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Progen Biotechnik synaptopodin antibody
Histopathological changes and Mfn2 expression in patients with DKD. (A) Histological changes in patients with DKD were determined by HE and PAS staining (original magnification, ×400). (B) Representative images of immunohistochemical staining of Mfn2 in glomeruli per group (original magnification, ×400). (C,D) Representative images of immunofluorescent staining of Mfn2, WT1 or <t>Synaptopodin</t> and DAPI in glomeruli per group (original magnification, ×600). CTL, control; DKD, diabetic kidney disease.
Synaptopodin Antibody, supplied by Progen Biotechnik, used in various techniques. Bioz Stars score: 86/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/synaptopodin antibody/product/Progen Biotechnik
Average 86 stars, based on 4 article reviews
Price from $9.99 to $1999.99
synaptopodin antibody - by Bioz Stars, 2022-11
86/100 stars

Images

1) Product Images from "Mfn2 Regulates High Glucose-Induced MAMs Dysfunction and Apoptosis in Podocytes via PERK Pathway"

Article Title: Mfn2 Regulates High Glucose-Induced MAMs Dysfunction and Apoptosis in Podocytes via PERK Pathway

Journal: Frontiers in Cell and Developmental Biology

doi: 10.3389/fcell.2021.769213

Histopathological changes and Mfn2 expression in patients with DKD. (A) Histological changes in patients with DKD were determined by HE and PAS staining (original magnification, ×400). (B) Representative images of immunohistochemical staining of Mfn2 in glomeruli per group (original magnification, ×400). (C,D) Representative images of immunofluorescent staining of Mfn2, WT1 or Synaptopodin and DAPI in glomeruli per group (original magnification, ×600). CTL, control; DKD, diabetic kidney disease.
Figure Legend Snippet: Histopathological changes and Mfn2 expression in patients with DKD. (A) Histological changes in patients with DKD were determined by HE and PAS staining (original magnification, ×400). (B) Representative images of immunohistochemical staining of Mfn2 in glomeruli per group (original magnification, ×400). (C,D) Representative images of immunofluorescent staining of Mfn2, WT1 or Synaptopodin and DAPI in glomeruli per group (original magnification, ×600). CTL, control; DKD, diabetic kidney disease.

Techniques Used: Expressing, Staining, Immunohistochemistry

2) Product Images from "Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1)"

Article Title: Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1)

Journal: Scientific Reports

doi: 10.1038/s41598-018-30115-3

Expression of TESK1 in glomerular podocytes. ( a ) ( b ) A monoclonal antibody to Hu TESK1 (#1) and polyclonal antibody to TESK1 (#2) confirmed expression of TESK1 in Hu podocytes. The antibody did not react with Ms TESK1. ( c ) We next investigated TESK1 expression in Hu kidney sections using the monoclonal antibody to TESK1 (green) and the podocyte marker synaptopodin (SYN) (red) as described in the Methods Section. Nuclei were counterstained with DAPI (blue). Merging of the images shows that TESK1 co-localized with the podocyte marker SYN at focal subcellular locations within the cell (insets). TESK1 was also found in tubular cells. TESK1 and SYN staining were not detected in the absence of the primary antibodies. ( d ) To determine if podocytes bound fibronectin, we performed attachment assays using fibronectin and collagen coated tissue dishes in the presence or absence of the integrin β3 inhibitor peptide cyclo-RGDfV. Mouse podocyte bound avidly to fibronectin and the binding was inhibited by cyclo-RGDfV. Podocytes bound collagen less avidly and cylco-RGDfV did not significantly affect binding to collagen-coated dishes. ( e , f ) Plating podocytes on fibronectin decreased CFL1 phosphorylation compared to cells plated on collagen. ( g , h ) Rho A activity was enhanced in podocytes plated on collagen compared to cells plated on fibronectin. **P
Figure Legend Snippet: Expression of TESK1 in glomerular podocytes. ( a ) ( b ) A monoclonal antibody to Hu TESK1 (#1) and polyclonal antibody to TESK1 (#2) confirmed expression of TESK1 in Hu podocytes. The antibody did not react with Ms TESK1. ( c ) We next investigated TESK1 expression in Hu kidney sections using the monoclonal antibody to TESK1 (green) and the podocyte marker synaptopodin (SYN) (red) as described in the Methods Section. Nuclei were counterstained with DAPI (blue). Merging of the images shows that TESK1 co-localized with the podocyte marker SYN at focal subcellular locations within the cell (insets). TESK1 was also found in tubular cells. TESK1 and SYN staining were not detected in the absence of the primary antibodies. ( d ) To determine if podocytes bound fibronectin, we performed attachment assays using fibronectin and collagen coated tissue dishes in the presence or absence of the integrin β3 inhibitor peptide cyclo-RGDfV. Mouse podocyte bound avidly to fibronectin and the binding was inhibited by cyclo-RGDfV. Podocytes bound collagen less avidly and cylco-RGDfV did not significantly affect binding to collagen-coated dishes. ( e , f ) Plating podocytes on fibronectin decreased CFL1 phosphorylation compared to cells plated on collagen. ( g , h ) Rho A activity was enhanced in podocytes plated on collagen compared to cells plated on fibronectin. **P

