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trpv2  (Alomone Labs)


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    Alomone Labs trpv2
    <t>TRPV2‐mediated</t> mechanosensing coordinates actomyosin‐Lamin A/C remodeling under hyperviscosity. (a) Expression of F‐actin and G‐actin quantified by western blotting, TRPV2 was knocked down in BMSCs using siRNA technology. (b) Expression of CaMKII and cofilin quantified by western blotting. (c) Quantitative analysis of calcium oscillations after si‐TRPV2 treatment ( n = 4). (d) Immunofluorescence images of F‐actin and nuclear. Scale bar: 40 µm ( n = 3). (e) Normalized F‐actin intensity profiles across nuclear equator. (f) Immunofluorescence image of vinculin focal adhesion angular distribution. Scale bar: 50 µm. (g) Dual‐channel confocal imaging of cPLA2 (Green) and Lamin A/C (Red). Scale bar: 10 µm ( n = 4).
    Trpv2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/acc-032/pmc12955904-260-17-18?v=Alomone+Labs
    Average 93 stars, based on 12 article reviews
    trpv2 - by Bioz Stars, 2026-07
    93/100 stars

    Images

    1) Product Images from "Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction"

    Article Title: Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction

    Journal: Advanced Science

    doi: 10.1002/advs.202509056

    TRPV2‐mediated mechanosensing coordinates actomyosin‐Lamin A/C remodeling under hyperviscosity. (a) Expression of F‐actin and G‐actin quantified by western blotting, TRPV2 was knocked down in BMSCs using siRNA technology. (b) Expression of CaMKII and cofilin quantified by western blotting. (c) Quantitative analysis of calcium oscillations after si‐TRPV2 treatment ( n = 4). (d) Immunofluorescence images of F‐actin and nuclear. Scale bar: 40 µm ( n = 3). (e) Normalized F‐actin intensity profiles across nuclear equator. (f) Immunofluorescence image of vinculin focal adhesion angular distribution. Scale bar: 50 µm. (g) Dual‐channel confocal imaging of cPLA2 (Green) and Lamin A/C (Red). Scale bar: 10 µm ( n = 4).
    Figure Legend Snippet: TRPV2‐mediated mechanosensing coordinates actomyosin‐Lamin A/C remodeling under hyperviscosity. (a) Expression of F‐actin and G‐actin quantified by western blotting, TRPV2 was knocked down in BMSCs using siRNA technology. (b) Expression of CaMKII and cofilin quantified by western blotting. (c) Quantitative analysis of calcium oscillations after si‐TRPV2 treatment ( n = 4). (d) Immunofluorescence images of F‐actin and nuclear. Scale bar: 40 µm ( n = 3). (e) Normalized F‐actin intensity profiles across nuclear equator. (f) Immunofluorescence image of vinculin focal adhesion angular distribution. Scale bar: 50 µm. (g) Dual‐channel confocal imaging of cPLA2 (Green) and Lamin A/C (Red). Scale bar: 10 µm ( n = 4).

    Techniques Used: Expressing, Western Blot, Immunofluorescence, Imaging

    Hyperviscous microenvironment drives chromatin remodeling through calcium‐mediated mechanotransduction to impair osteoregeneration. (a) Chromatin Transmission Electron Microscopy of Lamin‐associated domains (LADs), with chromatin density heatmaps generated by ImageJ. Scale bar: 2 µm ( n = 3). (b) Expression of H3K9me3 quantified by western blotting. (c) H3K9me3 immunostaining with DAPI counterstain. Scale bar: 10 µm ( n = 3). (d) Expression of H3K9me3 quantified by western blotting in BMSCs after si‐TRPV2 treatment. (e) After treatment with BAPTA‐AM, expression of H3K9me3 quantified by western blotting. (f) Intersectional analysis via Venn diagram ( n = 2). (g) GO enrichment analysis of DEGs in the MHC group ( n = 2). (h) Representative Integrative Genomics Viewer (IGV) tracks demonstrating increased H3K9me3 binding enrichment within heterochromatic regions of the Colgalt1 gene in the DM and MHC groups compared to the control ( n = 2).
    Figure Legend Snippet: Hyperviscous microenvironment drives chromatin remodeling through calcium‐mediated mechanotransduction to impair osteoregeneration. (a) Chromatin Transmission Electron Microscopy of Lamin‐associated domains (LADs), with chromatin density heatmaps generated by ImageJ. Scale bar: 2 µm ( n = 3). (b) Expression of H3K9me3 quantified by western blotting. (c) H3K9me3 immunostaining with DAPI counterstain. Scale bar: 10 µm ( n = 3). (d) Expression of H3K9me3 quantified by western blotting in BMSCs after si‐TRPV2 treatment. (e) After treatment with BAPTA‐AM, expression of H3K9me3 quantified by western blotting. (f) Intersectional analysis via Venn diagram ( n = 2). (g) GO enrichment analysis of DEGs in the MHC group ( n = 2). (h) Representative Integrative Genomics Viewer (IGV) tracks demonstrating increased H3K9me3 binding enrichment within heterochromatic regions of the Colgalt1 gene in the DM and MHC groups compared to the control ( n = 2).

