Core Binding Factors
Core Binding Factor alpha Subunits
Core Binding Factor Alpha 1 Subunit
Core Binding Factor beta Subunit
Core Binding Factor Alpha 2 Subunit
Core Binding Factor Alpha 3 Subunit
Transcription Factor AP-2
Transcription Factors
Chromosomes, Human, Pair 16
DNA-Binding Proteins
Chromosome Inversion
Leukemia, Myeloid, Acute
Molecular Sequence Data
Oncogene Proteins, Fusion
Base Sequence
Chromosomes, Human, Pair 21
Protein Binding
Neoplasm Proteins
Binding Sites
Osteoblasts
Enhancer Elements, Genetic
Translocation, Genetic
Osteocalcin
Mutation
Transforming Growth Factor alpha
Promoter Regions, Genetic
Tumor Necrosis Factor-alpha
Proto-Oncogene Proteins
Amino Acid Sequence
Cell Differentiation
Transcription, Genetic
Leukemia, Myeloid
Pol1 Transcription Initiation Complex Proteins
Three distinct domains in TEL-AML1 are required for transcriptional repression of the IL-3 promoter. (1/859)
A cytogenetically cryptic (12;21) translocation is the most common molecular abnormality identified in childhood acute lymphoblastic leukemia (ALL), and it generates a chimeric TEL-AML1 protein. Fusion of the Helix-Loop-Helix (HLH) (also called the pointed) domain of TEL to AML1 has been suggested to convert AML1 from a transcriptional activator to a repressor. To define the structural features of this chimeric protein required for repression, we analysed the transcriptional activity of a series of TEL-AML1 mutants on the AML1-responsive interleukin-3 (IL-3) promoter, a potentially relevant gene target. Our results demonstrate that TEL-AML1 represses basal IL-3 promoter activity in lymphoid cells, and deletion mutant analysis identified three distinct domains of TEL-AML1 that are required for repression; the HLH (pointed) motif contained in the TEL portion of TEL-AML1, and both the runt homology domain (Rhd) and the 74 amino acids downstream of the Rhd that are present in the AML1 portion of the fusion protein. Although AML1B (and a shorter AML1 isoform, AML1A) have transcriptional activating activity on the IL-3 promoter, fusion of the AML1 gene to the TEL gene generates a repressor of IL-3 expression. Consistent with this activity, freshly isolated human ALL cells that contain TEL-AML1 do not express IL-3. (+info)Biallelic and heterozygous point mutations in the runt domain of the AML1/PEBP2alphaB gene associated with myeloblastic leukemias. (2/859)
The AML1 gene encoding the DNA-binding alpha-subunit in the Runt domain family of heterodimeric transcription factors has been noted for its frequent involvement in chromosomal translocations associated with leukemia. Using reverse transcriptase-polymerase chain reaction (RT-PCR) combined with nonisotopic RNase cleavage assay (NIRCA), we found point mutations of the AML1 gene in 8 of 160 leukemia patients: silent mutations, heterozygous missense mutations, and biallelic nonsense or frameshift mutations in 2, 4, and 2 cases, respectively. The mutations were all clustered within the Runt domain. Missense mutations identified in 3 patients showed neither DNA binding nor transactivation, although being active in heterodimerization. These defective missense mutants may be relevant to the predisposition or progression of leukemia. On the other hand, the biallelic nonsense mutants encoding truncated AML1 proteins lost almost all functions examined and may play a role in leukemogenesis leading to acute myeloblastic leukemia. (+info)Mutual activation of Ets-1 and AML1 DNA binding by direct interaction of their autoinhibitory domains. (3/859)
The transcription factors Ets-1 and AML1 (the alphaBl subunit of PEBP2/CBF) play critical roles in hematopoiesis and leukemogenesis, and cooperate in the transactivation of the T cell receptor (TCR) beta chain enhancer. The DNA binding capacity of both factors is blocked intramolecularly but can be activated by the removal of negative regulatory domains. These include the exon VII domain for Ets-1 and the negative regulatory domain for DNA binding (NRDB) for alphaB1. Here we report that the direct interaction between the two factors leads to a reciprocal stimulation of their DNA binding activity and activation of their transactivation function. Detailed mapping revealed two independent contact points involving the exon VII and NRDB regions as well as the two DNA binding domains. Using deletion variants and dominant interfering mutants, we demonstrate that the interaction between exon VII and NRDB is necessary and sufficient for cooperative DNA binding. The exon VII and NRDB motifs are highly conserved in evolution yet deleted in natural variants, suggesting that the mechanism described is of biological relevance. The mutual activation of DNA binding of Ets and AML1 through the intermolecular interaction of autoinhibitory domains may represent a novel principle for the regulation of transcription factor function. (+info)A novel ubiquitin-specific protease, UBP43, cloned from leukemia fusion protein AML1-ETO-expressing mice, functions in hematopoietic cell differentiation. (4/859)
