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Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. Additionally we are shipping RUNX1 Kits (14) and RUNX1 Proteins (8) and many more products for this protein.
Showing 10 out of 279 products:
Human Polyclonal RUNX1 Primary Antibody for WB - ABIN2668716
Zaidi, Dowdy, van Wijnen, Lian, Raza, Stein, Croce, Stein: Altered Runx1 subnuclear targeting enhances myeloid cell proliferation and blocks differentiation by activating a miR-24/MKP-7/MAPK network. in Cancer research 2009
Show all 19 references for 2668716
Human Polyclonal RUNX1 Primary Antibody for FACS, IF - ABIN650732
Moosavi, Sanchez, Adeyinka: Marker chromosomes are a significant mechanism of high-level RUNX1 gene amplification in hematologic malignancies. in Cancer genetics and cytogenetics 2009
Show all 2 references for 650732
Human Polyclonal RUNX1 Primary Antibody for 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. in Blood 1993
Cow (Bovine) Polyclonal RUNX1 Primary Antibody for 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. in Leukemia 2008
Cow (Bovine) Polyclonal RUNX1 Primary Antibody for WB - ABIN2780380
Ghozi, Bernstein, Negreanu, Levanon, Groner: Expression of the human acute myeloid leukemia gene AML1 is regulated by two promoter regions. in Proceedings of the National Academy of Sciences of the United States of America 1996
Leukaemogenesis by AML1-ETO (show RUNX1T1 Antibodies) requires enhanced C/D box snoRNA/RNP (show RNPC3 Antibodies) formation.
In this study, we found upregulation of several hemostasis-related genes, including the thrombin (show F2 Antibodies)-activatable receptor PAR-1 (protease-activated receptor-1 (show F2R Antibodies)), in Runx1/Cbfb (show CBFB Antibodies)-deleted MLL (show MLL Antibodies)-AF9 (show MLLT3 Antibodies) cells. Similar to the effect of Runx1/Cbfb (show CBFB Antibodies) deletion, PAR-1 (show MARK2 Antibodies) overexpression induced CDKN1A/p21 (show CDKN1A Antibodies) expression and attenuated proliferation in MLL (show MLL Antibodies)-AF9 (show MLLT3 Antibodies) cells
Immunohistochemical staining for RUNX1 showed reactivity in angiogenic tufts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis.
The Runx1-persistent group is involved in transmitting mechanical and thermal information, whereas the Runx1-transient group transmits pruriceptive information. Such hierarchical control mechanisms may provide a developmental solution for the formation of sensory circuits that transmit distinct modalities.
RUNX1 was expressed in both mesenchymal and epithelial compartments of the developing and postnatal lung. Increased respiratory distress, inflammation, and proinflammatory cytokines were observed in the Runx1-deleted mice after pulmonary LPS (show TLR4 Antibodies) exposure. RUNX1 deletion was associated with the activation of NF-kappaB (show NFKB1 Antibodies) in respiratory epithelial cells. RUNX1 was required for the suppression of NF-kappaB (show NFKB1 Antibodies) signaling pathway.
both repressor and activator functions of Runx1 at multiple hematopoietic stages and lineages likely contribute to the tumor suppressor activity in MDS (show MECOM Antibodies) and AML.
Knock-down of PLC-gamma-1 (show PLCG1 Antibodies) 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 (show PLCG1 Antibodies)-transfected cells strongly inhibited foreign body giant cell formation.
this study shows that distinct, asynchronous and stage-specific transcription factors (TCF-1 (show HNF1A Antibodies), GATA-3 (show GATA3 Antibodies) and Runx1) activate Bcl11b (show BCL11B Antibodies) 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 (show TLR4 Antibodies)-induced IL-1beta (show IL1B Antibodies) and IL-6 (show IL6 Antibodies) production levels, but the TNF-alpha (show TNF Antibodies) levels were not affected. Overexpression of RUNX1 promoted IL-1beta (show IL1B Antibodies) and IL-6 (show IL6 Antibodies) production in response to LPS (show TLR4 Antibodies) stimulation.
LRG1 (show LRG1 Antibodies) plays a crucial role in the proliferation and apoptosis of colorectal cancer (CRC (show CALR Antibodies)) by regulating RUNX1 expression.
RUNX1 RNA and protein are upregulated in proliferative diabetic retinopathy and in response to high glucose in vitro. Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived fibrovascular membranes, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis.
RUNX1 overexpression induced partial DNA demethylation at SPI1 (show SPI1 Antibodies) proximal promoter.
mutations in the SRSF2 (show SRSF2 Antibodies)/ASXL1 (show ASXL1 Antibodies)/RUNX1 gene panel identified as significant prognostic markers in systemic mastocytosis
HHEX (show HHEX Antibodies) could replace RUNX1 in cooperating with FLT3 (show FLT3 Antibodies)-ITD to induce Acute myeloid leukemia (show BCL11A Antibodies) (AML).
RUNX1-mutated AML is associated with a complex mutation cluster and is correlated with distinct clinico-pathologic features and inferior prognosis.
It was found that the absence of mutations in the SRSF2 (show SRSF2 Antibodies), ASXL1 (show ASXL1 Antibodies), and/or RUNX1gene panel at baseline and a reduction of the KIT D816V allele burden more than 25% at month 6 are the most favorable predictors for improved survival in midostaurin-treated advanced systemic mastocytosis patients.
Our findings suggest ETV6 (show ETV6 Antibodies)-RUNX1 is associated with space-time clustering of childhood leukemia (CL) and are consistent with an infection interacting with that oncogene (show RAB1A Antibodies) in early life leading to clinical leukemia.
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 (show CTCF Antibodies) have distinct functions in the regulation of runx1 during zebrafish embryogenesis.
Morpholino knockdown of Myef2 (show MYEF2 Antibodies) 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 (show RAD21 Antibodies), or cohesin subunit Smc3 (show SMC3 Antibodies), fail to express runx3 (show RUNX3 Antibodies) 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 (show RUNX2 Antibodies) 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