anti-BMX Non-Receptor Tyrosine Kinase (BMX) Antibodies

Human BMX Non-Receptor Tyrosine Kinase (BMX) interaction partners

1. results demonstrate that hypoxia-dependent upregulation of BMX contributes to therapeutic resistance through a compensatory prosurvival signaling mechanism. These results also reveal the role of off-target drug effects on tumor microenvironment and development of acquired drug resistance.

2. These results suggested that BMX can promote cell proliferation through PI3K/AKT/mTOR and STAT3 signaling pathways in cervical cancer cells.

3. The studies suggested that BMXDeltaN might play roles in lung tumorigenicity, with expression of BMXDeltaN promoting cell growth, cell migration, and cell transformation.

4. results demonstrate that cleaved BMX is a novel N-end rule substrate, and its degradation exhibits a novel interplay between substrate phosphorylation and N-end rule degradation, revealing an increasing complex regulatory network of apoptotic proteolytic signaling cascades.

5. Data indicate that EPHA3 is involved in regulating the multidrug resistance (MDR) of small cell lung cancer (SCLC) via PI3K/BMX/STAT3 signaling and may be a therapeutic target in SCLC.

6. BMX directly inhibits a core component of the intrinsic apoptosis machinery opens opportunities to improve the efficacy of existing chemotherapy by potentiating BAK-driven cell death in cancer cells.

7. Report BMX-ARHGAP gene fusion in gastric cardia adenocarcinoma.

8. These findings suggested that polymorphisms of the BMX gene could be a potential predictor of clinical symptoms following mTBI.

9. BMX is an antiapoptotic downstream effector of PI3K, independent of AKT.

10. The effects of dietary K(+) on Bmx were more pronounced

11. Overexpression of ETK is associated with the malignancy and disease progression of renal cell carcinoma.

12. This review characterizes the role of BMX in inflamamtion, cardiovascular disease and cancer.

13. Etk/BMX may play a role in protection of NPC cells from apoptosis.

14. study concludes that BMX is an essential component of inflammatory cytokine signaling and that catalytic, as well as noncatalytic functions of BMX are involved

15. Deregulation of ETK may attribute to the elevated activity of STAT3 and AKT frequently detected in bladder cancer.

16. BMX is associated with multi-drug resistance of K562/HHT cell line.

17. Constitutively active STAT3 rescued the effects of BMX downregulation, supporting that BMX signals through STAT3 in glioblastoma stem cells (GSCs).

18. possible role in regulation of vesicle trafficking

19. Investigate Bmx mediates VEGF-dependent lymphangiogenic signaling.

20. by preventing binding of Etk/Bmx to PAR(1) -C-tail, hPar1 oncogenic properties are abrogated

Mouse (Murine) BMX Non-Receptor Tyrosine Kinase (BMX) interaction partners

1. results suggest that the endothelial Bmx tyrosine kinase could provide a target to attenuate the development of cardiac hypertrophy

2. Btk, Tec, Bmx are required for TLR-dependent signaling in many types of myeloid cells while being tissue-specific.

3. Tyrosine kinase BMX phosphorylates phosphotyrosine-primed motif mediating the activation of multiple receptor tyrosine kinases.

4. Our findings therefore indicate that Bmx activity contributes to tumor angiogenesis and growth.

5. genetic ablation of BMX conferred protection in arthritis model confirming BMX an essential mediator of inflammation in vivo; conclude BMX an essential component of inflammatory cytokine signaling and catalytic as well noncatalytic functions are involved

6. Investigate Bmx mediates VEGF-dependent lymphangiogenic signaling.

7. by preventing binding of Etk/Bmx to PAR(1) -C-tail, hPar1 oncogenic properties are abrogated

8. activation of Etk largely co-localizes with TNFR2 in vascular endothelial cells and cardiomyocytes.

9. Bmx overexpression accelerates keratinocyte proliferation and wound reepithelialization. Bmx expression also induces chronic inflammation and angiogenesis in the skin.

10. Role of Bmx in ischemia-mediated arteriogenesis/angiogenesis: response to ischemia, reduced in knockout mice and enhanced in transgenic mice.

11. BMX knockout mice are resistant to cardiac hypertrophy induced by transverse aortic constriction compared to wild-type mice.