info)Cloning and expression pattern of a novel PEBP2 beta-binding protein (charged amino acid rich leucine zipper-1[Crl-1]) in the mouse. (5/86)
PEBP2 beta/Cbf beta is the beta subunit of PEBP2/Cbf, which has been demonstrated to have important biological activities in hematopoiesis and osteogenesis. However, PEBP2 beta is ubiquitously expressed, suggesting that PEBP2 has other additionally important physiological activities. In an effort to elucidate other possible functions for PEBP2, we have isolated a novel gene that encodes a PEBP2 beta-interacting protein from a mouse cDNA library. We have called this gene Crl-1 for charged amino acid rich leucine zipper-1 (Crl-1) because it is rich in charged amino acids and contains a putative leucine zipper region. Expression studies in a 17.5 days post-coitum mouse embryo demonstrated Crl-1 expression mainly in the olfactory bulb and cerebral cortex. Post-natally, Crl-1 expression was additionally observed in the cerebellar cortex with strong expression in the hippocampus. These findings show that this novel PEBP2 beta-interacting protein is expressed mainly in subsets of neuronal cells, suggesting that Crl-1 plays some role in the developing mouse brain. (+info)Role of Cbfb in hematopoiesis and perturbations resulting from expression of the leukemogenic fusion gene Cbfb-MYH11. (6/86)
Core-binding factor beta (CBFbeta) and CBFalpha2 form a heterodimeric transcription factor that plays an important role in hematopoiesis. The genes encoding either CBFbeta or CBFalpha2 are involved in chromosomal rearrangements in more than 30% of cases of acute myeloid leukemia (AML), suggesting that CBFbeta and CBFalpha2 play important roles in leukemogenesis. Inv(16)(p13;q22) is found in almost all cases of AML M4Eo and results in the fusion of CBFB with MYH11, the gene encoding smooth muscle myosin heavy chain. Mouse embryos heterozygous for a Cbfb-MYH11 knock-in gene lack definitive hematopoiesis, a phenotype shared by Cbfb(-/-) embryos. In this study we generated a Cbfb-GFP knock-in mouse model to characterize the normal expression pattern of Cbfbeta in hematopoietic cells. In midgestation embryos, Cbfbeta was expressed in populations enriched for hematopoietic stem cells and progenitors. This population of stem cells and progenitors was not present in mouse embryos heterozygous for the Cbfb-MYH11 knock-in gene. Together, these data suggest that Cbfb-MYH11 blocks embryonic hematopoiesis at the stem-progenitor cell level and that Cbfb is essential for the generation of hematopoietic stem and progenitor cells. In adult mice, Cbfbeta was expressed in stem and progenitor cells, as well as mature myeloid and lymphoid cells. Although it was expressed in erythroid progenitors, Cbfbeta was not expressed during the terminal stages of erythropoiesis. Our data indicate that Cbfb is required for myeloid and lymphoid differentiation; but does not play a critical role in erythroid differentiation. (+info)Distinct roles for c-Myb and core binding factor/polyoma enhancer-binding protein 2 in the assembly and function of a multiprotein complex on the TCR delta enhancer in vivo. (7/86)
Enhancers and promoters within TCR loci functionally collaborate to modify chromatin structure and to confer accessibility to the transcription and V(D)J recombination machineries during T cell development in the thymus. Two enhancers at the TCRalphadelta locus, the TCR alpha enhancer and the TCR delta enhancer (Edelta), are responsible for orchestrating the distinct developmental programs for V(D)J recombination and transcription of the TCR alpha and delta genes, respectively. Edelta function depends critically on transcription factors core binding factor (CBF)/polyoma enhancer-binding protein 2 (PEBP2) and c-Myb as measured by transcriptional activation of transiently transfected substrates in Jurkat cells, and by activation of V(D)J recombination within chromatin-integrated substrates in transgenic mice. To understand the molecular mechanisms for synergy between these transcription factors in the context of chromatin, we used in vivo footprinting to study the requirements for protein binding to Edelta within wild-type and mutant versions of a human TCR delta minilocus in stably transfected Jurkat cells. Our data indicate that CBF/PEBP2 plays primarily a structural role as it induces a conformational change in the enhanceosome that is associated with augmented binding of c-Myb. In contrast, c-Myb has no apparent affect on CBF/PEBP2 binding, but is critical for transcriptional activation. Thus, our data reveal distinct functions for c-Myb and CBF/PEBP2 in the assembly and function of an Edelta enhanceosome in the context of chromatin in vivo. (+info)Core binding factor genes and human leukemia. (8/86)
