anti-Homeobox A9 (HOXA9) 抗体

Human Homeobox A9 (HOXA9) interaction partners

1. we show that HOXA9 and JAK3/STAT5 are bona fide cooperating factors in driving leukemia development and that the cooperation is situated at the transcriptional level where STAT5 and HOXA9 co-occupy similar genomic regions

2. These data indicate that NPMc+ leukemic cell survival requires upregulation of PBX3 and HOXA9.

3. High HOXA9 expression is associated with increased metabolic dysregulation and leukemogenesis.

4. Results identified HOXA9 as a potential target of miR873. 3'UTR of HOXA9 was recognized and targeted by miR873 in osteosarcoma (OS) cells. HOXA9 expression was upregulated in OS tissues, and inversely correlated with miR873 expression.

5. HOXA9, RASSF1A and SCGB3A1 promoter methylation significantly associated with testicular germ cell tumor stage.

6. this study shows HOXA9 methylation and blood vessel invasion in formalin-fixed paraffin-embedded tissues for prognostic stratification of stage I lung adenocarcinoma patients

7. that therapeutic targeting of HOXA9-dependent enhancer reorganization can be an effective therapeutic strategy in acute leukemia with HOXA9 overexpression

8. High HOXA9 expression is associated with hematogical malignancy.

9. Downregulation of HOXA9 in myeloid leukaemia cells led to increased differentiation capacity in vitro.

10. Based on the human, animal and cellular data, the transcription factor HOXA9 may promote the expression of pro-myopia genes and retinal pigment epithelial proliferation, which eventually contribute to myopia development.

11. HOXA9 inhibits HIF1A-mediated glycolysis through interacting with CRIP2 to repress cutaneous squamous cell carcinoma development.

12. MiR-182/HOXA9 was involved in the process of RUNX3-mediated GC tumor growth.

13. The present study demonstrated that miR-139-5p, functioning as a suppressor in the tumorigenesis process, suppressed oral squamous carcinoma cells mobility by targeting HOXA9 directly.

14. NHA9 (NUP98-HOXA9 fusion protein) deregulates the expression of key leukemic genes, including MEIS1-HOXA9-PBX3 complex, through the enhancer binding and the direct interaction of the fusion protein with HDAC and p300 transcriptional regulators

15. Results show that a combination of HOXA9 and HOXA10 promoter methylation markers is significantly associated with the prognosis of breast cancer patients a subtype-independent manner.

16. knockdown of HOXA9 abrogated NAC1induced drug resistance.

17. HOXA9 expression is upregulated in three-dimensional organotypic culture of claudin-low breast cancer cells.

18. HOXA9 transcriptionally regulated EPHB4 expression to modulate trophoblasts migration and invasion, which may suggest a contribution of HOXA9-EPHB4 in the poor placentation in the pathogenesis of preeclampsia.

19. Overexpression of HOXA4 and HOXA9 contributes to self-renewal and overpopulation of stem cells in colorectal cancers.

20. HOTTIP/WDR5/HOXA9/Wnt axis contributes to pancreatic tumor stem cell stemness.

Mouse (Murine) Homeobox A9 (HOXA9) interaction partners

1. DOT1L, LSD1, and HDAC Class I Inhibitors Reduce HOXA9 Expression in MLL-AF9 Rearranged Leukemia Cells, But Dysregulate the Expression of Many Histone-Modifying Enzymes

2. HOXA9 inhibits HIF1A-mediated glycolysis through interacting with CRIP2 to repress cutaneous squamous cell carcinoma development.

3. Beta-catenin regulates expression of downstream targets of a key transcriptional memory gene, Hoxa9 that is highly enriched in myeloid leukemia cancer stem cells and helps sustain leukemic self-renewal.

4. The analysis points to a critical role for Hoxa9 and PU.1 in distal regulation of c-myb expression in murine myeloid cells during iL-6-induced cell differentiation.

5. the Hoxa9- and Meis1-associated upregulation of Flt3 is a passive event with regard to leukemia development in mice and with limited relevance to the AML pathology.

6. the cohesin complex regulates PRC2 targeting to silence Hoxa7 and Hoxa9 and negatively regulate self-renewal. Our studies identify a novel epigenetic mechanism underlying leukemogenesis in AML patients with cohesin mutations.

7. data delineate an altered epigenetic stress response in activated satellite cells from aged mice, which limits satellite cell function and muscle regeneration by Hoxa9-dependent activation of developmental pathways

8. Pbx3 contributes to Hoxa9 leukemogenesis through stabilization of the Meis1 protein.

9. IGF-1 is a direct HOXA9 target important for hematopoietic transformation.

10. deficiency of tumor suppressor prep1 accelerates the onset of meis1- hoxa9 leukemogenesis

11. Hoxa9 collaborates with E2A-PBX1 in mouse B cell leukemia in association with Flt3 activation and decrease of B cell gene expression.

12. results suggest a previously unidentified role for C/EBPalpha in maintaining the proliferation required for Hoxa9/Meis1-mediated leukemogenesis

13. This is the first description of a molecular link between HoxA9 and the regulation of Bcl-2 family members in acute myeloid leukemia.

14. HOXA9 may, therefore, stimulate ovarian cancer progression by promoting an immunosuppressive microenvironment via paracrine effects on peritoneal macrophages.

15. there is an extremely early checkpoint in hematopoietic differentiation critical for B and T lymphopoiesis that can only be transversed through the cooperative action of Hoxa9 and Flt3 signaling.

16. High Hoxa9 transgene expression in the embryonic hematopoietic compartment was lethal. Mice with lower levels of Hoxa9 developed a precursor-T-cell lymphoblastic leukemia/lymphoma, accompanied by spontaneous Notch1 mutations.

17. These findings reveal distinct requirements for Hoxa9 or Hoxa9/Flt3 molecular circuits in regulation of B versus natural killer and dendritic cell development in bone marrow.

18. Collectively, our data suggest that PBX3 is a critical cofactor of HOXA9 in leukemogenesis.

19. Loss of Scmh1 caused derepression of Hoxb4 and Hoxa9, direct targets of Polycomb-group complex 1-mediated transcriptional silencing in hematopoietic cells.

20. Female nude mice inoculated i.p. with MOSEC cells that overexpressed Hoxa9 developed larger tumors and had significantly shorter survival times than controls.