Techniques Used: Expressing, Mass Spectrometry, Marker, Staining, Binding Assay, Activity Assay

3) Product Images from "Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1)"

Article Title: Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1)

Journal: Scientific Reports

doi: 10.1038/s41598-018-30115-3

Expression of TESK1 in glomerular podocytes. ( a ) PCR products of the appropriate size were amplified from human (Hu) and mouse (Ms) podocytes using intron spanning primers. DNA sequencing confirmed amplification of TESK1. (Supplementary Figure S1 ) ( b ) A monoclonal antibody to Hu TESK1 (#1) and polyclonal antibody to TESK1 (#2) confirmed expression of TESK1 in Hu podocytes. The antibody did not react with Ms TESK1. ( c ) We next investigated TESK1 expression in Hu kidney sections using the monoclonal antibody to TESK1 (green) and the podocyte marker synaptopodin (SYN) (red) as described in the Methods Section. Nuclei were counterstained with DAPI (blue). Merging of the images shows that TESK1 co-localized with the podocyte marker SYN at focal subcellular locations within the cell (insets). TESK1 was also found in tubular cells. TESK1 and SYN staining were not detected in the absence of the primary antibodies. ( d ) To determine if podocytes bound fibronectin, we performed attachment assays using fibronectin and collagen coated tissue dishes in the presence or absence of the integrin β3 inhibitor peptide cyclo-RGDfV. Mouse podocyte bound avidly to fibronectin and the binding was inhibited by cyclo-RGDfV. Podocytes bound collagen less avidly and cylco-RGDfV did not significantly affect binding to collagen-coated dishes. ( e , f ) Plating podocytes on fibronectin decreased CFL1 phosphorylation compared to cells plated on collagen. ( g , h ) Rho A activity was enhanced in podocytes plated on collagen compared to cells plated on fibronectin. **P
Figure Legend Snippet: Expression of TESK1 in glomerular podocytes. ( a ) PCR products of the appropriate size were amplified from human (Hu) and mouse (Ms) podocytes using intron spanning primers. DNA sequencing confirmed amplification of TESK1. (Supplementary Figure S1 ) ( b ) A monoclonal antibody to Hu TESK1 (#1) and polyclonal antibody to TESK1 (#2) confirmed expression of TESK1 in Hu podocytes. The antibody did not react with Ms TESK1. ( c ) We next investigated TESK1 expression in Hu kidney sections using the monoclonal antibody to TESK1 (green) and the podocyte marker synaptopodin (SYN) (red) as described in the Methods Section. Nuclei were counterstained with DAPI (blue). Merging of the images shows that TESK1 co-localized with the podocyte marker SYN at focal subcellular locations within the cell (insets). TESK1 was also found in tubular cells. TESK1 and SYN staining were not detected in the absence of the primary antibodies. ( d ) To determine if podocytes bound fibronectin, we performed attachment assays using fibronectin and collagen coated tissue dishes in the presence or absence of the integrin β3 inhibitor peptide cyclo-RGDfV. Mouse podocyte bound avidly to fibronectin and the binding was inhibited by cyclo-RGDfV. Podocytes bound collagen less avidly and cylco-RGDfV did not significantly affect binding to collagen-coated dishes. ( e , f ) Plating podocytes on fibronectin decreased CFL1 phosphorylation compared to cells plated on collagen. ( g , h ) Rho A activity was enhanced in podocytes plated on collagen compared to cells plated on fibronectin. **P

