anti-Runt-Related Transcription Factor 1 (RUNX1) 抗体

Mouse (Murine) Runt-Related Transcription Factor 1 (RUNX1) interaction partners

1. The current study shows a crucial role for Runx1 in hematopoietic stem cells development in the aorta-gonad-mesonephros region prior to liver colonization, and emphasizes the value of in vitro models recapitulating developmental processes.

2. Embryos lacking the KH domain poly(C) binding protein, Pcbp2, are selectively deficient in the definitive erythroid lineage. Compared to wild-type controls, transcript splicing analysis of the Pcbp2(-/-) embryonic liver reveals accentuated exclusion of an exon (exon 6) that encodes a highly conserved transcriptional control segment of the hematopoietic master regulator, Runx1.

3. that RUNX1/ETO maintains leukemia by promoting cell cycle progression and identifies G1 CCND-CDK complexes as promising therapeutic targets for treatment of RUNX1/ETO-driven acute myeloid leukemia

4. RUNX1 is found only in the relatively rare wave 2 and 3 progenitors in the embryo.RUNX1 loss blocked the formation of wave 2 and 3 progenitors from this rare population of "hemogenic" endothelial cells (HE). RUNX1 was required for blood cell formation from HE. Review.

5. RUNX1 may be involved in the transition of the myometrium from a quiescent into a contractile state in preparation for labor.

6. Reducing Runx1 function drives increased contractility after myocardial infarction, thereby preserving LV systolic function and preventing adverse cardiac remodeling.

7. Runx/Cbfb complexes protect group 2 innate lymphoid cells from exhausted-like hyporesponsiveness during allergic airway inflammation.

8. Deletion of Runx1 in mouse T-ALL impairs cell growth. RUNX1 depletion consistently resulted in reduced cell proliferation and increased apoptosis.

9. Ezh2 and Runx1 mutations collaborate to initiate lympho-myeloid leukemia in early thymic progenitors

10. RUNX1 promoted TGF-beta-induced partial EMT by increasing transcription of the PI3K subunit p110delta, which mediated Akt activation.

11. The promoter regions of Runx1 is targets of STAT4 and that STAT4 binding during NK cell activation induces epigenetic modifications of Runx1 gene loci resulting in increased expression.

12. 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

13. Gene expression profiling of HEPs revealed a RUNX1c-induced proinflammatory molecular signature, supporting previous studies demonstrating proinflammatory signaling as a regulator of HSC emergence.

14. Histones showed limited activation in regions of single TF binding, while enhancers that bind NF-E2 and either RUNX1, FLI1 or both TFs gave the highest signals for TF occupancy and H3K4me2; these enhancers associated best with genes activated late in MK maturation.

15. the ability of Runx1 to induce endothelial-to-hematopoietic transition (EHT) in non-hemogenic endothelial cells depends on the anatomical location of the cell and the developmental age of the conceptus

16. CDK6 kinase activity negatively regulates the conversion of fat-storing cells into fat-burning cells by suppressing RUNX1, and may be a therapeutic target for the treatment of obesity and related metabolic diseases

17. RUNX1 dosage plays a pivotal role in hemogenic endothelium maturation and the establishment of the hematopoietic system.

18. These results suggest that RUNX1 may be an essential modulator in BMP9- induced osteogenic differentiation of mesenchymal stem cells.

19. Loss of Runx1 and Runx2 inhibits prostate cell motility.

20. In vivo, in vitro and systems biology results show that Runx1 exerts a pro-neurogenic function in neural precursor cells in vitro, while in vivo data remained inconclusive.

Human Runt-Related Transcription Factor 1 (RUNX1) interaction partners

1. expression of GFI1 is higher in RUNX1/ETO+ AML samples compared to other AML types and that absence of Gfi1 delays the growth of RUNX1/ETO9a+ cells both in vitro and in vivo.

2. All de novo and relapsed AMLs with CSF3R mutations were associated with genetic alterations in transcription factors, including RUNX1-RUNX1T1, CBFB-MYH11, double-mutated CCAAT/enhancer binding protein alpha (CEBPAdm), and NPM1 mutations; and core-binding factor gene abnormalities and CEBPAdm accounted for 90.5% (19 of 21 patients)

3. study demonstrated that der(1;7)(q10;p10) is associated with a high frequency of mutations in RUNX1 in myelodysplastic syndrome patients

4. Results find reduced RUNX1 expression to be associated with decreased survival probability in patients with breast cancer (BC). Its ectopic expression inhibits stemness properties of BC cell lines through repressing the expression of ZEB1 providing evidence that RUNX1 has antitumor activity in breast cancer cells.

