Anti Trpm2 Antibodies, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction"
Article Title: The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction
Journal: Nature communications
Figure Legend Snippet: Aβ 1–40 activates sustained TRPM2 currents in brain endothelial cells for the specificity of the immunostain) ( a ). Aβ 1–40 (Aβ) and the channel activator ADPR induce inward currents with the conductance characteristics of TRPM2 currents ( b ). The currents are blocked by the TRPM2 inhibitor 2-APB or 2-ACA, or TRPM2 knockdown ( b–d ). Aβ-induced TRPM2 currents are antagonized by the ROS scavenger MnTBAP, the NADPH oxidase peptide inhibitor gp91ds-tat, the NOS inhibitor L-NNA, the PARP inhibitor PJ34 and the PARG inhibitor ADP-HPD. ADPR-induced TRPM2 currents are unaffected by these antagonists. Data are presented as mean ± s.e.m. * P
Figure Legend Snippet: Aβ 1–40 -induced neurovascular dysfunction is not observed in TRPM2-null mice Neocortical superfusion of Aβ 1–40 (Aβ) does not attenuate resting CBF ( a ), or the increase in CBF induced by whisker stimulation ( b ) or acetylcholine ( c ) in TRPM2-null mice. Responses to adenosine were not altered ( d ). Data are presented as mean ± s.e.m. * P
Techniques Used: Mouse Assay, Whisker Assay
Figure Legend Snippet: TRPM2 inhibition rescues the endothelial dysfunction induced by Aβ 1–40 in vivo Neocortical application of 2-APB or ACA has no effect on resting CBF ( a ), but it prevents the reduction in resting CBF induced by neocortical superfusion of Aβ 1–40 (Aβ) ( a ). 2-APB or ACA also rescues the attenuation in the CBF increase evoked by whisker stimulation ( b ) or acetylcholine ( c ) induced by Aβ 1–40 or observed in tg2576 mice. The CBF increase induced by adenosine is unaffected ( d ). Data are presented as mean ± s.e.m. * P
Techniques Used: Inhibition, In Vivo, Whisker Assay, Mouse Assay
Figure Legend Snippet: Presumed signalling pathways through which Aβ 1–40 activates endothelial TRPM2 channels Aβ 1–40 (Aβ) activates the innate immunity receptor CD36 leading to production of superoxide via NADPH oxidase. Superoxide reacts with NO, made continuously in endothelial cells, to form peroxynitrite (PN). PN induces DNA damage, which, in turn, activates PARP. ADPR formation by PARG cleavage of PAR activates the Nudix (Nu) domain of TRPM2 leading to massive increases in intracellular Ca 2+ , which induce endothelial dysfunction. However, the involvement of other TRPM2-permeable anions, such as Na + , cannot be ruled out. In a multicellular context, for example, in vivo , PN, a diffusible agent, could also be produced by other vascular cells, and diffuse into endothelial cells to activate this pathway.
Techniques Used: In Vivo, Produced
Figure Legend Snippet: Aβ 1–40 induces large and sustained increases in intracellular Ca2þ via TRPM2 channels in brain endothelial cells The Aβ 1–40 are attenuated by the mechanistically distinct TRPM2 inhibitors 2-APB and ACA ( a,c ) or by TRPM2 knockdown using siRNA, but not control siRNA (control si) ( b,d ). Data are presented as mean ± s.e.m. * P