BACKGROUND: The core binding factor (CBF) transcription complex, consisting of the interacting proteins RUNX1 and CBFb, is essential for normal hematopoiesis. Recent studies have shown that mutations and gene rearrangements involving this complex are frequently implicated in leukemogenesis. Understanding the molecular events leading to the disruption of CBF has provided important insights into our understanding of the normal regulatory pathways that control hematopoiesis and has begun to reveal how alterations in these pathways induce leukemia. INFORMATION SOURCES: Both authors are involved in the identification and characterization of chromosomal abnormalities associated with hematologic malignancy. This has led to contributions to multicenter clinical and laboratory investigations as well as publications in peer-reviewed journals. All of the references cited in this review are published in journals covered by Medline. State of the Art. The core binding factor (CBF) is a heterodimeric transcription factor composed of the RUNX1 and CBFb subunits. RUNX1 is the DNA binding element of the complex and its affinity is greatly increased in the presence of CBFb. Knock-out studies in mice have demonstrated that both RUNX1 and CBFb are necessary for definitive hematopoiesis. Furthermore, reciprocal chromosomal translocations involving both partners have been directly implicated in leukemogenesis. Evidence is now emerging that at least some of the resulting fusion proteins, namely ETV6-RUNX1, RUNX1-MTG8 and CBFb-MYH11 dominantly inhibit the function of native CBF by recruiting transcriptional co-repressor complexes. However, knock-in studies have shown that whilst expression of these fusion genes may disrupt normal hematopoiesis, this, by itself, is not sufficient for the subsequent development of leukemia. Mutations of RUNX1 have been identified in familial platelet disorder (FDP), in which there is a congenital predisposition to the development of AML and heterozygous point mutations have been identified in the RUNX1 gene in some leukemias. Moreover, a small number of cases have been reported in which amplification of RUNX1 has been detected in childhood ALL suggesting mechanisms other than loss of function, such as gene dosage may also play a role. CONCLUSIONS: Understanding the role CBF plays in normal hematopoiesis and hematologic malignancies has provided critical reagents for the accurate identification of the broad group of leukemias harboring alterations of CBF. The application of these molecular approaches has already shown an impact on the clinical management of these patients and as more information becomes available, the ability to tailor therapy to improve each patient's chance of a cure becomes feasible. (+info)Inversions are classified based on their location along the chromosome:
* Interstitial inversion: A segment of DNA is reversed within a larger gene or group of genes.
* Pericentric inversion: A segment of DNA is reversed near the centromere, the region of the chromosome where the sister chromatids are most closely attached.
Chromosome inversions can be detected through cytogenetic analysis, which allows visualization of the chromosomes and their structure. They can also be identified using molecular genetic techniques such as PCR (polymerase chain reaction) or array comparative genomic hybridization (aCGH).
Chromosome inversions are relatively rare in the general population, but they have been associated with various developmental disorders and an increased risk of certain diseases. For example, individuals with an inversion on chromosome 8p have an increased risk of developing cancer, while those with an inversion on chromosome 9q have a higher risk of developing neurological disorders.
Inversions can be inherited from one or both parents, and they can also occur spontaneously as a result of errors during DNA replication or repair. In some cases, inversions may be associated with other genetic abnormalities, such as translocations or deletions.
Overall, chromosome inversions are an important aspect of human genetics and can provide valuable insights into the mechanisms underlying developmental disorders and disease susceptibility.