Using PCR-coupled subtractive screening-representational difference analysis, we have cloned a novel gene from AML1-ETO knockin mice. This gene is highly expressed in the yolk sac and fetal liver of the knockin mice. Nucleotide sequence analysis indicates that its cDNA contains an 1,107-bp open reading frame encoding a 368-amino-acid polypeptide. Further protein sequence and protein translation analysis shows that it belongs to a family of ubiquitin-specific proteases (UBP), and its molecular mass is 43 kDa. Therefore, we have named this gene UBP43. Like other ubiquitin proteases, the UBP43 protein has deubiquitinating enzyme activity. Protein ubiquitination has been implicated in many important cellular events. In wild-type adult mice, UBP43 is highly expressed in the thymus and in peritoneal macrophages. Among nine different murine hematopoietic cell lines analyzed, UBP43 expression is detectable only in cell lines related to the monocytic lineage. Furthermore, its expression is regulated during cytokine-induced monocytic cell differentiation. We have investigated its function in the hematopoietic myeloid cell line M1. UBP43 was introduced into M1 cells by retroviral gene transfer, and several high-expressing UBP43 clones were obtained for further study. Morphologic and cell surface marker examination of UBP43/M1 cells reveals that overexpression of UBP43 blocks cytokine-induced terminal differentiation of monocytic cells. These data suggest that UBP43 plays an important role in hematopoiesis by modulating either the ubiquitin-dependent proteolytic pathway or the ubiquitination state of another regulatory factor(s) during myeloid cell differentiation. (+info)Regulation of c-fos gene transcription and myeloid cell differentiation by acute myeloid leukemia 1 and acute myeloid leukemia-MTG8, a chimeric leukemogenic derivative of acute myeloid leukemia 1. (5/859)
Both acute myeloid leukemia 1 and c-Fos are regulatory factors of hematopoietic cell differentiation. We identified that the c-fos promoter contains an acute myeloid leukemia 1 binding site at nucleotide positions -6-+14. c-fos promoter activity was induced by transient overexpression of acute myeloid leukemia 1 in Jurkat T-cells, but not by that of the short form of acute myeloid leukemia 1-MTG8, a chimeric acute myeloid leukemia 1 protein. In 32Dcl3 myeloid cells, stable overexpression of acute myeloid leukemia 1-MTG8 blocked the c-fos gene transcription and cell differentiation, but that of acute myeloid leukemia did not. These data suggest that acute myeloid leukemia 1 and acute myeloid leukemia 1-MTG8 reciprocally regulate the myeloid cell differentiation, possibly by the way of regulating c-fos gene transcription. (+info)Solution properties of the free and DNA-bound Runt domain of AML1. (6/859)
The Runt domain is responsible for specific DNA and protein-protein interactions in a family of transcription factors which includes human AML1. Structural data on the Runt domain has not yet become available, possibly due to solubility and stability problems with expressed protein fragments. Here we describe the optimization and characterization of a 140-residue fragment, containing the Runt domain of AML1, which is suitable for structural studies. The fragment of AML1 including amino acids 46-185 [AML1 Dm(46-185)] contains a double cysteine-->serine mutation which does not affect Runt domain structure or DNA-binding affinity. Purified AML1 Dm(46-185) is soluble and optimally stable in a buffer containing 200 mm MgSO4 and 20 mm sodium phosphate at pH 6.0. Nuclear magnetic resonance and circular dichroism spectroscopy indicate that the Runt domain contains beta-sheet, but little or no alpha-helical secondary structure elements. The 45 N-terminal residues of AML1 are unstructured and removal of the N-terminal enhances sequence-specific DNA binding. The NMR spectrum of AML1 Dm(46-185) displays a favorable chemical shift dispersion and resolved NOE connectivities are readily identified, suggesting that a structure determination of this Runt domain fragment is feasible. A titration of 15N-labelled AML1 Dm(46-185) with a 14-bp cognate DNA duplex results in changes in the 15N NMR heteronuclear single quantum coherence spectrum which indicate the formation of a specific complex and structural changes in the Runt domain upon DNA binding. (+info)Induction of apoptosis in myeloid leukaemic cells by ribozymes targeted against AML1/MTG8. (7/859)
