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The protein encoded by TRPM2 is a calcium-permeable cation channel that is regulated by free intracellular ADP-ribose. Additionally we are shipping TRPM2 Proteins (6) and many more products for this protein.
Showing 10 out of 94 products:
Mouse (Murine) Polyclonal TRPM2 Primary Antibody for ICC, IHC (fro) - ABIN259658
Bai, Lipski: Differential expression of TRPM2 and TRPV4 channels and their potential role in oxidative stress-induced cell death in organotypic hippocampal culture. in Neurotoxicology 2010
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Human Polyclonal TRPM2 Primary Antibody for ICC, IHC (fro) - ABIN153042
Partida-Sanchez, Gasser, Fliegert, Siebrands, Dammermann, Shi, Mousseau, Sumoza-Toledo, Bhagat, Walseth, Guse, Lund: Chemotaxis of mouse bone marrow neutrophils and dendritic cells is controlled by adp-ribose, the major product generated by the CD38 enzyme reaction. in Journal of immunology (Baltimore, Md. : 1950) 2007
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Human Polyclonal TRPM2 Primary Antibody for ICC, IF - ABIN153041
Moreau, Kirchberger, Swarbrick, Bartlett, Fliegert, Yorgan, Bauche, Harneit, Guse, Potter: Structure-activity relationship of adenosine 5'-diphosphoribose at the transient receptor potential melastatin 2 (TRPM2) channel: rational design of antagonists. in Journal of medicinal chemistry 2013
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Mouse (Murine) Polyclonal TRPM2 Primary Antibody for ICC, IF - ABIN4362934
Rah, Kwak, Chung, Kim: ADP-ribose/TRPM2-mediated Ca2+ signaling is essential for cytolytic degranulation and antitumor activity of natural killer cells. in Scientific reports 2015
Cow (Bovine) Polyclonal TRPM2 Primary Antibody for IHC, WB - ABIN2781840
Hecquet, Ahmmed, Vogel, Malik: Role of TRPM2 channel in mediating H2O2-induced Ca2+ entry and endothelial hyperpermeability. in Circulation research 2008
Study determined the sequence of pig TRPC1 and TRPC3-7 channels and found pig TRPC cDNAs resemble their human homologs more than the others .
heteromeric cation channels comprised of the TRPP2 mutant and the TRPC3 (show TRPC3 Antibodies) or TRPC7 protein induce enhanced receptor-activated Ca(2 (show CA2 Antibodies)+) influx that may lead to dysregulated cell growth in ADPKD
oxidative stress activated the TRPM2 (show CLU Antibodies)-CaMKII (show CAMK2G Antibodies) cascade to further induce intracellular ROS (show ROS1 Antibodies) production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential
The work summarized here shows that TRPM2 (show CLU Antibodies) 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 (show ROS1 Antibodies)
Activation of TRPM2 (show CLU Antibodies) channels, however, caused intracellular release of not only Ca(2 (show CA2 Antibodies)+) but also of Zn(2+) Intriguingly, elevation of intracellular Zn(2+) faithfully reproduced all of the effects of H2O2, whereas Ca(2 (show CA2 Antibodies)+) 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.
neutrophils sense reactive oxygen species via the TRPM2 (show CLU Antibodies) channel to arrest migration at their target site.
The inhibitory function of oxidant sensing by TRPM2 (show CLU Antibodies) requires the oxidation of Cys549, which then induces TRMP2 binding to formyl peptide receptor 1 (FPR1 (show FPR1 Antibodies)) and subsequent FPR1 (show FPR1 Antibodies) internalization and signaling inhibition
findings demonstrate the important function of TRPM2 (show CLU Antibodies) in modulation of cell survival through mitochondrial ROS (show ROS1 Antibodies), and the potential of targeted inhibition of TRPM2 (show CLU Antibodies) as a therapeutic approach to reduce cellular bioenergetics, tumor growth, and enhance susceptibility to chemotherapeutic agents.
Study demonstrate that PRL (show PRL Antibodies) is necessary for the survival of (retinal pigment epithelium) RPE (show RPE Antibodies) under normal and advancing age conditions and, identified SIRT2 (show SIRT2 Antibodies) and TRPM2 (show CLU Antibodies) as molecular targets for the antioxidant and antiapoptotic actions of PRL (show PRL Antibodies) in the RPE (show RPE Antibodies).
TRPM2 (show CLU Antibodies) has a role in the DNA damage response of T cell leukemia cells in a BCL-2 (show BCL2 Antibodies) dependent manner
Data show that HEK293 cells expressing low levels of receptor potential melastatin 2 (TRPM2) chan (show TRPM3 Antibodies)nel wer (show CLU Antibodies)e more susceptible to silica nanoparticles (NPs) than those expressing high levels of TRPM2.
This is expected to provide a basis for inhibiting TRPM2 (show CLU Antibodies) for the improved treatment of breast cancer, which potentially includes treating breast tumors that are resistant to chemotherapy due to their evasion of apoptosis.
These findings of this study suggest that TRPM2 channels play an essential role in mediating hypoxic-ischemic brain injury in neonatal mice.
TRPM2 regulates phagosomal acidification, and is essential for the bacterial killing function of macrophages.
Lysophosphatidylcholine induces intracellular Ca(2 (show CA2 Antibodies)+) influx and increases phosphorylation of p38 MAPK (show MAPK14 Antibodies) via TRPM2, which in turn activates microglia.
The current study demonstrated that a physiological concentration of adrenaline attenuates insulin (show INS Antibodies) release via coupling of alpha2A-adrenoceptor to cAMP/TRPM2 signaling.
Trpm2 does not seem to play a major role in myeloid leukemogenesis. Additionally, loss of Trpm2 does not augment the cytotoxicity of standard AML (show RUNX1 Antibodies) chemotherapeutic agents.
TRPM2 channels contribute to visceral nociception in response to noxious stimuli under normal conditions and visceral hypersensitivity in pathological conditions.
Data show that macrophages from young mice showed lower transient receptor potential melastatin 2 (show TRPM3 Antibodies) (TRPM2) expression than those from senescent mice and had lower viability after silica nanoparticles (NPs (show NPS Antibodies)) exposure than those from senescent ones.
TRPM2 activation is likely to be mediated by ADP-ribose production via PARP (show PARP1 Antibodies) pathway
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
findings provide compelling evidence that F. tularensis catalase (show CAT Antibodies) restricts reactive oxygen species to temper macrophage TRPM2-mediated Ca(2 (show CA2 Antibodies)+) signaling and limit host immune function.
The protein encoded by this gene is a calcium-permeable cation channel that is regulated by free intracellular ADP-ribose. The encoded protein is activated by oxidative stress and confers susceptibility to cell death. Several alternatively spliced transcript variants of this gene have been described, but their full-length nature is not known.
transient receptor potential cation channel, subfamily M, member 2
, transient receptor potential cation channel, subfamily C, member 7
, transient receptor potential cation channel, subfamily C, member 7-like
, short transient receptor potential channel 7-like
, transient receptor potential cation channel subfamily M member 2-like
, transient receptor potential channel subfamily C member 7
, estrogen-responsive element-associated gene 1 protein
, long transient receptor potential channel 2
, transient receptor potential cation channel subfamily M member 2
, transient receptor potential channel 7
, transient receptor protein 7
, transient receptor potential melastatin family 2