Techniques Used: Expressing, Polymerase Chain Reaction, Amplification, DNA Sequencing, Marker, Staining, Binding Assay, Activity Assay

4) Product Images from "Mild Electrical Stimulation and Heat Shock Ameliorates Progressive Proteinuria and Renal Inflammation in Mouse Model of Alport Syndrome"

Article Title: Mild Electrical Stimulation and Heat Shock Ameliorates Progressive Proteinuria and Renal Inflammation in Mouse Model of Alport Syndrome

Journal: PLoS ONE

doi: 10.1371/journal.pone.0043852

MES+HS activates Akt and induces Hsp72 expression in podocytes of Alport mice in vivo. ( a , c e ) One hour after the final treatment, whole kidney protein lysates or glomeruli protein lysates were isolated from 8 weeks-MES+HS-treated and control Alport mice, and immunoblotted to detect p-Akt and total Akt proteins. Actin was used as loading control ( a, c ). Renal cryosections were subjected to immunohistochemical analysis to assess phosphorylated Akt. Arrowheads indicate phosphorylated Akt in podocytes. Cryosections were counterstained with DAPI ( e ). ( b, d f ) Eight hours ( b f ) or five hours ( d ) after the final treatment, whole kidney or glomeruli protein lysates were isolated from MES+HS-treated (8 weeks treated for b f , or 4 weeks treated for d ) and control Alport mice, and immunoblotted to assess Hsp72 and HSC70 expression. α-Tubulin or actin was used as loading control ( b, d ). Renal cryosections were subjected to immunohistochemical analysis to assess Hsp72. Arrowheads indicate up-regulated Hsp72 in podocytes. Cryosections were counterstained with DAPI ( f ). ( e f ) Representative glomeruli images of three independent experiments are shown. Renal sections were immunostained with anti-synaptopodin antibody to assess podocyte localization ( lower panels ). Sections were counterstained with DAPI. White bars; 10 µm.
Figure Legend Snippet: MES+HS activates Akt and induces Hsp72 expression in podocytes of Alport mice in vivo. ( a , c e ) One hour after the final treatment, whole kidney protein lysates or glomeruli protein lysates were isolated from 8 weeks-MES+HS-treated and control Alport mice, and immunoblotted to detect p-Akt and total Akt proteins. Actin was used as loading control ( a, c ). Renal cryosections were subjected to immunohistochemical analysis to assess phosphorylated Akt. Arrowheads indicate phosphorylated Akt in podocytes. Cryosections were counterstained with DAPI ( e ). ( b, d f ) Eight hours ( b f ) or five hours ( d ) after the final treatment, whole kidney or glomeruli protein lysates were isolated from MES+HS-treated (8 weeks treated for b f , or 4 weeks treated for d ) and control Alport mice, and immunoblotted to assess Hsp72 and HSC70 expression. α-Tubulin or actin was used as loading control ( b, d ). Renal cryosections were subjected to immunohistochemical analysis to assess Hsp72. Arrowheads indicate up-regulated Hsp72 in podocytes. Cryosections were counterstained with DAPI ( f ). ( e f ) Representative glomeruli images of three independent experiments are shown. Renal sections were immunostained with anti-synaptopodin antibody to assess podocyte localization ( lower panels ). Sections were counterstained with DAPI. White bars; 10 µm.

