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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. Additionally we are shipping RUNX1T1 Antibodies (40) and RUNX1T1 Proteins (6) and many more products for this protein.
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Altogether, these results revealed an unexpected and important epigenetic mini-circuit of AML1-ETO/THAP10/miR-383 in t(8;21) acute myeloid leukaemia, in which epigenetic suppression of THAP10 predicts a poor clinical outcome and represents a novel therapeutic target.
RUNX1 (show RUNX1 ELISA Kits)-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 (show RUNX1 ELISA Kits)-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 (show TFF1 ELISA Kits) are mechanistically connected to CEBPB (show CEBPB ELISA Kits) and that cross-regulation between CEBPB (show CEBPB ELISA Kits)-RUNX1t1-TFF1 (show TFF1 ELISA Kits) 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 (show RUNX1 ELISA Kits)-ETO requires enhanced C/D box snoRNA/RNP (show RNPC3 ELISA Kits) formation.
Study demonstrated that TRiC's contribution to the activity of the DNA-binding domain (AML1 (show RUNX1 ELISA Kits)-175) of AML1 (show RUNX1 ELISA Kits)-ETO is consistent with its contribution to the activity of full-length AML1 (show RUNX1 ELISA Kits)-ETO and is mediated through its direct association with the DNA-binding domain
the AML1 (show RUNX1 ELISA Kits)-ETO fusion protein increases the expression of SIRT1 (show SIRT1 ELISA Kits), possibly by binding to the promoter region of SIRT1 (show SIRT1 ELISA Kits) to activate its transcription in t(8;21) AML (show RUNX1 ELISA Kits).
A feedback circuitry involving miR (show MLXIP ELISA Kits)-9-1 and RUNX1 (show RUNX1 ELISA Kits)-RUNX1T1.
The role of RUNX1T1 in t(8;21) acute myeloid leukemia (show BCL11A ELISA Kits) and miRNA expression regulation
Our data revealed a novel role for RUNX1T1 as a tumor-suppressor gene in colorectal cancer through modulation of multiple cellular pathways affecting the cell cycle, DNA damage, DNA replication, estrogen signaling, and drug resistance
Data show that RUNX1 (show RUNX1 ELISA Kits)-ETO;c-Kit (show KIT ELISA Kits)(T417IDelta418-419) coexpression promoted exclusively acute myeloid leukemia (show BCL11A ELISA Kits) (AML (show RUNX1 ELISA Kits)) in a fraction (51%) of reconstituted mice.
Self-renewal induced by AML1 (show RUNX1 ELISA Kits)/ETO in primary murine progenitors was inhibited when Aes (show AES ELISA Kits) was decreased or absent.
AML1 (show RUNX1 ELISA Kits)-ETO synergizes with an ICSBP (show IRF8 ELISA Kits) 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 (show CEBPB ELISA Kits) and a novel regulator of early adipogenesis
the loss of the molecular events of AML1 (show RUNX1 ELISA Kits)-ETO C-terminal NCoR (show NCOR1 ELISA Kits)/SMRT-interacting domain transforms AML1 (show RUNX1 ELISA Kits)-ETO into a potent leukemogenic protein
p15(Ink4b (show CDKN2B ELISA Kits)) loss must be accompanied by additional oncogenic changes for RUNX1 (show RUNX1 ELISA Kits)-ETO-associated AML (show RUNX1 ELISA Kits) to develop
AML1 DNA-binding domain and the ETO NHR2-dimerization domain, but not the ETO NHR1 domain, are critical for the induction of acute myeloid leukemia by AML1-ETO9a
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