anti trpm2 antibodies  (Alomone Labs)


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    Structured Review

    Alomone Labs anti trpm2 antibodies
    Aβ 1–40 activates sustained <t>TRPM2</t> 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
    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
    https://www.bioz.com/result/anti trpm2 antibodies/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti trpm2 antibodies - by Bioz Stars, 2022-10
    86/100 stars

    Images

    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

    doi: 10.1038/ncomms6318

    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 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

    Techniques Used:

    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
    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

    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
    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

    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.
    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

    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
    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

    Techniques Used:

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    Alomone Labs anti trpm2 antibodies
    Aβ 1–40 activates sustained <t>TRPM2</t> 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
    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
    https://www.bioz.com/result/anti trpm2 antibodies/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti trpm2 antibodies - by Bioz Stars, 2022-10
    86/100 stars
      Buy from Supplier

    92
    Alomone Labs anti transient receptor potential canonical
    Blockade of <t>transient</t> <t>receptor</t> <t>potential</t> <t>canonical</t> 6 (TRPC6) channels significantly inhibits extracellular Ca 2+ -induced increase in cytosolic free Ca 2+ concentration ([Ca 2+ ] cyt ) in idiopathic pulmonary (IPAH)-pulmonary arterial smooth muscle cells (PASMC). A : representative images ( left ) and traces ( middle ) showing the changes of [Ca 2+ ] cyt before, during, and after extracellular application of 2.2 mM Ca 2+ (2.2Ca) in normal (Nor) and IPAH-PASMC. Lathanum (La 3+ ) was added into the perfusate when 2.2Ca-induced increase in [Ca 2+ ] cyt reached the plateau phase. Summarized data ( n = 43 cells; right ) showing the amplitude of 2.2Ca-induced transient and plateau increases in [Ca 2+ ] cyt in IPAH-PASMC with (La) or without (control) extracellular La 3+ . ** P
    Anti Transient Receptor Potential Canonical, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti transient receptor potential canonical/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti transient receptor potential canonical - by Bioz Stars, 2022-10
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    Image Search Results


    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

    Journal: Nature communications

    Article Title: The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction

    doi: 10.1038/ncomms6318

    Figure Lengend 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

    Article Snippet: The reduction of TRPM2 protein in whole-cell lysates was confirmed with western blot analysis using anti-TRPM2 antibodies (1:200; ant-rabbit; alomone labs).

    Techniques:

    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

    Journal: Nature communications

    Article Title: The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction

    doi: 10.1038/ncomms6318

    Figure Lengend 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

    Article Snippet: The reduction of TRPM2 protein in whole-cell lysates was confirmed with western blot analysis using anti-TRPM2 antibodies (1:200; ant-rabbit; alomone labs).

    Techniques: Mouse Assay, Whisker Assay

    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

    Journal: Nature communications

    Article Title: The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction

    doi: 10.1038/ncomms6318

    Figure Lengend 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

    Article Snippet: The reduction of TRPM2 protein in whole-cell lysates was confirmed with western blot analysis using anti-TRPM2 antibodies (1:200; ant-rabbit; alomone labs).

    Techniques: Inhibition, In Vivo, Whisker Assay, Mouse Assay

    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.

    Journal: Nature communications

    Article Title: The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction

    doi: 10.1038/ncomms6318

    Figure Lengend 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.

    Article Snippet: The reduction of TRPM2 protein in whole-cell lysates was confirmed with western blot analysis using anti-TRPM2 antibodies (1:200; ant-rabbit; alomone labs).

    Techniques: In Vivo, Produced

    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

    Journal: Nature communications

    Article Title: The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction

    doi: 10.1038/ncomms6318

    Figure Lengend 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

    Article Snippet: The reduction of TRPM2 protein in whole-cell lysates was confirmed with western blot analysis using anti-TRPM2 antibodies (1:200; ant-rabbit; alomone labs).