    Techniques Used: Transmission Assay, Electron Microscopy, Generated, Expressing, Western Blot, Immunostaining, Binding Assay, Control

    Schematic illustration of mechanotransduction in BMSCs within a diabetic high viscosity marrow microenvironment. In the high viscosity niche, elevated confining stress imposes loading on the plasma membrane, gating the mechanosensitive Ca 2 ⁺ channel TRPV2. The resultant Ca 2 ⁺ influx triggers CaMKII phosphorylation, which in turn phosphorylates cofilin, shifting the G‐/F‐actin equilibrium toward perinuclear F‐actin disassembly. This cytoskeletal remodeling deforms Lamin A/C and repositions lamina‐associated domains (LADs), ultimately expanding H3K9me3‐marked heterochromatin and driving transcriptional repression of osteogenic genes.
    Figure Legend Snippet: Schematic illustration of mechanotransduction in BMSCs within a diabetic high viscosity marrow microenvironment. In the high viscosity niche, elevated confining stress imposes loading on the plasma membrane, gating the mechanosensitive Ca 2 ⁺ channel TRPV2. The resultant Ca 2 ⁺ influx triggers CaMKII phosphorylation, which in turn phosphorylates cofilin, shifting the G‐/F‐actin equilibrium toward perinuclear F‐actin disassembly. This cytoskeletal remodeling deforms Lamin A/C and repositions lamina‐associated domains (LADs), ultimately expanding H3K9me3‐marked heterochromatin and driving transcriptional repression of osteogenic genes.

    Techniques Used: Viscosity, Clinical Proteomics, Membrane, Phospho-proteomics



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    Image Search Results


    TRPV2‐mediated mechanosensing coordinates actomyosin‐Lamin A/C remodeling under hyperviscosity. (a) Expression of F‐actin and G‐actin quantified by western blotting, TRPV2 was knocked down in BMSCs using siRNA technology. (b) Expression of CaMKII and cofilin quantified by western blotting. (c) Quantitative analysis of calcium oscillations after si‐TRPV2 treatment ( n = 4). (d) Immunofluorescence images of F‐actin and nuclear. Scale bar: 40 µm ( n = 3). (e) Normalized F‐actin intensity profiles across nuclear equator. (f) Immunofluorescence image of vinculin focal adhesion angular distribution. Scale bar: 50 µm. (g) Dual‐channel confocal imaging of cPLA2 (Green) and Lamin A/C (Red). Scale bar: 10 µm ( n = 4).

    Journal: Advanced Science

    Article Title: Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction

    doi: 10.1002/advs.202509056

    Figure Lengend Snippet: TRPV2‐mediated mechanosensing coordinates actomyosin‐Lamin A/C remodeling under hyperviscosity. (a) Expression of F‐actin and G‐actin quantified by western blotting, TRPV2 was knocked down in BMSCs using siRNA technology. (b) Expression of CaMKII and cofilin quantified by western blotting. (c) Quantitative analysis of calcium oscillations after si‐TRPV2 treatment ( n = 4). (d) Immunofluorescence images of F‐actin and nuclear. Scale bar: 40 µm ( n = 3). (e) Normalized F‐actin intensity profiles across nuclear equator. (f) Immunofluorescence image of vinculin focal adhesion angular distribution. Scale bar: 50 µm. (g) Dual‐channel confocal imaging of cPLA2 (Green) and Lamin A/C (Red). Scale bar: 10 µm ( n = 4).

    Article Snippet: Primary antibodies: F‐actin (Abcam, ab205), G‐actin (Abcam, ab200046), p‐CaMKII (Abcam, ab124880), p‐cofilin (Abcam, ab283500), cofilin (Abcam, ab54532), TRPV2 (Alomone Labs, ACC‐032), Histone H3 (tri methyl K9) (PTM BIO, PTM‐616), and Histone H3 (PTM BIO, PTM‐6621), Histone H3 (tri methyl K27) (PTM BIO, PTM‐647RM), Histone H3 (tri methyl K4) (PTM BIO, PTM‐5019), GAPDH (Abcam, ab181602).