The translocation (8;21)(q22;q22) is a karyotypic abnormality detected in acute myeloid leukaemia (AML) M2 and results in the formation of the chimeric fusion gene AML1/MTG8. We previously reported that two hammerhead ribozymes against AML1/MTG8 cleave this fusion transcript and also inhibit the proliferation of myeloid leukaemia cell line Kasumi-1 which possesses t(8;21)(q22;q22). In this study, we investigated the mechanisms of inhibition of proliferation in myeloid leukaemic cells with t(8;21)(q22;q22) by ribozymes. These ribozymes specifically inhibited the growth of Kasumi-1 cells, but did not affect the leukaemic cells without t(8;21)(q22;q22). We observed the morphological changes including chromatin condensation, fragmentation and the formation of apoptotic bodies in Kasumi-1 cells incubated with ribozymes for 7 days. In addition, DNA ladder formation was also detected after incubation with ribozymes which suggested the induction of apoptosis in Kasumi-1 cells by the AML1/MTG8 ribozymes. However, the ribozymes did not induce the expression of CD11b and CD14 antigens in Kasumi-1 cells. The above data suggest that these ribozymes therefore inhibit the growth of myeloid leukaemic cells with t(8;21)(q22;q22) by the induction of apoptosis, but not differentiation. We conclude therefore that the ribozymes targeted against AML1/MTG8 may have therapeutic potential for patients with AML carrying t(8;21)(q22;q22) while, in addition, the product of the chimeric gene is responsible for the pathogenesis of myeloid leukaemia. (+info)Expression of AML1-d, a short human AML1 isoform, in embryonic stem cells suppresses in vivo tumor growth and differentiation. (8/859)
The human AML1 gene encodes a heterodimeric transcription factor which plays an important role in mammalian hematopoiesis. Several alternatively spliced AML1 mRNA species were identified, some of which encode short protein products that lack the transactivation domain. When transfected into cells these short isoforms dominantly suppress transactivation mediated by the full length AML1 protein. However, their biological function remains obscure. To investigate the role of these short species in cell proliferation and differentiation we generated embryonic stem (ES) cells overexpressing one of the short isoforms, AML1-d, as well as cells expressing the full length isoforms AML1-b and AML2. The in vitro growth rate and differentiation of the transfected ES cells were unchanged. However, overexpression of AML1-d significantly affected the ES cells' ability to form teratocarcinomas in vivo in syngeneic mice, while a similar overexpression of AML1-b and AML2 had no effect on tumor formation. Histological analysis revealed that the AML1-d derived tumors were poorly differentiated and contained numerous apoptotic cells. These data highlight the pleiotropic effects of AML1 gene products and demonstrate for the first time an in vivo growth regulation function for the short isoform AML1-d. (+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.
AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.
There are several subtypes of AML, including:
1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.
The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:
* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures
AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:
1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.
Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:
1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.
It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.
https://www.medicinenet.com › Medical Dictionary › G
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Definition & Facts | Britannica
https://www.britannica.com › science › Genetic-tr...
Genetic translocation, also called chromosomal translocation, a type of chromosomal aberration in which a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material. Genetic translocations are often found in cancer cells and may play a role in the development and progression of cancer.
Translocation, Genetic | health Encyclopedia - UPMC
https://www.upmc.com › health-library › gene...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Genetics Home Reference - NIH
https://ghr.nlm.nih.gov › condition › ge...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
In conclusion, Genetic Translocation is an abnormality in the number or arrangement of chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome, resulting in a gain or loss of genetic material that can have significant effects on the individual.
Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:
1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.
The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.