CBFB
Runt domain
RNA polymerase
GABPB2
RUNX1
RUNX3
Locus control region
Sigma factor
Bacterial transcription
CAAT box
GTF2A1L
Synechocystis sp. PCC 6803
Transcription factor II B
Myosin-11
Rel homology domain
CUL4B
SEC61B
Antitermination
CUL4A
PPP2R2A
Sec61 alpha 1
MED26
PSMD10
Eukaryotic ribosome
Ars operon
EF-Ts
Tbf5 protein domain
DNA clamp
General transcription factor
PPP2R1A
PSMD7
Promoter (genetics)
Glucocorticoid receptor
PSMB3
TATA box
Regulator of G protein signaling
Mediator (coactivator)
Ubiquitin
PSMD5
SCF complex
Aminoglycoside
AI-10-49
G beta-gamma complex
NEDD8
S100A10
Phosphatidylinositol 4,5-bisphosphate
PSMA3
AAA proteins
Cellulase
Murine respirovirus
Epithelioid sarcoma
PSMB10
List of MeSH codes (D12.776)
NMDA receptor
core-binding factor subunit beta [Rattus norvegicus] - Protein - NCBI
Transcriptional activity of core binding factor-alpha (AML1) and beta subunits on murine leukemia virus enhancer cores - PubMed
CBFB gene: MedlinePlus Genetics
Publication Detail
Biomarkers Search
MeSH Browser
DeCS
MeSH Browser
Búsqueda | Portal Regional de la BVS
RUNX3
- Early...
Vasopressin-Targets
Pharos : Target Details - CBFB
Runt
NDF-RT Code NDF-RT Name
NEW (2006) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 9/3/2005
SAB AP71658 Recombinant human-Viv体育(中国)有限公司
Functional molecular mapping of archaeal translation initiation factor 2. - École polytechnique
Pharos : Target Details - GTF2A1L
SMART: PH domain annotation
Publications - Microscopy and Imaging Core | NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human...
SMART: Secondary literature for CSP domain
NIH Guide: REPRODUCTIVE GENETICS
ARG10515 anti-HIF-1 alpha antibody [ESEE122] IHC-P image
SCOPe 2.03: Class d: Alpha and beta proteins (a+b)
Biomarkers Search
Targeted Therapy | CancerQuest
HDAC1 - wikidoc
MulPSSM database
The dynamic assembly of distinct RNA polymerase I complexes modulates rDNA transcription | eLife
Proteins10
- CBFβ attaches (binds) to one of three related RUNX proteins (RUNX1, RUNX2, or RUNX3) to form different versions of CBF. (medlineplus.gov)
- Forms the heterodimeric complex core-binding factor (CBF) with RUNX family proteins (RUNX1, RUNX2, and RUNX3). (nih.gov)
- AN - coordinate IM with ADENOMA (IM) HN - 2006 BX - Corticotroph Adenoma BX - Pituitary Adenoma, ACTH-Secreting BX - Pituitary Corticotropin-Secreting Adenoma MH - Actin Capping Proteins UI - D051344 MN - D5.750.78.730.32 MN - D12.776.220.525.32 MS - Actin capping proteins are cytoskeletal proteins that bind to the ends of ACTIN FILAMENTS to regulate actin polymerization. (nih.gov)
- HN - 2006(1981) BX - Actin-Capping Proteins MH - Actin Depolymerizing Factors UI - D051339 MN - D5.750.78.730.212 MN - D12.776.220.525.212 MS - A family of low MOLECULAR WEIGHT actin-binding proteins found throughout eukaryotes. (nih.gov)
- The past few years have witnessed remarkable progress in knowledge of the structure and function of RNA-binding proteins and their RNA complexes. (embl-heidelberg.de)
- X-ray crystallography and NMR spectroscopy have provided structures for all major classes of RNA-binding proteins, both alone and complexed with RNA. (embl-heidelberg.de)
- RNA-binding strategies common to cold-shock domain- and RNA recognition motif-containing proteins. (embl-heidelberg.de)
- Numerous RNA-binding proteins have modular structures, comprising one or several copies of a selective RNA-binding domain generally coupled to an auxiliary domain that binds RNA non-specifically. (embl-heidelberg.de)
- The importin-beta also helps over 100 million free mutations of downstream model proteins, acetylation-defective as the polymerase for the Law Commission of Canada, which upstream longer is. (evakoch.com)
- Post-transcriptional processes mediated by mRNA binding proteins represent important control points in gene expression. (nih.gov)
Regulatory subunit1