    Techniques:

    Western blot analysis of TRPC protein expression in 2–4-, 10–12- and 16–20-month-old rat aorta. Representative blot images for TRPC1 and TRPC6 proteins isolated from rat aorta were shown. β-actin protein was used as loading control. Protein levels were expressed as relative optical density. Shown are mean ± SEM; * P

    Journal: Age

    Article Title: Expression levels of TRPC1 and TRPC6 ion channels are reciprocally altered in aging rat aorta: implications for age-related vasospastic disorders

    doi: 10.1007/s11357-009-9126-z

    Figure Lengend Snippet: Western blot analysis of TRPC protein expression in 2–4-, 10–12- and 16–20-month-old rat aorta. Representative blot images for TRPC1 and TRPC6 proteins isolated from rat aorta were shown. β-actin protein was used as loading control. Protein levels were expressed as relative optical density. Shown are mean ± SEM; * P

    Article Snippet: Proteins were separated on 8% sodium dodecyl sulfate polyacrylamide gel electrophoresis and transferred to membranes (Immobilon-P polyvinylidene difluoride, Millipore) at 25°C for 2 h at 15 V. Following 2 h blocking (with 5% skim milk in Tris-buffered saline with Tween-20), membranes were incubated with TRPC primary antibodies (1:200, Alomone Laboratories) and anti-β-actin (1:1,500, Abcam Ltd.) overnight at 4°C, then with horseradish peroxidase (HRP)-conjugated goat antirabbit secondary antibody (DakoCytomation; 1:1,500) for 1 h at room temperature.

    Techniques: Western Blot, Expressing, Isolation

    Blockade of transient receptor potential canonical 6 (TRPC6) channels significantly inhibits extracellular Ca 2+ -induced increase in cytosolic free Ca 2+ concentration ([Ca 2+ ] cyt ) in idiopathic pulmonary (IPAH)-pulmonary arterial smooth muscle cells (PASMC). A : representative images ( left ) and traces ( middle ) showing the changes of [Ca 2+ ] cyt before, during, and after extracellular application of 2.2 mM Ca 2+ (2.2Ca) in normal (Nor) and IPAH-PASMC. Lathanum (La 3+ ) was added into the perfusate when 2.2Ca-induced increase in [Ca 2+ ] cyt reached the plateau phase. Summarized data ( n = 43 cells; right ) showing the amplitude of 2.2Ca-induced transient and plateau increases in [Ca 2+ ] cyt in IPAH-PASMC with (La) or without (control) extracellular La 3+ . ** P

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: Pathogenic role of calcium-sensing receptors in the development and progression of pulmonary hypertension

    doi: 10.1152/ajplung.00050.2016

    Figure Lengend Snippet: Blockade of transient receptor potential canonical 6 (TRPC6) channels significantly inhibits extracellular Ca 2+ -induced increase in cytosolic free Ca 2+ concentration ([Ca 2+ ] cyt ) in idiopathic pulmonary (IPAH)-pulmonary arterial smooth muscle cells (PASMC). A : representative images ( left ) and traces ( middle ) showing the changes of [Ca 2+ ] cyt before, during, and after extracellular application of 2.2 mM Ca 2+ (2.2Ca) in normal (Nor) and IPAH-PASMC. Lathanum (La 3+ ) was added into the perfusate when 2.2Ca-induced increase in [Ca 2+ ] cyt reached the plateau phase. Summarized data ( n = 43 cells; right ) showing the amplitude of 2.2Ca-induced transient and plateau increases in [Ca 2+ ] cyt in IPAH-PASMC with (La) or without (control) extracellular La 3+ . ** P

    Article Snippet: Protein was loaded on an 8% acrylamide gel, transferred to an Immobilon-P transfer membrane (Millipore, Bedford, MA), and immunoblotted with anti-CaSR (1:1,000; Alomone Laboratories) and anti-transient receptor potential canonical (TRPC)6 monoclonal antibody (1:1,000; Alomone Laboratories).

    Techniques: Concentration Assay