CBFA2T3
CBFA2T2
RUNX2
RUNX1
TAF11
CBFB
Sigma factor
STAT4
TBP-associated factor
GTF2A1L
CAAT box
SEC61B
TAF15
Sec61 alpha 1
Histone fold
EGLN1
RNA polymerase
PSMD10
POLR2J
EIF-W2 protein domain
PSMC5
Promoter (genetics)
Cyclin D
TAF9
CUL4A
General transcription factor
Bacterial transcription
SMARCC2
PPP2R1A
Tbf5 protein domain
PSMD7
Glucocorticoid receptor
PSMB3
DDB1
Chromosome 16
Regulator of G protein signaling
Cadherin-catenin complex in learning and memory
H4K8ac
Anticancer gene
Ubiquitin
PSMD5
SNAP25
Endophenotype
PSMD14
G beta-gamma complex
Homeobox protein MSX-1
S100A10
Phosphatidylinositol 4,5-bisphosphate
PSMA3
AAA proteins
Francis Crick
Cellulase
Murine respirovirus
Iron
PSMB10
List of MeSH codes (D12.776)
PAK1
Transcriptional activity of core binding factor-alpha (AML1) and beta subunits on murine leukemia virus enhancer cores - PubMed
RUNX1T1 gene: MedlinePlus Genetics
Haematopoietic stem and progenitor cells from human pluripotent stem cells - PubMed
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Conservation and function of the transcriptional regulatory protein Runt - Fingerprint - Experts@Syracuse
Genatlas sheet
Allogeneic stem cell transplantation for AML patients with RUNX1 mutation in first complete remission: a study on behalf of the...
Hind Bouzid, Ph.D. | Harvard Catalyst Profiles | Harvard Catalyst
Transcription Co-Regulators
Notch signalling and haematopoietic stem cell formation during embryogenesis. - Oxford Cardiovascular Science
NEW (2006) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 9/3/2005
Functional molecular mapping of archaeal translation initiation factor 2. - École polytechnique
Nonredundant roles for Runx1 alternative promoters reflect their activity at discrete stages of developmental hematopoiesis. -...
Calcitriol and enamel matrix derivative differentially regulated cemento-induction and mineralization in human periodontal...
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Pharos : Target Details - PSMD2
SMART: Pfam domain Ribosomal L16
NDF-RT Code NDF-RT Name
Proteins15
- It performs this function by attaching (binding) to proteins that normally turn genes on and blocking their activity. (medlineplus.gov)
- Guo C, Hu Q, Yan C, Zhang J. Multivalent binding of the ETO corepressor to E proteins facilitates dual repression controls targeting chromatin and the basal transcription machinery. (medlineplus.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)
- HN - 2006(1998) MH - Actin-Related Protein 2-3 Complex UI - D051376 MN - D5.750.78.730.246 MN - D12.776.220.525.246 MS - A complex of seven proteins including ARP2 PROTEIN and ARP3 PROTEIN that plays an essential role in maintenance and assembly of the CYTOSKELETON. (nih.gov)
- The proteins are named in accordance with the subunit of the ribosome which they belong to - the small (S1 to S31) and the large (L1 to L44). (embl.de)
- Many ribosomal proteins, particularly those of the large subunit, are composed of a globular, surfaced-exposed domain with long finger-like projections that extend into the rRNA core to stabilise its structure. (embl.de)
- 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)
- SWIRM (Swi3p, Rsc8p, and Moira) domain is an alpha-helical domain of about 85 residues in chromosomal proteins. (hindawi.com)
- SWIRM domain-containing proteins make up large multisubunit complexes by interacting with other chromatin modification factors and may have an important function in plants. (hindawi.com)
- Generally, the SWIRM domain forms a helix-turn-helix motif commonly found in DNA-binding proteins. (hindawi.com)
- We'll be at how subunits neurotransmitter grassroots identify tissues that proteins are. (evakoch.com)
Enhancer factor1
- Core binding factor (CBF), also known as polyomavirus enhancer-binding protein 2 and SL3 enhancer factor 1, is a mammalian transcription factor that binds to an element termed the core within the enhancers of the murine leukemia virus family of retroviruses. (nih.gov)
Highly conserved3
- It contains a highly conserved DNA-binding domain known as the runt domain. (nih.gov)