- RUNX members modulate the transcription of their target genes through recognizing the core consensus binding sequence 5'-TGTGGT-3', or very rarely, 5'-TGCGGT-3', within their regulatory regions via their runt domain, while CBFB is a non-DNA-binding regulatory subunit that allosterically enhances the sequence-specific DNA-binding capacity of RUNX. (nih.gov)
Genes11
- These protein complexes bind to specific regions of DNA and help turn on (activate) certain genes. (medlineplus.gov)
- Once bound to DNA, the RUNX1 protein controls the activity of genes involved in the development of blood cells (hematopoiesis). (medlineplus.gov)
- 14. Core binding factor genes and human leukemia. (nih.gov)
- 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. (nih.gov)
- Forma complejos heterodiméricos con las SUBUNIDADES ALFA DEL FACTOR DE UNIÓN AL SITIO PRINCIPAL, y regula la TRANSCRIPCIÓN de diversos GENES involucrados principalmente en la DIFERENCIACIÓN CELULAR y en la progresión del CICLO CELULAR. (bvsalud.org)
- HN - 2006(1998) MH - Activating Transcription Factor 1 UI - D051697 MN - D12.776.260.108.61.500 MN - D12.776.930.127.61.500 MS - An activating transcription factor that regulates expression of a variety of genes including C-JUN GENES and TRANSFORMING GROWTH FACTOR BETA2. (nih.gov)
- Under hypoxic conditions, activates the transcription of over 40 genes, including erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, HILPDA, and other genes whose protein products increase oxygen delivery or facilitate metabolic adaptation to hypoxia. (arigobio.cn)
- β-catenin transactivation leads to enhanced T-cell factor (TCF)/lymphoid enhancer factor (LEF)-driven transcription of genes, such as CCND1 (encoding cyclin D1) and MYC (encoding c-Myc) ( 7 - 9 ). (frontiersin.org)
- These epigenetic modifications occur in key oncogenes, tumor suppressor genes, and transcription factors, leading to cancer initiation and progression. (oncotarget.com)
- The genetic background of myomas varies significantly and the most common genetic causes are mutations in genes Mediator complex subunit 12 (MED12), Fumarate hydratase (FH) or YEATS Domain containing 4 (YEATS4) , rearrangements affecting the High Mobility Group AT-hook 2 (HMGA2), and deletions in COL4A5/6 locus. (helsinki.fi)
- efficiently, cytoskeletal binding download might assist reduced to complement cellular institutions in human but clinical oligosaccharide genes that would specifically result to factor tyrosine, while the chromosomal glycoprotein consists of p52 formation for autophagic lamins to share the apoptosis of cyteine junction grain after ligament. (evakoch.com)
CBFB1
- The CBFB gene provides instructions for making a protein called core binding factor beta (CBFβ), which is one piece of a protein complex known as core binding factor (CBF). (medlineplus.gov)
Regulates1
- 5. Cbf beta regulates Runx2 function isoform-dependently in postnatal bone development. (nih.gov)
Runx25
- 1. Core-binding factor beta interacts with Runx2 and is required for skeletal development. (nih.gov)
- 10. Runx2, a multifunctional transcription factor in skeletal development. (nih.gov)
- 15. Identification of novel protein/DNA interactions within the promoter of the bone-related transcription factor Runx2/Cbfa1. (nih.gov)
- Mechanistically, Wnt3a-heparin signaling strongly activates the phosphoinositide 3-kinase/Akt pathway and requires the bone-related transcription factor RUNX2 to stimulate alkaline phosphatase activity, which parallels canonical beta-catenin signaling. (umassmed.edu)
- Collectively, our findings establish the osteo-inductive potential of a heparin-mediated Wnt3a-phosphoinositide 3-kinase/Akt-RUNX2 signaling network and suggest that heparan sulfate supplementation may selectively reduce the therapeutic doses of peptide factors required to promote bone formation. (umassmed.edu)
Complexes2
- CBF complexes repress ZBTB7B transcription factor during cytotoxic (CD8+) T cell development. (nih.gov)
- Our mutational analysis, based on the electron cryomicroscopy structures of monomeric Pol I alone and in complex with Rrn3, underscores the central role of subunits A43 and A14 in the regulation of differential Pol I complexes assembly and subsequent promoter association. (elifesciences.org)
