anti-Transient Receptor Potential Cation Channel, Subfamily M, Member 2 (TRPM2) Antibodies

Human Transient Receptor Potential Cation Channel, Subfamily M, Member 2 (TRPM2) interaction partners

1. Our study indicates that TRPM2 is a potential target for protecting melanocytes against oxidative damages in vitiligo.

2. Wild-type TRPM2 but not Ca(2+)-impermeable mutant E960D reconstituted phosphorylation and expression of Pyk2 and CREB in TRPM2-depleted cells exposed to doxorubicin. Results demonstrate that TRPM2 expression protects the viability of neuroblastoma through Src, Pyk2, CREB, and MCU activation, which play key roles in maintaining mitochondrial function and cellular bioenergetics

3. comparison of TRPM2 and TRPM7 ion channel gene expression and immunohistochemical staining in endometrial hyperplasia and endometrium adenocarcinoma

4. Study shows that combination therapy with selenium and dcetaxel may represent an effective strategy for the treatment of glioblastoma cells and may be associated with TRPM2-mediated increases in oxidative stress and [Ca2+]i.

5. We showed that the autophagy-TRPM2 association may take place in the molecular basis of PCa and accordingly this connection may be targeted as a new therapeutic approach in PCa.

6. Cell culture, animal models, and patient samples established that TRPM2 expression/function is important for dopaminergic neuronal survival and is increased in neurotoxin models that mimic Parkinson's Disease.

7. These findings explain the molecular mechanism of concerted TRPM2 gating by adenosine diphosphate (ADP)-ribose and Ca(2+) and provide insights into the gating mechanism of other TRP channels.

8. Data suggest that TRPM2 plays roles in viability of gastric cancer cell line and in survival of gastric cancer patients; TRPM2 appears to regulate autophagy, mitophagy (mitochondrial degradation), and apoptosis; TRPM2 modulates autophagy through a c-Jun N-terminal kinase (JNK)-dependent mechanism.

9. TRPM2 overexpression in a PDAC cell line (PANC1) promoted cell proliferation, invasion and metastatic ability. TRPM2 represents a potential therapeutic target and prognostic marker for patients with PDAC.

10. The expression of TRPM2-AS was higher in most HCC tissues and was significantly correlated with tumor size, AJCC stage, tumor differentiation, and the prognosis of HCC patients. Interfering TRPM2-AS expression using siRNA significantly inhibited cell proliferation and promoted cell apoptosis in two HCC cell lines.

11. Results reveal a novel, potentially druggable signalling pathway for FFA-induced beta-cell death. The cascade involves NOX-2-dependent production of ROS, activation of TRPM2 channels, rise in mitochondrial Zn(2+), Drp-1 recruitment and abnormal mitochondrial fission.

12. TRPM2 is essential for the survival and migration of squamous cell cancer cells.

13. Results provide compelling evidence to support a role for nitrosative stress in linking the TRPM2 turnover with the disturbance of autophagy in brain pericyte injury.

14. oxidative stress activates the TRPM2-Ca(2+)-CAMK2 cascade to phosphorylate BECN1 resulting in autophagy inhibition

15. We conclude from these studies that inhibition of ROS production, and the subsequent abrogation of TRPM2-mediated Ca(2+) influx, is the primary mechanism underlying RE-1's inhibitory effect on LNs-induced inflammasome activation.

16. oxidative stress activated the TRPM2-CaMKII cascade to further induce intracellular ROS production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential

17. The work summarized here shows that TRPM2 channels protect cardiac myocytes from ischaemia-reperfusion injury and tumour cells from doxorubicin toxicity, and demonstrates that the mechanisms involve preservation of mitochondrial bioenergetics and modulation of ROS

18. Activation of TRPM2 channels, however, caused intracellular release of not only Ca(2+) but also of Zn(2+) Intriguingly, elevation of intracellular Zn(2+) faithfully reproduced all of the effects of H2O2, whereas Ca(2+) showed opposite effects. Interestingly, H2O2 caused increased trafficking of Zn(2+)-enriched lysosomes to the leading edge of migrating cells, presumably to impart polarisation of Zn(2+) location.

19. neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site.