- The general subunit of all three eukaryotic RNA polymerases, Rpb12, and subunit P of the archaeal enzyme show sequence similarities in their N-terminal zinc ribbon and some highly conserved residues in the C-terminus. (cipsm.de)
- Here, we show that the middle module of the Mediator core contains a submodule of unique structure and function that comprises the N-terminal part of subunit Med7 (Med7N) and the highly conserved subunit Med31 (Soh1). (cipsm.de)
Genes5
- One of the genes that encodes a CBF alpha subunit is AML1, also called Cbf alpha 2. (nih.gov)
- 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)
- Prediction of Core Cancer Genes Using Multitask Classification Framework. (nih.gov)
- Regardless, many genes with distinct functions are co-regulated by the two transcription factors. (nature.com)
AML12
Mammalian1
- 17. Cloning, mapping and expression of PEBP2 alpha C, a third gene encoding the mammalian Runt domain. (nih.gov)
Proteasome1
- The 26S proteasome is a multicatalytic proteinase complex with a highly ordered structure composed of 2 complexes, a 20S core and a 19S regulator. (nih.gov)
Cofactor2
- A transcription factor that dimerizes with the cofactor CORE BINDING FACTOR BETA SUBUNIT to form core binding factor. (nih.gov)
- Factor de transcripción que dimeriza con el cofactor SUBUNIDAD BETA DEL FACTOR DE UNIÓN AL SITIO PRINCIPAL para formar el factor de unión al sitio principal. (bvsalud.org)
Polyomavirus2
- 1. Cytoplasmic sequestration of the polyomavirus enhancer binding protein 2 (PEBP2)/core binding factor alpha (CBFalpha) subunit by the leukemia-related PEBP2/CBFbeta-SMMHC fusion protein inhibits PEBP2/CBF-mediated transactivation. (nih.gov)
- 5. Intrinsic transcriptional activation-inhibition domains of the polyomavirus enhancer binding protein 2/core binding factor alpha subunit revealed in the presence of the beta subunit. (nih.gov)
Catalytic1
- These changes in chromatin involve activities of many chromatin-modifying complexes, consisting of both catalytic and noncatalytic subunits [ 5 ]. (hindawi.com)
Transcription factors3
- RUNX3 is a member of the runt domain-containing family of transcription factors. (nih.gov)
- It also interacts with other transcription factors. (nih.gov)
- EOMES and T-BET are related T-box transcription factors that control natural killer (NK) cell development. (nature.com)
Ribosomal2
Regulator1
- The transcription factor Runx1 is a pivotal regulator of definitive hematopoiesis in mouse ontogeny. (ox.ac.uk)
Transcriptional5
- The core elements of the SL3 virus are important genetic determinants of the ability of this virus to induce T-cell lymphomas and the transcriptional activity of the viral long terminal repeat in T lymphocytes. (nih.gov)
- The longest form, CBF beta-187, increased the transcriptional stimulation by CBF alpha 2-451 twofold in HeLa cells, although it had no effect in P19 cells. (nih.gov)
- 2. The chimeric protein, PEBP2 beta/CBF beta-SMMHC, disorganizes cytoplasmic stress fibers and inhibits transcriptional activation. (nih.gov)
- Vertebrate Runx1 is transcribed from 2 promoters, the distal P1 and proximal P2, which provide a paradigm of the complex transcriptional and translational control of Runx1 function. (ox.ac.uk)
- Characterization of DNA binding, transcriptional activation, and regulated nuclear association of recombinant human NFATp. (colorado.edu)
Drosophila1
- 18. Molecular cloning and characterization of PEBP2 beta, the heterodimeric partner of a novel Drosophila runt-related DNA binding protein PEBP2 alpha. (nih.gov)
Hypoxia2
- 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)
- Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. (arigobio.cn)
Chromatin2
- The reversibly dynamic changes in chromatin structure modulate the access of regulatory factors to DNA [ 1 , 2 ]. (hindawi.com)
- By generating two gene-modified mice facilitating chromatin immunoprecipitation of endogenous EOMES and T-BET, we show a strong overlap in their DNA binding targets, as well as extensive epigenetic changes during NK cell differentiation. (nature.com)
Recombinant1
- Effect of single-point mutations on the stability and immunogenicity of a recombinant ricin chain subunit vaccine antigen. (nih.gov)
Receptors3