Techniques Used: Expressing, Mouse Assay, In Vivo, Isolation, Immunohistochemistry

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    Progen Biotechnik mouse anti synaptopodin
    Mouse Anti Synaptopodin, supplied by Progen Biotechnik, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti synaptopodin/product/Progen Biotechnik
    Average 90 stars, based on 1 article reviews
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    88
    Progen Biotechnik synaptopodin
    In vitro drug evaluation in human kidney organoids. ( A ) Current-voltage relationship, 500-ms voltage ramp from −80 mV to +80 mV before/after GFB-887 (0.1 μM) or ML204 (100 μM). ( B ) Concentration-dependent inhibition of human TRPC5 after GFB-887 at +80 mV. Means ± SEM ( n = 3 to 4 measurements per concentration). IC 50 , median inhibitory concentration. ( C ) Up-regulation of human TRPC5 mRNA expression during organoid differentiation in vitro. Error bars, SD. BLOQ, below limit of quantitation. ( D ) Double labeling of podocytes with <t>synaptopodin</t> (SYNPO, green) and TRPC5 (red). ( E ) CsA and GFB-887 protect podocytes from PS-induced injury, region of interest in blue. Inset: Scale of representative images for injury quantification (top left). Representative images of glomeruli for podocyte injury quantification in organoids treated with DMSO (vehicle), PS, PS + CsA, PS + GFB-887, or PS + CsA + GFB-887. Cyan, synaptopodin; red, phalloidin. ( F ) Quantification of PS-induced actin aggregation. GFB-887 and CsA are nonadditive. DMSO versus PS, P
    Synaptopodin, supplied by Progen Biotechnik, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/synaptopodin/product/Progen Biotechnik
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    Progen Biotechnik anti mouse synpo
    In vitro drug evaluation in human kidney organoids. ( A ) Current-voltage relationship, 500-ms voltage ramp from −80 mV to +80 mV before/after GFB-887 (0.1 μM) or ML204 (100 μM). ( B ) Concentration-dependent inhibition of human TRPC5 after GFB-887 at +80 mV. Means ± SEM ( n = 3 to 4 measurements per concentration). IC 50 , median inhibitory concentration. ( C ) Up-regulation of human TRPC5 mRNA expression during organoid differentiation in vitro. Error bars, SD. BLOQ, below limit of quantitation. ( D ) Double labeling of podocytes with <t>synaptopodin</t> (SYNPO, green) and TRPC5 (red). ( E ) CsA and GFB-887 protect podocytes from PS-induced injury, region of interest in blue. Inset: Scale of representative images for injury quantification (top left). Representative images of glomeruli for podocyte injury quantification in organoids treated with DMSO (vehicle), PS, PS + CsA, PS + GFB-887, or PS + CsA + GFB-887. Cyan, synaptopodin; red, phalloidin. ( F ) Quantification of PS-induced actin aggregation. GFB-887 and CsA are nonadditive. DMSO versus PS, P
    Anti Mouse Synpo, supplied by Progen Biotechnik, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti mouse synpo/product/Progen Biotechnik
    Average 90 stars, based on 1 article reviews
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    In vitro drug evaluation in human kidney organoids. ( A ) Current-voltage relationship, 500-ms voltage ramp from −80 mV to +80 mV before/after GFB-887 (0.1 μM) or ML204 (100 μM). ( B ) Concentration-dependent inhibition of human TRPC5 after GFB-887 at +80 mV. Means ± SEM ( n = 3 to 4 measurements per concentration). IC 50 , median inhibitory concentration. ( C ) Up-regulation of human TRPC5 mRNA expression during organoid differentiation in vitro. Error bars, SD. BLOQ, below limit of quantitation. ( D ) Double labeling of podocytes with synaptopodin (SYNPO, green) and TRPC5 (red). ( E ) CsA and GFB-887 protect podocytes from PS-induced injury, region of interest in blue. Inset: Scale of representative images for injury quantification (top left). Representative images of glomeruli for podocyte injury quantification in organoids treated with DMSO (vehicle), PS, PS + CsA, PS + GFB-887, or PS + CsA + GFB-887. Cyan, synaptopodin; red, phalloidin. ( F ) Quantification of PS-induced actin aggregation. GFB-887 and CsA are nonadditive. DMSO versus PS, P