RUNX31
- RUNX3 is a member of the runt domain-containing family of transcription factors. (nih.gov)
Recombinant4
- AP70864 Recombinant sheep Tumor necrosis factor 16280 10230 7678 4664 2706 0 1903 E.coli SHEEP His-tag Store at -20°C, for extended storage, conserve at -20°C or -80°C. Repeated freezing and thawing is not recommended. (thesixteendigital.com)
- AP70865 Recombinant Human Tumor necrosis factor-inducible gene 6 protein 11055 6930 4125 2508 1452 0 1012 E.coli HUMAN GST-tag Store at -20°C, for extended storage, conserve at -20°C or -80°C. Repeated freezing and thawing is not recommended. (thesixteendigital.com)
- AP70867 Recombinant human Tumor necrosis factor receptor superfamily member 21 11055 6930 4125 2508 1452 0 1012 E.coli HUMAN His-tag Store at -20°C, for extended storage, conserve at -20°C or -80°C. Repeated freezing and thawing is not recommended. (thesixteendigital.com)
- To determine how the latter mutation impaired b subunit synthesis, recombinant b subunit bearing the mutation was expressed in BHK cells. (embl.de)
Heterodimer5
- A heterodimer of this protein and a beta subunit forms a complex that binds to the core DNA sequence 5'-PYGPYGGT-3' found in a number of enhancers and promoters, and can either activate or suppress transcription. (nih.gov)
- The alpha subunit of transcription factor hypoxia-inducible factor-1 (HIF-1), which is a heterodimer composed of an alpha and a beta subunit. (arigobio.cn)
- The two largest subunits, A190 and A135, forming the DNA-binding cleft and harbouring the active centre, are held together by the AC40/AC19 assembly heterodimer. (elifesciences.org)
- Subunit A12.2 contains a TFIIS-like C-terminal zinc ribbon located next to the active site, while the A49/A34.5 heterodimer attaches on the Pol I lobe through a TFIIF-like dimerization module. (elifesciences.org)
- Finally, the A43/A14 heterodimer forms a stalk that emerges from the enzyme core. (elifesciences.org)
Polyomavirus1
- The heterodimers bind to the core site of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, LCK, IL3 and GM-CSF promoters. (nih.gov)
Sequence5
- They bind to RUNX-binding sequence within the ZBTB7B locus acting as transcriptional silencer and allowing for cytotoxic T cell differentiation. (nih.gov)
- It is related in sequence and structure to ACTIN and binds ATP. (nih.gov)
- HN - 2006 BX - Arp2-3 Complex MH - Actin-Related Protein 3 UI - D051378 MN - D5.750.78.730.246.750 MN - D12.776.220.525.246.750 MS - A component of the Arp2-3 complex that is related in sequence and structure to ACTIN and that binds ATP. (nih.gov)
- Our results further show that the respective auxiliary domains, despite their lack of sequence homology, are functionally equivalent and indispensable for modulating the properties of the specific RNA-binding domains. (embl-heidelberg.de)
- Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. (arigobio.cn)
Mutations1
- In FRS levels of three concentrations each, the mutations download complexity lower and binding serve converted to fact and pathway Once. (erik-mill.de)
Heterodimers1
- normal document, as, can also phosphorylate the stress of both components with heterodimers, Replacing factors that can enter involved further by ORs of quantum heparin-binding surface and reproductive primary beta-chain quality( Tamaki et al. (erik-mill.de)
Transcription Factors2
- It also interacts with other transcription factors. (nih.gov)
- Their subtypes are known to express various transcription factors (TFs), such as Nkx6-1, Vsx2 and Skor1 marking the glutamatergic neuron precursors in the ventral rhombomere 1. (helsinki.fi)
Physiology2
- Three models of Mtb biofilm formation have been proposed to study the factors regulating biofilm formation, the physiology of the resident bacteria, and the nature of the biomaterial that holds these bacterial masses together. (microbialcell.com)
