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The protein encoded by TRPM2 is a calcium-permeable cation channel that is regulated by free intracellular ADP-ribose. 再加上，我们可以发TRPM2 蛋白 (6)和数多这个蛋白质的别的产品。
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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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Polyclonal TRPM2 Primary Antibody for WB - ABIN540252
Zhang, Chu, Tong, Cheung, Conrad, Masker, Miller: A novel TRPM2 isoform inhibits calcium influx and susceptibility to cell death. in The Journal of biological chemistry 2003
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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
Results provide compelling evidence to support a role for nitrosative stress in linking the TRPM2 (显示 CLU 抗体) turnover with the disturbance of autophagy in brain pericyte injury.
oxidative stress activates the TRPM2 (显示 CLU 抗体)-Ca(2 (显示 CA2 抗体)+)-CAMK2 (显示 CAMK2B 抗体) cascade to phosphorylate BECN1 (显示 BECN1 抗体) resulting in autophagy inhibition
We conclude from these studies that inhibition of ROS (显示 ROS1 抗体) production, and the subsequent abrogation of TRPM2 (显示 CLU 抗体)-mediated Ca(2 (显示 CA2 抗体)+) influx, is the primary mechanism underlying RE-1's inhibitory effect on LNs-induced inflammasome activation.
oxidative stress activated the TRPM2 (显示 CLU 抗体)-CaMKII (显示 CAMK2G 抗体) cascade to further induce intracellular ROS (显示 ROS1 抗体) production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential
The work summarized here shows that TRPM2 (显示 CLU 抗体) 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 (显示 ROS1 抗体)
Activation of TRPM2 (显示 CLU 抗体) channels, however, caused intracellular release of not only Ca(2 (显示 CA2 抗体)+) but also of Zn(2+) Intriguingly, elevation of intracellular Zn(2+) faithfully reproduced all of the effects of H2O2, whereas Ca(2 (显示 CA2 抗体)+) 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 (显示 CLU 抗体) channel to arrest migration at their target site.
The inhibitory function of oxidant sensing by TRPM2 (显示 CLU 抗体) requires the oxidation of Cys549, which then induces TRMP2 binding to formyl peptide receptor 1 (FPR1 (显示 FPR1 抗体)) and subsequent FPR1 (显示 FPR1 抗体) internalization and signaling inhibition
findings demonstrate the important function of TRPM2 (显示 CLU 抗体) in modulation of cell survival through mitochondrial ROS (显示 ROS1 抗体), and the potential of targeted inhibition of TRPM2 (显示 CLU 抗体) as a therapeutic approach to reduce cellular bioenergetics, tumor growth, and enhance susceptibility to chemotherapeutic agents.
Study demonstrate that PRL (显示 PRL 抗体) is necessary for the survival of (retinal pigment epithelium) RPE (显示 RPE 抗体) under normal and advancing age conditions and, identified SIRT2 (显示 SIRT2 抗体) and TRPM2 (显示 CLU 抗体) as molecular targets for the antioxidant and antiapoptotic actions of PRL (显示 PRL 抗体) in the RPE (显示 RPE 抗体).
Studied the role of transient receptor potential melastatin 2 (显示 TRPM3 抗体) (TRPM2) in activating caspase-1 (显示 CASP1 抗体) and caspase-1 (显示 CASP1 抗体)-dependent pyroptosis in mouse BMDMs. Found TRPM2 knockout caused higher caspase-1 (显示 CASP1 抗体) activation and pyrotopsis.
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.
this study shows that TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection
Overexpression of TRPM2 channel prevented neutrophil transendothelial migration and vascular injury.
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 (显示 CA2 抗体)+) influx and increases phosphorylation of p38 MAPK (显示 MAPK14 抗体) via TRPM2, which in turn activates microglia.
The current study demonstrated that a physiological concentration of adrenaline attenuates insulin (显示 INS 抗体) 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 (显示 RUNX1 抗体) chemotherapeutic agents.
TRPM2 channels contribute to visceral nociception in response to noxious stimuli under normal conditions and visceral hypersensitivity in pathological conditions.
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 (显示 TRPC3 抗体) or TRPC7 protein induce enhanced receptor-activated Ca(2 (显示 CA2 抗体)+) influx that may lead to dysregulated cell growth in ADPKD
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.
, 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 potential melastatin family 2
, 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 protein 7
, transient receptor potential channel subfamily C member 7