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The protein encoded by TRPM2 is a calcium-permeable cation channel that is regulated by free intracellular ADP-ribose. Zusätzlich bieten wir Ihnen TRPM2 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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Mouse (Murine) Polyclonal TRPM2 Primary Antibody für 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 für 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 für 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 für 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 für 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
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 (zeige TRPC3 Antikörper) or TRPC7 protein induce enhanced receptor-activated Ca(2 (zeige CA2 Antikörper)+) influx that may lead to dysregulated cell growth in ADPKD
oxidative stress activated the TRPM2 (zeige CLU Antikörper)-CaMKII (zeige CAMK2G Antikörper) cascade to further induce intracellular ROS (zeige ROS1 Antikörper) production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential
The work summarized here shows that TRPM2 (zeige CLU Antikörper) 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 (zeige ROS1 Antikörper)
Activation of TRPM2 (zeige CLU Antikörper) channels, however, caused intracellular release of not only Ca(2 (zeige CA2 Antikörper)+) but also of Zn(2+) Intriguingly, elevation of intracellular Zn(2+) faithfully reproduced all of the effects of H2O2, whereas Ca(2 (zeige CA2 Antikörper)+) 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 (zeige CLU Antikörper) channel to arrest migration at their target site.
The inhibitory function of oxidant sensing by TRPM2 (zeige CLU Antikörper) requires the oxidation of Cys549, which then induces TRMP2 binding to formyl peptide receptor 1 (FPR1 (zeige FPR1 Antikörper)) and subsequent FPR1 (zeige FPR1 Antikörper) internalization and signaling inhibition
findings demonstrate the important function of TRPM2 (zeige CLU Antikörper) in modulation of cell survival through mitochondrial ROS (zeige ROS1 Antikörper), and the potential of targeted inhibition of TRPM2 (zeige CLU Antikörper) as a therapeutic approach to reduce cellular bioenergetics, tumor growth, and enhance susceptibility to chemotherapeutic agents.
Study demonstrate that PRL (zeige PRL Antikörper) is necessary for the survival of (retinal pigment epithelium) RPE (zeige RPE Antikörper) under normal and advancing age conditions and, identified SIRT2 (zeige SIRT2 Antikörper) and TRPM2 (zeige CLU Antikörper) as molecular targets for the antioxidant and antiapoptotic actions of PRL (zeige PRL Antikörper) in the RPE (zeige RPE Antikörper).
TRPM2 (zeige CLU Antikörper) has a role in the DNA damage response of T cell leukemia cells in a BCL-2 (zeige BCL2 Antikörper) dependent manner
Data show that HEK293 cells expressing low levels of receptor potential melastatin 2 (TRPM2) chan (zeige TRPM3 Antikörper)nel wer (zeige CLU Antikörper)e more susceptible to silica nanoparticles (NPs) than those expressing high levels of TRPM2.
This is expected to provide a basis for inhibiting TRPM2 (zeige CLU Antikörper) for the improved treatment of breast cancer, which potentially includes treating breast tumors that are resistant to chemotherapy due to their evasion of apoptosis.
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 (zeige CA2 Antikörper)+) influx and increases phosphorylation of p38 MAPK (zeige MAPK14 Antikörper) via TRPM2, which in turn activates microglia.
The current study demonstrated that a physiological concentration of adrenaline attenuates insulin (zeige INS Antikörper) 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 (zeige RUNX1 Antikörper) 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 (zeige TRPM3 Antikörper) (TRPM2) expression than those from senescent mice and had lower viability after silica nanoparticles (NPs (zeige NPS Antikörper)) exposure than those from senescent ones.
TRPM2 activation is likely to be mediated by ADP-ribose production via PARP (zeige PARP1 Antikörper) pathway
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