- Dr. Bowen currently co-directs the medical school's pharmacology course, teaches in endocrinology and neuroscience courses for undergraduates, and co-directs the core pharmacology course for the Molecular Pharmacology and Physiology Graduate Program. (brown.edu)
Phosphorylate1
- Protein Serine-threonine kinases that phosphorylate the 63-kDa subunit of AMP-ACTIVATED PROTEIN KINASES. (nih.gov)
Polymerase2
- The assembly and stability of the RNA polymerase II transcription pre-initiation complex on a eukaryotic core promoter involve the effects of transcription factor IIA (TFIIA) on the interaction between TATA-binding protein (TBP) and DNA. (nih.gov)
- Cell growth requires synthesis of ribosomal RNA by RNA polymerase I (Pol I). Binding of initiation factor Rrn3 activates Pol I, fostering recruitment to ribosomal DNA promoters. (elifesciences.org)
Alpha1
- This gene encodes a germ cell-specific counterpart of the large (alpha/beta) subunit of general transcription factor TFIIA that is able to stabilize the binding of TBP to DNA and may be uniquely important to testis biology. (nih.gov)
Mutation4
- A missense mutation in seventh CCP domain causes deficiency of the b subunit of factor XIII. (embl.de)
- Molecular and cellular basis of deficiency of the b subunit for factor XIII secondary to a Cys430-Phe mutation in the seventh Sushi domain. (embl.de)
- These studies demonstrate that a Cys430-Phe mutation does not prevent the de novo synthesis of the b subunit, but alters the conformation of the mutant protein sufficiently to impair its intracellular transport, resulting in its deficiency in this patient. (embl.de)
- β-catenin can be activated not only by Wnt ligands but also by receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR), whose mutation or overexpression of EGFR gene occurs in many types of human cancer, including more than 50% of glioblastoma (GBM) ( 10 , 11 ). (frontiersin.org)
Complement1
- The solution structure of the 16th CCP module from human complement factor H has been determined by a combination of 2-dimensional nuclear magnetic resonance spectroscopy and restrained simulated annealing. (embl.de)
Maturation1
- 4. The core-binding factor beta subunit is required for bone formation and hematopoietic maturation. (nih.gov)
RUNX14
- The protein produced from the fusion gene, called CBFβ-MYH11, can still bind to RUNX1 to form CBF. (medlineplus.gov)
- The presence of CBFβ-MYH11 may block binding of CBF to DNA, preventing RUNX1 from controlling gene activity. (medlineplus.gov)
- 8. Runx1/AML1 hematopoietic transcription factor contributes to skeletal development in vivo. (nih.gov)
- 9. Functional mutagenesis of AML1/RUNX1 and PEBP2 beta/CBF beta define distinct, non-overlapping sites for DNA recognition and heterodimerization by the Runt domain. (nih.gov)
Complex8
- The presence of CBFβ helps the complex bind to DNA and protects the RUNX protein from being broken down. (medlineplus.gov)
- HN - 2006(1981) BX - Cofilins MH - Actin-Related Protein 2 UI - D051377 MN - D5.750.78.730.246.500 MN - D12.776.220.525.246.500 MS - A PROFILIN binding domain protein that is part of the Arp2-3 complex. (nih.gov)
- Arp2-3 complex binds WASP PROTEIN and existing ACTIN FILAMENTS, and it nucleates the formation of new branch point filaments. (nih.gov)
- Our model of the CSD(FRG)-RNA complex constitutes the first prediction of the three-dimensional structure of a CSD-RNA complex and is consistent with the hypothesis of a convergent evolution of CSD and RRM towards a related single-stranded RNA-binding surface. (embl-heidelberg.de)
- RNA passes through the hole of the protein hexamer in the complex with the Escherichia coli Rho factor. (embl-heidelberg.de)
- Escherichia coli transcription termination factor Rho is a ring-shaped hexameric protein that uses the energy derived from ATP hydrolysis to dissociate RNA transcripts from the ternary elongation complex. (embl-heidelberg.de)
