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

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

1. 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.

2. Data indicate that EPHA3 (show EPHA3 Antibodies) is involved in regulating the multidrug resistance (MDR) of small cell lung cancer (SCLC) via PI3K (show PIK3CA Antibodies)/BMX/STAT3 (show STAT3 Antibodies) signaling and may be a therapeutic target in SCLC.

3. BMX directly inhibits a core component of the intrinsic apoptosis machinery opens opportunities to improve the efficacy of existing chemotherapy by potentiating BAK (show BAK1 Antibodies)-driven cell death in cancer cells.

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

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

6. BMX is an antiapoptotic downstream effector of PI3K (show PIK3CA Antibodies), independent of AKT (show AKT1 Antibodies).

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

8. Overexpression of ETK is associated with the malignancy and disease progression of renal cell carcinoma (show MOK Antibodies).

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

10. Etk/BMX may play a role in protection of NPC (show NPC1 Antibodies) cells from apoptosis.

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

1. results suggest that the endothelial Bmx tyrosine kinase (show TYRO3 Antibodies) could provide a target to attenuate the development of cardiac hypertrophy

2. Btk (show BTK Antibodies), Tec (show NR4A3 Antibodies), Bmx are required for TLR-dependent signaling in many types of myeloid cells while being tissue-specific.

3. Tyrosine kinase (show TYRO3 Antibodies) 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 (show VEGFA Antibodies)-dependent lymphangiogenic signaling.

7. by preventing binding of Etk/Bmx to PAR(1 (show MARK2 Antibodies)) -C-tail, hPar1 oncogenic properties are abrogated

8. activation of Etk largely co-localizes with TNFR2 (show TNFRSF1B Antibodies) 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.