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Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. De plus, nous expédions RUNX1 Kits (14) et RUNX1 Protéines (8) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 272 products:
Human Polyclonal RUNX1 Primary Antibody pour EIA, WB - ABIN500646
Lee, Jenner, Boyer, Guenther, Levine, Kumar, Chevalier, Johnstone, Cole, Isono, Koseki, Fuchikami, Abe, Murray, Zucker, Yuan, Bell, Herbolsheimer, Hannett, Sun, Odom, Otte, Volkert, Bartel, Melton, Gifford, Jaenisch, Young: Control of developmental regulators by Polycomb in human embryonic stem cells. dans Cell 2006
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Human Polyclonal RUNX1 Primary Antibody pour FACS, IF - ABIN650732
Moosavi, Sanchez, Adeyinka: Marker chromosomes are a significant mechanism of high-level RUNX1 gene amplification in hematologic malignancies. dans Cancer genetics and cytogenetics 2009
Show all 2 references for ABIN650732
Human Polyclonal RUNX1 Primary Antibody pour ELISA, WB - ABIN1532121
Nucifora, Birn, Espinosa, Erickson, LeBeau, Roulston, McKeithan, Drabkin, Rowley: Involvement of the AML1 gene in the t(3,21) in therapy-related leukemia and in chronic myeloid leukemia in blast crisis. dans Blood 1993
Cow (Bovine) Polyclonal RUNX1 Primary Antibody pour WB - ABIN2792628
Takeshita, Ichikawa, Nitta, Goyama, Asai, Ogawa, Chiba, Kurokawa: AML1-Evi-1 specifically transforms hematopoietic stem cells through fusion of the entire Evi-1 sequence to AML1. dans Leukemia 2008
Cow (Bovine) Polyclonal RUNX1 Primary Antibody pour WB - ABIN2780380
Ghozi, Bernstein, Negreanu, Levanon, Groner: Expression of the human acute myeloid leukemia gene AML1 is regulated by two promoter regions. dans Proceedings of the National Academy of Sciences of the United States of America 1996
Knock-down of PLC-gamma-1 (Montrer PLCG1 Anticorps) induced foreign body giant cell formation.PLC-gamma-1-deficiency caused a decrease in RUNX1 and subsequent PU.1 upregulation while subsequent rescue of RUNX1 in sh-PLC-gamma-1 (Montrer PLCG1 Anticorps)-transfected cells strongly inhibited foreign body giant cell formation.
this study shows that distinct, asynchronous and stage-specific transcription factors (TCF-1 (Montrer HNF1A Anticorps), GATA-3 (Montrer GATA3 Anticorps) and Runx1) activate Bcl11b (Montrer BCL11B Anticorps) for T cell commitment
Inhibition of Runx1 in multipotential myeloid precursor cells is important for osteoclast formation and function.
Silencing of Runx1 attenuated the LPS (Montrer TLR4 Anticorps)-induced IL-1beta (Montrer IL1B Anticorps) and IL-6 (Montrer IL6 Anticorps) production levels, but the TNF-alpha (Montrer TNF Anticorps) levels were not affected. Overexpression of RUNX1 promoted IL-1beta (Montrer IL1B Anticorps) and IL-6 (Montrer IL6 Anticorps) production in response to LPS (Montrer TLR4 Anticorps) stimulation.
the Acute Myeloid Leukemia-1a (AML-1a) transcription factor, a regulator of immune gene expression, was identified as potentially sensitive to nucleosomal regulation within the Ly49 gene family. This result was confirmed in RMA, a cell line with natural expression of Ly49, using MNase-Seq to generate a nucleosome map of chromosome 6, where the Ly49 gene family is located
Data show that immature Runx1-deficient CD4 (Montrer CD4 Anticorps)(+) T cells are eliminated in the periphery by the activation and fixation of the classical complement pathway.
Runx1 deficiency enhanced CGRP expression and disrupted BMP4-induced neurite outgrowth inhibition in DRG.
Runx1 could be manipulated after injury to promote neuronal differentiation to facilitate repair of the CNS.
Runx1 haploinsufficiency appears to predispose FPD patients to MM by expanding the pool of stem/progenitor cells and blocking myeloid differentiation in response to G-CSF (Montrer CSF3 Anticorps).
Runx1 has an important role in Nf1 (Montrer NF1 Anticorps) neurofibroma initiation
RUNX1-RUNX1T1 (Montrer RUNX1T1 Anticorps) fusion is associated with acute myeloid leukemia (Montrer BCL11A Anticorps).