    Techniques: Expressing, Western Blot, Immunofluorescence, Imaging

    Hyperviscous microenvironment drives chromatin remodeling through calcium‐mediated mechanotransduction to impair osteoregeneration. (a) Chromatin Transmission Electron Microscopy of Lamin‐associated domains (LADs), with chromatin density heatmaps generated by ImageJ. Scale bar: 2 µm ( n = 3). (b) Expression of H3K9me3 quantified by western blotting. (c) H3K9me3 immunostaining with DAPI counterstain. Scale bar: 10 µm ( n = 3). (d) Expression of H3K9me3 quantified by western blotting in BMSCs after si‐TRPV2 treatment. (e) After treatment with BAPTA‐AM, expression of H3K9me3 quantified by western blotting. (f) Intersectional analysis via Venn diagram ( n = 2). (g) GO enrichment analysis of DEGs in the MHC group ( n = 2). (h) Representative Integrative Genomics Viewer (IGV) tracks demonstrating increased H3K9me3 binding enrichment within heterochromatic regions of the Colgalt1 gene in the DM and MHC groups compared to the control ( n = 2).

    Journal: Advanced Science

    Article Title: Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction

    doi: 10.1002/advs.202509056

    Figure Lengend Snippet: Hyperviscous microenvironment drives chromatin remodeling through calcium‐mediated mechanotransduction to impair osteoregeneration. (a) Chromatin Transmission Electron Microscopy of Lamin‐associated domains (LADs), with chromatin density heatmaps generated by ImageJ. Scale bar: 2 µm ( n = 3). (b) Expression of H3K9me3 quantified by western blotting. (c) H3K9me3 immunostaining with DAPI counterstain. Scale bar: 10 µm ( n = 3). (d) Expression of H3K9me3 quantified by western blotting in BMSCs after si‐TRPV2 treatment. (e) After treatment with BAPTA‐AM, expression of H3K9me3 quantified by western blotting. (f) Intersectional analysis via Venn diagram ( n = 2). (g) GO enrichment analysis of DEGs in the MHC group ( n = 2). (h) Representative Integrative Genomics Viewer (IGV) tracks demonstrating increased H3K9me3 binding enrichment within heterochromatic regions of the Colgalt1 gene in the DM and MHC groups compared to the control ( n = 2).

    Article Snippet: Primary antibodies: F‐actin (Abcam, ab205), G‐actin (Abcam, ab200046), p‐CaMKII (Abcam, ab124880), p‐cofilin (Abcam, ab283500), cofilin (Abcam, ab54532), TRPV2 (Alomone Labs, ACC‐032), Histone H3 (tri methyl K9) (PTM BIO, PTM‐616), and Histone H3 (PTM BIO, PTM‐6621), Histone H3 (tri methyl K27) (PTM BIO, PTM‐647RM), Histone H3 (tri methyl K4) (PTM BIO, PTM‐5019), GAPDH (Abcam, ab181602).

    Techniques: Transmission Assay, Electron Microscopy, Generated, Expressing, Western Blot, Immunostaining, Binding Assay, Control

    Schematic illustration of mechanotransduction in BMSCs within a diabetic high viscosity marrow microenvironment. In the high viscosity niche, elevated confining stress imposes loading on the plasma membrane, gating the mechanosensitive Ca 2 ⁺ channel TRPV2. The resultant Ca 2 ⁺ influx triggers CaMKII phosphorylation, which in turn phosphorylates cofilin, shifting the G‐/F‐actin equilibrium toward perinuclear F‐actin disassembly. This cytoskeletal remodeling deforms Lamin A/C and repositions lamina‐associated domains (LADs), ultimately expanding H3K9me3‐marked heterochromatin and driving transcriptional repression of osteogenic genes.

    Journal: Advanced Science

    Article Title: Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction

    doi: 10.1002/advs.202509056

    Figure Lengend Snippet: Schematic illustration of mechanotransduction in BMSCs within a diabetic high viscosity marrow microenvironment. In the high viscosity niche, elevated confining stress imposes loading on the plasma membrane, gating the mechanosensitive Ca 2 ⁺ channel TRPV2. The resultant Ca 2 ⁺ influx triggers CaMKII phosphorylation, which in turn phosphorylates cofilin, shifting the G‐/F‐actin equilibrium toward perinuclear F‐actin disassembly. This cytoskeletal remodeling deforms Lamin A/C and repositions lamina‐associated domains (LADs), ultimately expanding H3K9me3‐marked heterochromatin and driving transcriptional repression of osteogenic genes.

    Article Snippet: Primary antibodies: F‐actin (Abcam, ab205), G‐actin (Abcam, ab200046), p‐CaMKII (Abcam, ab124880), p‐cofilin (Abcam, ab283500), cofilin (Abcam, ab54532), TRPV2 (Alomone Labs, ACC‐032), Histone H3 (tri methyl K9) (PTM BIO, PTM‐616), and Histone H3 (PTM BIO, PTM‐6621), Histone H3 (tri methyl K27) (PTM BIO, PTM‐647RM), Histone H3 (tri methyl K4) (PTM BIO, PTM‐5019), GAPDH (Abcam, ab181602).

    Techniques: Viscosity, Clinical Proteomics, Membrane, Phospho-proteomics