Use your antibodies-online credentials, if available.
Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. 再加上，我们可以发RUNX1 试剂盒 (14) 和 RUNX1 蛋白 (8)和数多这个蛋白质的别的产品。
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 (显示 RUNX1T1 抗体) requires enhanced C/D box snoRNA/RNP (显示 RNPC3 抗体) formation.
In this study, we found upregulation of several hemostasis-related genes, including the thrombin (显示 F2 抗体)-activatable receptor PAR-1 (protease-activated receptor-1 (显示 F2R 抗体)), in Runx1/Cbfb (显示 CBFB 抗体)-deleted MLL (显示 MLL 抗体)-AF9 (显示 MLLT3 抗体) cells. Similar to the effect of Runx1/Cbfb (显示 CBFB 抗体) deletion, PAR-1 (显示 MARK2 抗体) overexpression induced CDKN1A/p21 (显示 CDKN1A 抗体) expression and attenuated proliferation in MLL (显示 MLL 抗体)-AF9 (显示 MLLT3 抗体) 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 (显示 TLR4 抗体) exposure. RUNX1 deletion was associated with the activation of NF-kappaB (显示 NFKB1 抗体) in respiratory epithelial cells. RUNX1 was required for the suppression of NF-kappaB (显示 NFKB1 抗体) signaling pathway.
both repressor and activator functions of Runx1 at multiple hematopoietic stages and lineages likely contribute to the tumor suppressor activity in MDS (显示 MECOM 抗体) and AML.
Knock-down of PLC-gamma-1 (显示 PLCG1 抗体) 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 (显示 PLCG1 抗体)-transfected cells strongly inhibited foreign body giant cell formation.
this study shows that distinct, asynchronous and stage-specific transcription factors (TCF-1 (显示 HNF1A 抗体), GATA-3 (显示 GATA3 抗体) and Runx1) activate Bcl11b (显示 BCL11B 抗体) 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 (显示 TLR4 抗体)-induced IL-1beta (显示 IL1B 抗体) and IL-6 (显示 IL6 抗体) production levels, but the TNF-alpha (显示 TNF 抗体) levels were not affected. Overexpression of RUNX1 promoted IL-1beta (显示 IL1B 抗体) and IL-6 (显示 IL6 抗体) production in response to LPS (显示 TLR4 抗体) stimulation.
LRG1 (显示 LRG1 抗体) plays a crucial role in the proliferation and apoptosis of colorectal cancer (CRC (显示 CALR 抗体)) 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 (显示 SPI1 抗体) proximal promoter.
mutations in the SRSF2 (显示 SRSF2 抗体)/ASXL1 (显示 ASXL1 抗体)/RUNX1 gene panel identified as significant prognostic markers in systemic mastocytosis
HHEX (显示 HHEX 抗体) could replace RUNX1 in cooperating with FLT3 (显示 FLT3 抗体)-ITD to induce Acute myeloid leukemia (显示 BCL11A 抗体) (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 (显示 SRSF2 抗体), ASXL1 (显示 ASXL1 抗体), 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 (显示 ETV6 抗体)-RUNX1 is associated with space-time clustering of childhood leukemia (CL) and are consistent with an infection interacting with that oncogene (显示 RAB1A 抗体) 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 (显示 CTCF 抗体) have distinct functions in the regulation of runx1 during zebrafish embryogenesis.
Morpholino knockdown of Myef2 (显示 MYEF2 抗体) 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 (显示 RAD21 抗体), or cohesin subunit Smc3 (显示 SMC3 抗体), fail to express runx3 (显示 RUNX3 抗体) 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 (显示 RUNX2 抗体) 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