    Journal: Science Advances

    Article Title: Transplanted organoids empower human preclinical assessment of drug candidate for the clinic

    doi: 10.1126/sciadv.abj5633

    Figure Lengend Snippet: In vitro drug evaluation in human kidney organoids. ( A ) Current-voltage relationship, 500-ms voltage ramp from −80 mV to +80 mV before/after GFB-887 (0.1 μM) or ML204 (100 μM). ( B ) Concentration-dependent inhibition of human TRPC5 after GFB-887 at +80 mV. Means ± SEM ( n = 3 to 4 measurements per concentration). IC 50 , median inhibitory concentration. ( C ) Up-regulation of human TRPC5 mRNA expression during organoid differentiation in vitro. Error bars, SD. BLOQ, below limit of quantitation. ( D ) Double labeling of podocytes with synaptopodin (SYNPO, green) and TRPC5 (red). ( E ) CsA and GFB-887 protect podocytes from PS-induced injury, region of interest in blue. Inset: Scale of representative images for injury quantification (top left). Representative images of glomeruli for podocyte injury quantification in organoids treated with DMSO (vehicle), PS, PS + CsA, PS + GFB-887, or PS + CsA + GFB-887. Cyan, synaptopodin; red, phalloidin. ( F ) Quantification of PS-induced actin aggregation. GFB-887 and CsA are nonadditive. DMSO versus PS, P

    Article Snippet: Primary antibodies included the following: CD31/PECAM1 (Bethyl Laboratories, IHC-00055), RECA-1 (Bio-Rad, MCA970GA), synaptopodin (Progen, GP94-N), E-cadherin (R & D Systems, AF648), TRPC5 [University of California Davis/National Institutes of Health (NIH) NeuroMab Facility, 75-104], and TRPC5 (Alomone Labs, ACC-020).

    Techniques: In Vitro, Concentration Assay, Inhibition, Expressing, Quantitation Assay, Labeling

    PD studies in rats with transplanted human kidney organoids bolster confidence in GFB-887, an investigational new drug. ( A ) Organoids differentiated for 14 days in vitro were transplanted under the kidney capsule of athymic male rats and followed for 2 (left) or 4 (right) weeks before oral dosing with GFB-887 (10 mg/kg) for three consecutive days. Extracted organoid and kidney samples were normalized to sample weights, and the final drug values were calculated as nanograms per gram tissue; nanograms per milliliter refers to GFB-887 concentration per milliliter of plasma. Oral dosing of GFB-887 resulted in equivalent drug exposure in organoids and rat plasma, thereby showing that the organoids had functional connectivity to the host vasculature at 2 weeks after transplantation. Organoid GFB-887 levels did not further increase at 4 weeks after tr ansplantation. Data show means ± SEM from at least four independent measurements. ( B ) Superresolution imaging reveals PS-induced loss of synaptopodin protein abundance in transplanted organoids, which was prevented by oral dosing of GFB-887; blue, nuclei; green, synaptopodin; red, RECA-1; HBSS, Hank’s balanced salt solution vehicle control. ( C ) Quantification of PS-induced podocyte injury and protection by GFB-887 in transplanted organoids. ( D ) Quantification of PS-induced podocyte injury and protection by GFB-887 in endogenous rat kidney adjacent to transplanted organoids. For both (C) and (D), synaptopodin mean intensity in podocytes was quantified for HBSS vehicle, PS, coperfusion PS + GFB-887, or PS perfusion after oral dosing of GFB-887. Data show means ± SEM; for all treatment conditions versus PS, P

