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

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

1. 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.

2. 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.

3. 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.

4. 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.

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

6. 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.

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

8. 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.

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

10. 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

11. 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.

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

13. 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

14. findings demonstrate the important function of TRPM2 in modulation of cell survival through mitochondrial ROS, and the potential of targeted inhibition of TRPM2 as a therapeutic approach to reduce cellular bioenergetics, tumor growth, and enhance susceptibility to chemotherapeutic agents.

15. Study demonstrate that PRL is necessary for the survival of (retinal pigment epithelium) RPE under normal and advancing age conditions and, identified SIRT2 and TRPM2 as molecular targets for the antioxidant and antiapoptotic actions of PRL in the RPE.

16. TRPM2 has a role in the DNA damage response of T cell leukemia cells in a BCL-2 dependent manner

17. Data show that HEK293 cells expressing low levels of receptor potential melastatin 2 (TRPM2) channel were more susceptible to silica nanoparticles (NPs) than those expressing high levels of TRPM2.

18. This is expected to provide a basis for inhibiting TRPM2 for the improved treatment of breast cancer, which potentially includes treating breast tumors that are resistant to chemotherapy due to their evasion of apoptosis.

19. In a transgenic mouse model of Alzheimer's disease, TRPM2 was involved in neuronal toxicity and memory impairment.

20. These findings shed new light on the evolution of TRPM2 and establish nvTRPM2 as a promising tool to decipher its complex gating mechanisms.

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

1. 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 ...

2. 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.

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

4. Trpm2 might promote hyperinflammation in Down Syndrome.

5. 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.

6. 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.

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

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

9. These findings of this study suggest that TRPM2 channels play an essential role in mediating hypoxic-ischemic brain injury in neonatal mice.

10. TRPM2 regulates phagosomal acidification, and is essential for the bacterial killing function of macrophages.

11. Lysophosphatidylcholine induces intracellular Ca(2+) influx and increases phosphorylation of p38 MAPK via TRPM2, which in turn activates microglia.

12. The current study demonstrated that a physiological concentration of adrenaline attenuates insulin release via coupling of alpha2A-adrenoceptor to cAMP/TRPM2 signaling.

13. Trpm2 does not seem to play a major role in myeloid leukemogenesis. Additionally, loss of Trpm2 does not augment the cytotoxicity of standard AML chemotherapeutic agents.

14. TRPM2 channels contribute to visceral nociception in response to noxious stimuli under normal conditions and visceral hypersensitivity in pathological conditions.

15. this study demonstrates that the ion channel TRPM] is a temperature sensor in a subpopulation of hypothalamic neurons.

16. Data show that macrophages from young mice showed lower transient receptor potential melastatin 2 (TRPM2) expression than those from senescent mice and had lower viability after silica nanoparticles (NPs) exposure than those from senescent ones.

17. TRPM2 activation is likely to be mediated by ADP-ribose production via PARP pathway

18. mice in which TRPM2 had been genetically deleted showed a striking deficit in their sensation of non-noxious warm temperatures, consistent with the idea that TRPM2 initiates a 'warm' signal which drives cool-seeking behaviour

19. findings provide compelling evidence that F. tularensis catalase restricts reactive oxygen species to temper macrophage TRPM2-mediated Ca(2+) signaling and limit host immune function.

20. TRPM2 plays roles in a wide range of pathological pain models based on peripheral and central neuroinflammation, rather than physiological nociceptive pain.