anti-Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) (RUNX1T1) Antibodies

Zebrafish Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) (RUNX1T1) interaction partners

1. Results found that runx1(W84X/W84X) mutation led to the reduction and disordering of B cells, as well as the failure of V(D)J rearrangements in B cells but not T cells, resulting in antibody-inadequate-mediated immunodeficiency. By contrast, T cell development was not affected. Furthermore, an evolutionarily conserved function of runx1 was demonstrated in maturation and differentiation of B cells in adult zebrafish.

Human Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) (RUNX1T1) interaction partners

1. fusion transcript level after the first induction therapy in RUNX1-RUNX1T1-positive AML children is an independent factor influencing the long-term prognosis

2. found that the binding capacity of RUNX1-ETO9a, a truncated RUNX1-ETO isoform, to the c-KIT promoter was stronger than that of RUNX1-ETO, suggesting RUNX1-ETO9a as another valuable therapeutic target in t(8;21) AML

3. At levels of condFDR < 0.01 and conjFDR < 0.05; we identified 5 ADHD-associated loci, 3 of these being shared between ADHD and EA.

4. In an analysis of an independent validation cohort, KIAA0125 again showed a significant influence with respect to the impact of the RUNX1/RUNX1T1 fusion in mediation of acute myeloid leukemia.

5. Minimal residual disease (MRD) monitoring and mutational landscape in AML with RUNX1-RUNX1T1.

6. Study reports differential regulation of gene expression by RUNX1-RUNX1T1 oncoprotein and MAPK1 as determined by genome-wide expression analysis responsible for the phenotypic features of acute myeloid leukaemia with karyotypic discernible translocation (t)(8;21)(q22;q22).

7. identified most of these factors as RUNX1-RUNX1T1 targets, with Ras Homolog Family Member (RHOB) overexpression being the core of this network

8. lncRNA RUNX1-IT1 was down regulated both in colorectal cancer tissues and cell lines; besides, lncRNA RUNX1-IT1 could serve as a potential diagnostic biomarker and play a tumour-suppressive role owing to its good diagnostic efficacy and inhibition of colorectal cancer cell proliferation and migration

9. As most transcriptional repressor proteins do not comprise tetramerization domains, our results provide a possible explanation as to the reason that RUNX1 is recurrently found translocated to ETO family members

10. PKM2 as a novel target of RUNX1-ETO and is specifically downregulated in RUNX1-ETO positive AML patients, indicating that PKM2 level might have a diagnostic potential in RUNX1-ETO associated AML.

11. The specific association of ZBTB7A mutations with t(8;21) rearranged acute myeloid leukaemia points towards leukemogenic cooperativity between mutant ZBTB7A and the RUNX1/RUNX1T1 fusion protein has been reported.

12. Data indicate miR-29b-1 as a regulator of the AML1-ETO protein (RUNX1-RUNX1T1), and that miR-29b-1 expression in t(8;21)-carrying leukemic cell lines partially rescues the leukemic phenotype.

13. 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.

14. RUNX1-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-RUNX1T1 transcript levels from the time of diagnosis at each time point after transplantation and a >/=4-log reduction at >/=12 months.

15. The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 are mechanistically connected to CEBPB and that cross-regulation between CEBPB-RUNX1t1-TFF1 plays an important role in gastric carcinogenesis.

16. RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells

17. Leukaemogenesis by AML1-ETO requires enhanced C/D box snoRNA/RNP formation.

18. Study demonstrated that TRiC's contribution to the activity of the DNA-binding domain (AML1-175) of AML1-ETO is consistent with its contribution to the activity of full-length AML1-ETO and is mediated through its direct association with the DNA-binding domain

19. the AML1-ETO fusion protein increases the expression of SIRT1, possibly by binding to the promoter region of SIRT1 to activate its transcription in t(8;21) AML.

20. A feedback circuitry involving miR-9-1 and RUNX1-RUNX1T1.

Mouse (Murine) Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) (RUNX1T1) interaction partners

1. Results suggest that AML1/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

2. The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 are mechanistically connected to CEBPB and that cross-regulation between CEBPB-RUNX1t1-TFF1 plays an important role in gastric carcinogenesis.

3. RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells

4. Leukaemogenesis by AML1-ETO requires enhanced C/D box snoRNA/RNP formation.

5. Data show that RUNX1-ETO;c-Kit(T417IDelta418-419) coexpression promoted exclusively acute myeloid leukemia (AML) in a fraction (51%) of reconstituted mice.

6. Self-renewal induced by AML1/ETO in primary murine progenitors was inhibited when Aes was decreased or absent.

7. AML1-ETO synergizes with an ICSBP deficiency to induce myeloblastic transformation in the bone marrow, reminiscent of acute myelogenous leukemia

8. molecular role for ETO in normal physiology as an inhibitor of C/EBPbeta and a novel regulator of early adipogenesis

9. the loss of the molecular events of AML1-ETO C-terminal NCoR/SMRT-interacting domain transforms AML1-ETO into a potent leukemogenic protein

10. p15(Ink4b) loss must be accompanied by additional oncogenic changes for RUNX1-ETO-associated AML to develop

11. 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

12. the eTAFH-E protein interaction appears to contribute relatively little to the activity of AML1-ETO