20. The inhibitory function of oxidant sensing by TRPM2 requires the oxidation of Cys549, which then induces TRMP2 binding to formyl peptide receptor 1 (FPR1) and subsequent FPR1 internalization and signaling inhibition

Zebrafish Transient Receptor Potential Cation Channel, Subfamily M, Member 2 (TRPM2) interaction partners

1. cryo-electron microscopy structures of the zebrafish TRPM2 in the apo resting (closed) state and in the ADP-ribose/Ca(2+)-bound active (open) state, in which the characteristic NUDT9-H domains hang underneath the MHR1/2 domain; results provide an insight into the mechanism of activation of the TRPM channel family and define a framework for the development of therapeutic agents to treat neurodegenerative diseases

Mouse (Murine) Transient Receptor Potential Cation Channel, Subfamily M, Member 2 (TRPM2) interaction partners

1. Study shows that TRPM2 Exacerbates Central Nervous System Inflammation in Experimental Autoimmune Encephalomyelitis by Increasing Production of CXCL2 Chemokines.

2. TRPM2-mediated Ca(2+) signaling is required for training-induced improvement in skeletal muscle mitochondrial function and fiber type transition.

3. Cognitive dysfunction and white matter injury following carotid artery stenosis were significantly improved in TRPM2 knock-out mice compared with WT.

4. Cells expressing reduced levels of TRPM2 were protected from neutrophil cytotoxicity and seeded more efficiently in the premetastatic lung. These data identify TRPM2 as the link between environmental cues at the primary tumor site, tumor cell susceptibility to neutrophil cytotoxicity, and disease progression.

5. The present study questions the role of TRPM2 in the catabolism of ADP ribose in the brain.

6. this study provides insight into the mechanism determining tumor cell susceptibility to neutrophil cytotoxicity. This mechanism depends on the expression of the H2O2-responsive Ca2+ channel TRPM2. TRPM2 expression is upregulated in cancerous tissues, making tumor cells more susceptible to neutrophil cytotoxicity.

7. TRPM2 silencing inhibits also lung cancer cells invasion ability and alters EMT processes and TRPM2 downregulation causes an increase in the intracellular levels of reactive oxygen (ROS) and nitrogen (RNS) species, which in turn causes DNA damage and JNK activation leading to G2/M arrest, and an ultimate cell death.

8. The trafficking of TRPM2 to the plasma membrane could potentially contribute to a positive feedback mechanism mediating Ca(2+) overload in hepatocytes under conditions of oxidative stress.

9. TRPM2 is a key agent in stress-induced depression and a possible target for treating depression.

10. Cell culture, animal models, and patient samples established that TRPM2 expression/function is important for dopaminergic neuronal survival and is increased in neurotoxin models that mimic Parkinson's Disease.

11. TRPM2 plays an important role in bacterial clearance in neutrophils, possibly by regulating elastase release

12. Tumor cell-expressed transient receptor potential channel, melastatin subfamily type 2 (TRPM2) regulates neutrophil chemoattraction via chemokine CXCL2 (CXCL2).

13. Results demonstrate a critical role for the TRPM2 channel in Abeta42-induced microglial activation and generation of TNF-alpha: PKC/NOX-mediated generation of ROS and activation of PARP-1 are required for Abeta42-induced TRPM2 channel activation and, furthermore, the PYK2/MEK/ERK signaling pathway as a positive feedback mechanism downstream of TRPM2 channel activation facilitates further activation of PARP-1 and TRPM2 ...

14. Results reveal a novel, potentially druggable signalling pathway for FFA-induced beta-cell death. The cascade involves NOX-2-dependent production of ROS, activation of TRPM2 channels, rise in mitochondrial Zn(2+), Drp-1 recruitment and abnormal mitochondrial fission.

15. High TRPM2 to trigger lysosomal membrane permeabilization and Zn(2+)-mediated mitochondrial fission.

16. Trpm2 might promote hyperinflammation in Down Syndrome.

17. Studied the role of transient receptor potential melastatin 2 (TRPM2) in activating caspase-1 and caspase-1-dependent pyroptosis in mouse BMDMs. Found TRPM2 knockout caused higher caspase-1 activation and pyrotopsis.

18. Transient receptor potential melastatin-2 (TRPM2) in pituitary nerve terminals plays a role in oxytocin release. Temperature- enhanced oxytocin release by CD38 and TRPM2. TRPM2 might be involved in the process of CD38-regulated oxytocin release.

19. this study shows that TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection

20. Overexpression of TRPM2 channel prevented neutrophil transendothelial migration and vascular injury.