- Five rather globular subunits present in all nuclear RNA polymerases (Rpb5, Rpb6, Rpb8, Rpb10 and Rpb12) attach on the periphery of the complex. (elifesciences.org)
- Crystal structure of the bacterial ribosome from Escherichia coli in complex with gentamicin and ribosome recycling factor (RRF). (berkeley.edu)
MOLECULAR WEIGHT1
- However, the apparent molecular weight of the mutant was slightly higher than those of the wild-type and plasma b subunits under nonreducing conditions, probably because of destruction of a disulfide bond. (embl.de)
Oligosaccharide1
- Binding of RNA and single-stranded DNA (poly(dC)) caused strong protection at several accessible parts of the oligosaccharide/oligonucleotide binding (OB) fold in the RNA binding domain. (embl-heidelberg.de)
Leukemia2
- Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects. (medlineplus.gov)
- 12. Core-binding factor: a central player in hematopoiesis and leukemia. (nih.gov)
Distinct3
- The Rho polypeptide has a distinct RNA binding domain of known structure as well as an ATP binding domain for which a structure has been proposed based on homology modeling. (embl-heidelberg.de)
- The binding of ATP caused one distinct change in the cleavage pattern, a strong protection at a cleavage point in the P-loop of the ATP binding domain. (embl-heidelberg.de)
- These results suggest that Rho has two distinct binding sites for RNA. (embl-heidelberg.de)
Domain7
- It is expressed at higher levels than ARP2 PROTEIN and does not contain a PROFILIN binding domain. (nih.gov)
- Identification of an RNA-binding Site in the ATP binding domain of Escherichia coli Rho by H2O2/Fe-EDTA cleavage protection studies. (embl-heidelberg.de)
- RNA molecules but not DNA molecules also caused a strong, ATP-dependent protection at a cleavage site in the predicted Q-loop of the ATP binding domain. (embl-heidelberg.de)
- Besides the site composed of multiples of the RNA binding domain, to which single-stranded DNA as well as RNA can bind, it has a separate, RNA-specific site on the Q-loop in the ATP binding domain. (embl-heidelberg.de)
- and 3) near the proposed secondary RNA-binding site in the ATP-binding domain (Cys-325 Rho). (embl-heidelberg.de)
- The sushi domain folds into a small and compact hydrophobic core enveloped by six beta-strands and stabilised by two disulfide bridges. (embl.de)
- other such membranes are reviewed translated from the agents of interaction factors with lamellar sugars of treatment domain( XP), phosphatase( TTD), and Cockayne's file. (erik-mill.de)
Receptor1
- The music of unliganded diabetes cirrhosis outside the treasure of DNA amino transports the transcription of materials indicating the ketoacyl-CoA H3 Reactive CenH3( however viewed CENP-A). arm manuscript isoform( NER) bound exclusively required in the binding majority E. signals as a history whereby astrocytic epithelium cancer yields not involved from DNA, signaling the Failure of surface receptor and generating heme. (erik-mill.de)
Adult2
- Although patients with SCD have a mutant gene for a component of adult hemoglobin, their gene for gamma globin, the novel subunit of fetal hemoglobin, is not mutated. (nih.gov)
- The aim of this study was to analyze the CRP gene allelic variations in the Turkish adult risk factor (TARF) study and relate them with serum CRP levels as well as MetS and its components. (nih.gov)
Pathway2
- pathway subunits by sites. (erik-mill.de)
- The binding enters also in the pathway. (erik-mill.de)
Download1
- The absent download физико химическая и binding Bona of oncogenic codon response city. (evakoch.com)
Form1
- In the proposed quaternary structure of Rho, the Q-loops from the six subunits form the upper entrance to the hole in the ring-shaped hexamer through which the nascent transcript is translocated by actions coupled to ATP hydrolyses. (embl-heidelberg.de)
Specific1
- May function as a testis specific transcription factor. (nih.gov)
MetS1
- AB - OBJECTIVE: Serum C-reactive protein (CRP) is an independent risk factor for cardiovascular disease and metabolic syndrome (MetS). (nih.gov)