    Journal: Science Advances

    Article Title: Transplanted organoids empower human preclinical assessment of drug candidate for the clinic

    doi: 10.1126/sciadv.abj5633

    Figure Lengend Snippet: PD studies in rats with transplanted human kidney organoids bolster confidence in GFB-887, an investigational new drug. ( A ) Organoids differentiated for 14 days in vitro were transplanted under the kidney capsule of athymic male rats and followed for 2 (left) or 4 (right) weeks before oral dosing with GFB-887 (10 mg/kg) for three consecutive days. Extracted organoid and kidney samples were normalized to sample weights, and the final drug values were calculated as nanograms per gram tissue; nanograms per milliliter refers to GFB-887 concentration per milliliter of plasma. Oral dosing of GFB-887 resulted in equivalent drug exposure in organoids and rat plasma, thereby showing that the organoids had functional connectivity to the host vasculature at 2 weeks after transplantation. Organoid GFB-887 levels did not further increase at 4 weeks after tr ansplantation. Data show means ± SEM from at least four independent measurements. ( B ) Superresolution imaging reveals PS-induced loss of synaptopodin protein abundance in transplanted organoids, which was prevented by oral dosing of GFB-887; blue, nuclei; green, synaptopodin; red, RECA-1; HBSS, Hank’s balanced salt solution vehicle control. ( C ) Quantification of PS-induced podocyte injury and protection by GFB-887 in transplanted organoids. ( D ) Quantification of PS-induced podocyte injury and protection by GFB-887 in endogenous rat kidney adjacent to transplanted organoids. For both (C) and (D), synaptopodin mean intensity in podocytes was quantified for HBSS vehicle, PS, coperfusion PS + GFB-887, or PS perfusion after oral dosing of GFB-887. Data show means ± SEM; for all treatment conditions versus PS, P

    Article Snippet: Primary antibodies included the following: CD31/PECAM1 (Bethyl Laboratories, IHC-00055), RECA-1 (Bio-Rad, MCA970GA), synaptopodin (Progen, GP94-N), E-cadherin (R & D Systems, AF648), TRPC5 [University of California Davis/National Institutes of Health (NIH) NeuroMab Facility, 75-104], and TRPC5 (Alomone Labs, ACC-020).

    Techniques: In Vitro, Concentration Assay, Functional Assay, Transplantation Assay, Imaging

    APOL1 expression is upregulated in podocytes and GECs of patients with COVAN. ( A – L ) IHC for APOL1 in biopsy tissue from ( A – F ) patient 1 and ( G – L ) patient 6. Original magnification, 40×. ( B , E , H , and K ) Co-staining of APOL1 with podocyte marker synaptopodin. ( C , F , I , and L ) Co-staining of APOL1 with endothelial marker CD31. Arrow represents a podocyte. Arrowhead represents a GEC.

    Journal: JCI Insight

    Article Title: JAK inhibitor blocks COVID-19 cytokine–induced JAK/STAT/APOL1 signaling in glomerular cells and podocytopathy in human kidney organoids

    doi: 10.1172/jci.insight.157432

    Figure Lengend Snippet: APOL1 expression is upregulated in podocytes and GECs of patients with COVAN. ( A – L ) IHC for APOL1 in biopsy tissue from ( A – F ) patient 1 and ( G – L ) patient 6. Original magnification, 40×. ( B , E , H , and K ) Co-staining of APOL1 with podocyte marker synaptopodin. ( C , F , I , and L ) Co-staining of APOL1 with endothelial marker CD31. Arrow represents a podocyte. Arrowhead represents a GEC.

    Article Snippet: Primary Abs against APOL1 (5.17D12, Genentech), synaptopodin (Progen Biotechnik, 61094), and CD31 (CST, 3528s) were applied at 1:4000 (final concentration 0.95 μg/mL), 1:100, and 1:1600, respectively, for 60 minutes at 36°C.

    Techniques: Expressing, Immunohistochemistry, Staining, Marker