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RUNX1T1 encodes a member of the myeloid translocation gene family which interact with DNA-bound transcription factors and recruit a range of corepressors to facilitate transcriptional repression. 再加上，我们可以发RUNX1T1 蛋白 (6) 和 RUNX1T1 试剂盒 (4)和数多这个蛋白质的别的产品。
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Human Polyclonal RUNX1T1 Primary Antibody for ELISA, WB - ABIN560189
Abdelhaleem: RNA helicases: regulators of differentiation. in Clinical biochemistry 2005
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Data indicate miR (显示 MLXIP 抗体)-29b-1 as a regulator of the AML1 (显示 RUNX1 抗体)-ETO protein (RUNX1 (显示 RUNX1 抗体)-RUNX1T1), and that miR (显示 MLXIP 抗体)-29b-1 expression in t(8;21)-carrying leukemic cell lines partially rescues the leukemic phenotype.
Altogether, these results revealed an unexpected and important epigenetic mini-circuit of AML1 (显示 RUNX1 抗体)-ETO/THAP10 (显示 THAP10 抗体)/miR (显示 MLXIP 抗体)-383 in t(8;21) acute myeloid leukaemia, in which epigenetic suppression of THAP10 (显示 THAP10 抗体) predicts a poor clinical outcome and represents a novel therapeutic target.
RUNX1 (显示 RUNX1 抗体)-RUNX1T1 transcript levels were measured in bone marrow samples collected from 208 patients at scheduled time points after transplantation. Over 90% of the 175 patients who were in continuous complete remission had a >/=3-log reduction in RUNX1 (显示 RUNX1 抗体)-RUNX1T1 transcript levels from the time of diagnosis at each time point after transplantation and a >/=4-log reduction at >/=12 months.
The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 (显示 TFF1 抗体) are mechanistically connected to CEBPB (显示 CEBPB 抗体) and that cross-regulation between CEBPB (显示 CEBPB 抗体)-RUNX1t1-TFF1 (显示 TFF1 抗体) plays an important role in gastric carcinogenesis.
RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells
Leukaemogenesis by AML1 (显示 RUNX1 抗体)-ETO requires enhanced C/D box snoRNA/RNP (显示 RNPC3 抗体) formation.
Study demonstrated that TRiC's contribution to the activity of the DNA-binding domain (AML1 (显示 RUNX1 抗体)-175) of AML1 (显示 RUNX1 抗体)-ETO is consistent with its contribution to the activity of full-length AML1 (显示 RUNX1 抗体)-ETO and is mediated through its direct association with the DNA-binding domain
the AML1 (显示 RUNX1 抗体)-ETO fusion protein increases the expression of SIRT1 (显示 SIRT1 抗体), possibly by binding to the promoter region of SIRT1 (显示 SIRT1 抗体) to activate its transcription in t(8;21) AML (显示 RUNX1 抗体).
A feedback circuitry involving miR (显示 MLXIP 抗体)-9-1 and RUNX1 (显示 RUNX1 抗体)-RUNX1T1.
The role of RUNX1T1 in t(8;21) acute myeloid leukemia (显示 BCL11A 抗体) and miRNA expression regulation
Results suggest that AML1 (显示 RUNX1 抗体)/ETO expression determines a more mobile and less adherent phenotype in preleukemic cells, therefore altering the interaction with the hematopoietic niche, potentially leading to the migration across the bone marrow barrier and to disease progression
Data show that RUNX1 (显示 RUNX1 抗体)-ETO;c-Kit (显示 KIT 抗体)(T417IDelta418-419) coexpression promoted exclusively acute myeloid leukemia (显示 BCL11A 抗体) (AML (显示 RUNX1 抗体)) in a fraction (51%) of reconstituted mice.
Self-renewal induced by AML1 (显示 RUNX1 抗体)/ETO in primary murine progenitors was inhibited when Aes (显示 AES 抗体) was decreased or absent.
AML1 (显示 RUNX1 抗体)-ETO synergizes with an ICSBP (显示 IRF8 抗体) deficiency to induce myeloblastic transformation in the bone marrow, reminiscent of acute myelogenous leukemia
molecular role for ETO in normal physiology as an inhibitor of C/EBPbeta (显示 CEBPB 抗体) and a novel regulator of early adipogenesis
the loss of the molecular events of AML1 (显示 RUNX1 抗体)-ETO C-terminal NCoR (显示 NCOR1 抗体)/SMRT-interacting domain transforms AML1 (显示 RUNX1 抗体)-ETO into a potent leukemogenic protein
p15(Ink4b (显示 CDKN2B 抗体)) loss must be accompanied by additional oncogenic changes for RUNX1 (显示 RUNX1 抗体)-ETO-associated AML (显示 RUNX1 抗体) to develop
This gene encodes a member of the myeloid translocation gene family which interact with DNA-bound transcription factors and recruit a range of corepressors to facilitate transcriptional repression. The t(8\;21)(q22\;q22) translocation is one of the most frequent karyotypic abnormalities in acute myeloid leukemia. The translocation produces a chimeric gene made up of the 5'-region of the runt-related transcription factor 1 gene fused to the 3'-region of this gene. The chimeric protein is thought to associate with the nuclear corepressor/histone deacetylase complex to block hematopoietic differentiation. Alternative splicing results in multiple transcript variants.
, expressed during postmitotic spinal neurons, most likely in motorneurons
, acute myelogenous leukemia 1 translocation 1, cyclin-D related
, core-binding factor, runt domain, alpha subunit 2; translocated to, 1; cyclin D-related
, eight twenty one protein
, myeloid translocation gene on 8q22
, zinc finger MYND domain-containing protein 2
, CBFA2T1 identified gene homolog
, acute myelogenous leukemia 1 translocation 1 protein
, core-binding factor, runt domain, alpha subunit 2
, cyclin D-related
, translocated to, 1