- ER-PM Junctions on GABAergic Interneurons Are Organized by Neuregulin 2/VAP Interactions and Regulated by NMDA Receptors. (nih.gov)
- However, they differ from ILC1s by their capacity to circulate in the blood, by their expression of multiple receptors of the Ly49 family, by their higher cytotoxic potential and by their expression of integrin subunits. (nature.com)
- These toxins bind to specific receptors of the intestinal epithelial cells and cause secretion of water and electrolytes into the intestinal lumen. (cdc.gov)
Intracellular1
- Binds to the intracellular domain of tumor necrosis factor type 1 receptor. (nih.gov)
Sequence6
- 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)
- 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)
- Based on the domain architectures and the amino acid sequence homology, the SWIRM domains can be classified into three main types: Swi3/MYSM1 (human MYb-like, Swirm, and Mpn domain-containing protein-1), LSD1 (Lysine-specific demethylase 1), and Ada2 (Adenosine deaminase isoenzymes 2) types [ 13 ]. (hindawi.com)
- Ubiquitin roles are expressed from larger diseases and anywhere bound by dimethylglycine of a polyA protein complex between differentiation and a precursor Activation of an cytosolic caring sequence( UBA1 or UBA6, Jin et al. (evakoch.com)
Runt1
- Acute myeloid leukemia with runt-related transcription factor 1 gene mutation (RUNX1+ AML) is associated with inferior response rates and outcome after conventional chemotherapy. (tau.ac.il)
Consists2
Regulate1
- The GTPase RbgA (YlqF) is essential for the assembly of the large subunit, and it is believed to regulate the incorporation of L16. (embl.de)
RUNX12
- The protein produced from the normal RUNX1 gene is part of a protein complex known as core binding factor (CBF). (medlineplus.gov)
- En las LEUCEMIAS humanas el Runx1 está mutado con frecuencia. (bvsalud.org)
Vaccine2
Acute2
- 11. Core binding factor beta-smooth muscle myosin heavy chain chimeric protein involved in acute myeloid leukemia forms unusual nuclear rod-like structures in transformed NIH 3T3 cells. (nih.gov)
- 13. Fusion between transcription factor CBF beta/PEBP2 beta and a myosin heavy chain in acute myeloid leukemia. (nih.gov)
Beta5
- 3. Overexpression of core-binding factor alpha (CBF alpha) reverses cellular transformation by the CBF beta-smooth muscle myosin heavy chain chimeric oncoprotein. (nih.gov)
- 4. The leukemic protein core binding factor beta (CBFbeta)-smooth-muscle myosin heavy chain sequesters CBFalpha2 into cytoskeletal filaments and aggregates. (nih.gov)
- 6. Core-binding factor beta (CBFbeta), but not CBFbeta-smooth muscle myosin heavy chain, rescues definitive hematopoiesis in CBFbeta-deficient embryonic stem cells. (nih.gov)
- 2 rings are composed of 7 alpha subunits and 2 rings are composed of 7 beta subunits. (nih.gov)
- This entry represents a structural domain with an alpha/beta-hammerhead fold, where the beta-hammerhead motif is similar to that in barrel-sandwich hybrids. (embl.de)
Domain11
- 8. The core binding factor (CBF) alpha interaction domain and the smooth muscle myosin heavy chain (SMMHC) segment of CBFbeta-SMMHC are both required to slow cell proliferation. (nih.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)
- It is expressed at higher levels than ARP2 PROTEIN and does not contain a PROFILIN binding domain. (nih.gov)
- The binding domain of TRAP1 and TRAP2 resides outside the death domain of TNFR1. (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)
- 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)
- 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)
- 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)
20222
- 33(2): 320-323, 2022 Feb 17. (bvsalud.org)
- AIM: To investigate the expression and correlation of C1q/tumor necrosis factor related protein 9(CTRP9)levels in the serum of patients with different stages of diabetic retinopathy(DR)and diabetic macular edema(DME).METHODS: A total of 135 patients with type 2 diabetes who were admitted to Gansu Provincial Hospital from April 2021 to April 2022 were selected as the experimental group. (bvsalud.org)
Complexes1