5. Aberrant CD79a and/or PAX5 expression can be found in Acute Myelogenous Leukemia cases with RUNX1 mutations even without the translocation t(8; 21).

6. Our work demonstrates for the first time the predominant co-repressive function of SKI in acute myeloid leukemia cells on a genome-wide scale and uncovers the transcription factor RUNX1 as an important mediator of SKI-dependent transcriptional repression.

7. our present study strongly suggests that an autonomous RUNX1-p53-CBFB regulatory triangle plays a vital role in the maintenance and the acquisition of chemo-resistance of AML cells, and potentially provides novel therapeutic targets for anti-leukemia strategy.

8. RUNX1 regulates the oncogene KIT, by binding to its enhancer, and through interaction with FUBP1.

9. this study suggests that RUNX1 mutations might be a poor prognostic factor in the risk classification for pediatric acute myeloid leukemia.

10. that RUNX1/ETO maintains leukemia by promoting cell cycle progression and identifies G1 CCND-CDK complexes as promising therapeutic targets for treatment of RUNX1/ETO-driven acute myeloid leukemia

11. Study found that CBFB binds to and enhances the translation of RUNX1 mRNA, which encodes the binding partner of CBFB. CBFB binds and regulates the translation of hundreds of mRNAs through hnRNPK and facilitate translation initiation by eIF4B. Data propose that breast cancer cells evade translation and transcription surveillance simultaneously through downregulating CBFB.

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

13. Data show that miR-20a attenuated the killing effect of NK cells to cervical cancer cells by directly targeting runt-related transcription factor 1 (RUNX1).

14. Serum NEF is a sensitive diagnostic and prognostic marker for gastric carcinoma. NEF siRNA silencing promoted, and overexpression inhibited, gastric carcinoma proliferation. In addition, NEF overexpression promoted, and NEF siRNA silencing inhibited, Runx1 expression. Therefore, it was concluded that lncRNA NEF may participate in the regulation of cancer cell proliferation by regulating Runx1 expression

15. identified RNF38 as a novel E3 ligase that modifies RUNX1 function without inducing its degradation

16. These data indicate that RUNX1 regulates A4GALT and thereby the expression of clinically important glycosphingolipids implicated in blood group incompatibility and host-pathogen interactions.

17. The human RUNX1 gene was cloned as one of a pair of genes disrupted by the (8;21)(q22;q22) translocation in acute myeloid leukemia. The human RUNX1 protein binds the "core-binding" DNA motif. The inv(16)(p13.1;q22) mutation associated with AML created a chimeric protein that fused the non-DNA-binding CBFbeta subunit to the coiled-coil tail region of a smooth muscle myosin heavy chain. Review.

18. RUNX1 may be involved in the transition of the myometrium from a quiescent into a contractile state in preparation for labor.

19. ZFP36L2 could be transactivated by AML1, which subsequently induced cell-cycle arrest and apoptosis of leukemia cells

Zebrafish Runt-Related Transcription Factor 1 (RUNX1) interaction partners

1. Our data suggest that runx1 and cbfb are required at 2 different steps during early hematopoietic stem cell development

2. We propose that cohesin and CTCF have distinct functions in the regulation of runx1 during zebrafish embryogenesis.

3. Morpholino knockdown of Myef2 or Runx1 in zebrafish results in reduced numbers of hematopoietic stem cells, suggesting that these two factors also interact in vivo to regulate hematopoiesis.

4. 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.

5. hematopoietic stem cell numbers depended on activity of the transcription factor Runx1, on blood flow, and on proper development of the dorsal aorta

6. in zebrafish adult HSCs can be formed without an intact runx1.

7. isolation and characterization by spatiotemporal expression detected in the developing zebrafish

8. Zebrafish embryos lacking Rad21, or cohesin subunit Smc3, fail to express runx3 and lose hematopoietic runx1 expression in early embryonic development.

Xenopus laevis Runt-Related Transcription Factor 1 (RUNX1) interaction partners

1. Xaml1/Runx1 is required for the specification of Rohon-Beard sensory neurons in Xenopus.

2. ETV6-RUNX1 (TEL-AML1) fusion and hyperdiploidy (>50 chromosomes) are favorable genetic features in childhood acute lymphoblastic leukemia (ALL).

3. reveal a shift in Runx2 function protein during vertebrate evolution towards its exclusive roles in cartilage hypertrophy and bone differentiation within the amniote lineage