Study demonstrated that TRiC's contribution to the activity of the DNA-binding domain (AML1-175) of AML1-ETO (Montrer RUNX1T1 Anticorps) is consistent with its contribution to the activity of full-length AML1-ETO (Montrer RUNX1T1 Anticorps) and is mediated through its direct association with the DNA-binding domain
results provide novel insight into RUNX1-mediated perturbations of higher-order genome organization that are functionally linked with RUNX1-dependent compromised gene expression in breast cancer cells
RUNX1 and AXIN1 (Montrer AXIN1 Anticorps) proteins are strongly correlated in ER(-) tumors as well.
he data suggest a central role for RUNX1 as master regulator of gene expression in the U87 glioblastoma multiforme cell line and mark RUNX1 as a potential target for novel future therapies for glioblastoma multiforme
Study highlights the importance of interactions among lncRNA HCP5, microRNA-139, and transcription factor RUNX1 in regulating the malignant behavior of glioma cells. HCP5 down-regulated miR-139 to up-regulate RUNX1. RUNX1 promoted AEG-1 expression, which was involved in a series of oncogenic effects in glioma cells. RUNX1 also up-regulated HCP5 expression, which formed a positive feedback loop.
Data suggest that RUNX1 functions in stem cells regulating cell differentiation; cancer cells appear to have corrupted this function of RUNX1 into promotion of oncogenesis. [REVIEW]
the AML1-ETO (Montrer RUNX1T1 Anticorps) fusion protein increases the expression of SIRT1 (Montrer SIRT1 Anticorps), possibly by binding to the promoter region of SIRT1 (Montrer SIRT1 Anticorps) to activate its transcription in t(8;21) AML.
the Notch (Montrer NOTCH1 Anticorps) pathway DNA-binding protein (Montrer UBE2V1 Anticorps) RBP-J (Montrer RBPJ Anticorps) is the key cellular factor hijacked by EBNA2 to direct activation of RUNX1 transcription via upstream super-enhancers.
revealed more than 170 NFAT (Montrer NFATC1 Anticorps)-associated proteins, half of which are involved in transcriptional regulation. Among them are many hitherto unknown interaction partners of NFATc1 (Montrer NFATC1 Anticorps) and NFATc2 (Montrer NFAT1 Anticorps) in T cells, such as Raptor (Montrer RPTOR Anticorps), CHEK1 (Montrer CHEK1 Anticorps), CREB1 (Montrer CREB1 Anticorps), RUNX1, SATB1 (Montrer SATB1 Anticorps), Ikaros (Montrer IKZF1 Anticorps), and Helios (Montrer ZNFN1A2 Anticorps).
Our data suggest that runx1 and cbfb are required at 2 different steps during early hematopoietic stem cell development
We propose that cohesin and CTCF (Montrer CTCF Anticorps) have distinct functions in the regulation of runx1 during zebrafish embryogenesis.
Morpholino knockdown of Myef2 (Montrer MYEF2 Anticorps) or Runx1 in zebrafish results in reduced numbers of hematopoietic stem cells, suggesting that these two factors also interact in vivo to regulate hematopoiesis.
Runx1 is induced by high Pu.1 level and in turn transrepresses pu.1 expression, thus constituting a negative feedback loop that fashions a favorable Pu.1 level required for balanced fate commitment to neutrophils versus macrophages.
hematopoietic stem cell numbers depended on activity of the transcription factor Runx1, on blood flow, and on proper development of the dorsal aorta
in zebrafish adult HSCs can be formed without an intact runx1.
Zebrafish embryos lacking Rad21 (Montrer RAD21 Anticorps), or cohesin subunit Smc3 (Montrer SMC3 Anticorps), fail to express runx3 (Montrer RUNX3 Anticorps) and lose hematopoietic runx1 expression in early embryonic development.
Xaml1/Runx1 is required for the specification of Rohon-Beard sensory neurons in Xenopus.
ETV6-RUNX1 (TEL-AML1) fusion and hyperdiploidy (>50 chromosomes) are favorable genetic features in childhood acute lymphoblastic leukemia (ALL).
reveal a shift in Runx2 (Montrer RUNX2 Anticorps) function protein during vertebrate evolution towards its exclusive roles in cartilage hypertrophy and bone differentiation within the amniote lineage
Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. The protein encoded by this gene represents the alpha subunit of CBF and is thought to be involved in the development of normal hematopoiesis. Chromosomal translocations involving this gene are well-documented and have been associated with several types of leukemia. Three transcript variants encoding different isoforms have been found for this gene.
runt-related transcription factor 1
, runt-related transcription factor 1 (acute myeloid leukemia 1; aml1 oncogene)
, runt-related transcription factor
, runt protein
, PEA2-alpha B
, PEBP2-alpha B
, SL3-3 enhancer factor 1 alpha B subunit
, SL3/AKV core-binding factor alpha B subunit
, acute myeloid leukemia 1 protein
, core binding factor alpha 2
, core-binding factor subunit alpha-2
, oncogene AML-1
, polyomavirus enhancer-binding protein 2 alpha B subunit
, runt domain, alpha subunit 2
, AML1-EVI-1 fusion protein
, core-binding factor, runt domain, alpha subunit 2
, runt-related transcription factor a
, Acute myeloid leukemia 1 protein
, Core-binding factor subunit alpha-2
, aml1 oncogene
, acute myeloid leukemia 1
, factor, runt domain, alpha subunit 2
, core-binding factor runt domain alpha subunit 2 (acute myeloid leukemia 1 oncogene)
, runt related transcription factor 1