- A membrane-bound membrane repair includes encoded by degradation of its potential design reviewed by processing of the C-terminus to a Co-Activator activity of the E1 complexes UBA1 or UBA6 via a survival full-length muscle( Jin et al. (evakoch.com)
Prognostic1
- By bringing together research institutions with large populations of patients with BE, we will perform a multi-center study of FISH and hypermethylation markers as possible prognostic factors in BE. (nih.gov)
Hydrolysis3
- Large subunits that lack L16 are defective in peptidyl transferase activity, peptidyl-tRNA hydrolysis activity, association with the 30S subunit, binding of aminoacyl-tRNA and interaction with antibiotics. (embl.de)
- Transcription factor Rho is a ring-shaped, homohexameric protein that causes transcript termination through actions on nascent RNAs that are coupled to ATP hydrolysis. (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)
MRNA1
- The codons of the mRNA are exposed on the ribosome to allow tRNA binding. (embl.de)
Enzyme5
- 9/3/2005) TOTAL DESCRIPTORS = 935 MH - 1-Acylglycerol-3-Phosphate O-Acyltransferase UI - D051103 MN - D8.811.913.50.173 MS - An enzyme that catalyzes the acyl group transfer of ACYL COA to 1-acyl-sn-glycerol 3-phosphate to generate 1,2-diacyl-sn-glycerol 3-phosphate. (nih.gov)
- HN - 2006(1981) MH - 2-Aminoadipate Transaminase UI - D051307 MN - D8.811.913.477.700.120 MS - A PYRIDOXAL PHOSPHATE containing enzyme that catalyzes the transfer of amino group of L-2-aminoadipate onto 2-OXOGLUTARATE to generate 2-oxoadipate and L-GLUTAMATE. (nih.gov)
- HN - 2006(1983) MH - 2-Oxoisovalerate Dehydrogenase (Acylating) UI - D050645 MN - D8.811.682.657.350.825 MS - An NAD+ dependent enzyme that catalyzes the oxidation 3-methyl-2-oxobutanoate to 2-methylpropanoyl-CoA. (nih.gov)
- use AMINO ACIDS, BRANCHED-CHAIN 1979, & KETO ACIDS & VALERATES 1973-1979 MH - 3-Hydroxyanthranilate 3,4-Dioxygenase UI - D050561 MN - D8.811.682.690.416.328 MS - An enzyme that catalyzes the conversion of 3-hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde. (nih.gov)
- use ANTHRANILIC ACID 1974-1979 MH - 3-Isopropylmalate Dehydrogenase UI - D050539 MN - D8.811.682.47.500 MS - An NAD+ dependent enzyme that catalyzes the oxidation of 3-carboxy-2-hydroxy-4-methylpentanoate to 3-carboxy-4-methyl-2-oxopentanoate. (nih.gov)
Regulation1
- 16. Regulation mechanisms for the heterodimeric transcription factor, PEBP2/CBF. (nih.gov)
Structural2
- Such subunits are characterized by specific structural frames that mediate protein-protein and protein-DNA interactions. (hindawi.com)
- The structural changes in activated CNFs were investigated using the following characterization techniques: N(2) adsorption isotherms at 77K, XRD, temperature-programmed desorption of hydrogen, TEM, TPO and elemental composition. (nih.gov)
Phosphorylation1
- In a mature phosphorylation muscle, largely 500 methylation of subunit is involved to myoglobin alleles organic( Russell 2003). (evakoch.com)
Developmental1
- Indeed, even though all ILCs share a common progenitor, NK cells rapidly branch out from the main ILC developmental pathway 6 , and the factors that promote this route remain unclear. (nature.com)
Complex4
- 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)
- By dying so we will initiate coordinate site about the mitotic ligands complex, and the rafts bound and activated will offer a different glutamine-N-acyltransferase of information for that glycoprotein. (evakoch.com)
Maturation1
- Our data thus suggest that EOMES and T-BET may distinctly govern, via differential expression and co-factors recruitment, NK cell maturation by inserting partially overlapping epigenetic regulations. (nature.com)
Nuclear2
Receptor1
- Genome-Wide Binding and Transcriptome Analysis of Human Farnesoid X Receptor in Primary Human Hepatocytes. (nih.gov)
Glycoprotein1
- This glycoprotein is you left-right into how the alpha-ketoglutarate mouse number here is. (evakoch.com)
Mice1
- Gene Editing and Mouse Model Core Laboratory is either involved in generating mutant mice and/or helped in the study that warranted authorship or core acknowledgement in the published article. (nih.gov)
Molecular1
- Molecular pathogenesis of core binding factor leukemia: current knowledge and future prospects. (medlineplus.gov)