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mouse anti-dsg2 (clone 10g11) (Progen Biotechnik)

Name: mouse anti-dsg2 (clone 10g11)
Brand: Progen Biotechnik
Rating: 90 (1 reviews)

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Progen Biotechnik mouse anti-dsg2 (clone 10g11)
Mouse Anti Dsg2 (Clone 10g11), 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-dsg2 (clone 10g11)/product/Progen Biotechnik
Average 90 stars, based on 1 article reviews

mouse anti-dsg2 (clone 10g11) - by Bioz Stars, 2026-02

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$Extradesmosomal Dsg2 is present at the cell surface of polarized cultured enterocytes. Cells were grown on coverslips for several days after reaching confluency, fixed with 2% PFA and stained for junctional components. ( A ) Confocal microscopy analysis of Caco2 cells shows linear and apical localization of the junctional components Dsg2 and Cld4 at cell borders. Scale bar, 10 µm. ( B ) Analysis with SIM shows Dsg2 being located at same level as microvilli, visualized with Alexa488-phalloidin, at the surface of Caco2 cells. Shown is a Z-projection. Bar, 5 µm. ( C ) Apical fraction of Dsg2 (right panel) is not co-localizing with DP in contrast to lower layers (left panel) where both can be found in close proximity as analysed via SIM. Scale bar, 5 µm. ( D ) Both, clusters consisting of Dsg2 and DP as well as single Dsg2 molecules are present on the cell surface of DLD1 cells, as revealed by STED. Scale bar, 5 µm (left panel), 1 µm (right panel). ( E ) Dsg2 was detected in both, the Triton X-100-soluble and -insoluble fraction in contrast to DP being present only in the insoluble fraction. GAPDH served as loading control. Cropped blots are displayed and full-length blots are included in the supplementary information.$

Journal: Scientific Reports

Article Title: Desmoglein 2 regulates the intestinal epithelial barrier via p38 mitogen-activated protein kinase

doi: 10.1038/s41598-017-06713-y

Figure Lengend Snippet: Extradesmosomal Dsg2 is present at the cell surface of polarized cultured enterocytes. Cells were grown on coverslips for several days after reaching confluency, fixed with 2% PFA and stained for junctional components. ( A ) Confocal microscopy analysis of Caco2 cells shows linear and apical localization of the junctional components Dsg2 and Cld4 at cell borders. Scale bar, 10 µm. ( B ) Analysis with SIM shows Dsg2 being located at same level as microvilli, visualized with Alexa488-phalloidin, at the surface of Caco2 cells. Shown is a Z-projection. Bar, 5 µm. ( C ) Apical fraction of Dsg2 (right panel) is not co-localizing with DP in contrast to lower layers (left panel) where both can be found in close proximity as analysed via SIM. Scale bar, 5 µm. ( D ) Both, clusters consisting of Dsg2 and DP as well as single Dsg2 molecules are present on the cell surface of DLD1 cells, as revealed by STED. Scale bar, 5 µm (left panel), 1 µm (right panel). ( E ) Dsg2 was detected in both, the Triton X-100-soluble and -insoluble fraction in contrast to DP being present only in the insoluble fraction. GAPDH served as loading control. Cropped blots are displayed and full-length blots are included in the supplementary information.

Article Snippet: Following primary antibodies were used: mouse anti Dsg2 (clone 10G11) and rabbit anti Dsg2 (rb5, both Progen, Heidelberg, Germany), rabbit anti DP (NW6, USA, self-made), mouse anti Dsc2/3 (clone 7G6, Life Technologies, Carlsbad, CA), rabbit anti Claudin-4, rabbit anti Claudin-1 and rabbit anti Claudin-2 (all from Life Technologies, Carlsbad, CA), mouse anti E-cadherin (clone 36, BD Bioscience, Heidelberg, Germany,) mouse anti GAPDH (Santa Cruz Biotechnology, Santa Cruz, CA), mouse anti α-tubulin (Abcam, Cambridge, UK), rabbit anti p38MAPK, rabbit anti phospho-Thr180/182 p38MAPK, (Cell Signaling, Danvers, MA, USA),.

Techniques: Cell Culture, Staining, Confocal Microscopy, Control

Dsg2-specific binding events can be detected on the surface of enterocytes. ( A ) Dsg2 force measurements were performed on living DLD1 cells at 37 °C. Cell topography was imaged to select specific areas at cell borders (upper panel). Force measurements revealed binding events along the cell border (lower panel) Bar, 10 µm (upper panel), 1 µm (lower panels). ( B ) Peak fit analysis of unbinding force resulted in a distribution-peak of 30,4 pN. ( C ) Application of a Dsg2-specific antibody significantly reduced the amount of binding events on living DLD1 cells as well as ( D ) in a cell-free setup (shown are means ± SE, n = 3, *p < 0,05). ( E ) Dsg2-specific antibody increased cell monolayer fragmentation in a dispase-based cell dissociation assay. (Shown is mean ± SE, n = 9, *p < 0,05 compared to control).

Journal: Scientific Reports

Article Title: Desmoglein 2 regulates the intestinal epithelial barrier via p38 mitogen-activated protein kinase

doi: 10.1038/s41598-017-06713-y

Figure Lengend Snippet: Dsg2-specific binding events can be detected on the surface of enterocytes. ( A ) Dsg2 force measurements were performed on living DLD1 cells at 37 °C. Cell topography was imaged to select specific areas at cell borders (upper panel). Force measurements revealed binding events along the cell border (lower panel) Bar, 10 µm (upper panel), 1 µm (lower panels). ( B ) Peak fit analysis of unbinding force resulted in a distribution-peak of 30,4 pN. ( C ) Application of a Dsg2-specific antibody significantly reduced the amount of binding events on living DLD1 cells as well as ( D ) in a cell-free setup (shown are means ± SE, n = 3, *p < 0,05). ( E ) Dsg2-specific antibody increased cell monolayer fragmentation in a dispase-based cell dissociation assay. (Shown is mean ± SE, n = 9, *p < 0,05 compared to control).

Techniques: Binding Assay, Control

Inhibition of Dsg2 binding resulted in increased p38MAPK activity which is critical for enterocyte cohesion. ( A ) Western blot analysis after incubation of DLD1 cells with a Dsg2-specific antibody for 30 min revealed increased phosphorylation of p38MAPK. Cropped blots are displayed and full-length blots are included in the supplementary information. ( B ) Band intensity of detected p-p38MAPK was quantified using ImageJ and normalized to control (shown is mean ± SE, n = 6, *p < 0,05 compared to control). ( C ) DLD1 cells were treated with the p38MAPK inhibitor SB202190 or the activator anisomycin and analysed in a dispase-based cell dissociation assay. Both resulted in increased cell monolayer fragmentation. (Shown is mean ± SE, n = 3, *p < 0,05 compared to control).

Journal: Scientific Reports

Article Title: Desmoglein 2 regulates the intestinal epithelial barrier via p38 mitogen-activated protein kinase

doi: 10.1038/s41598-017-06713-y

Figure Lengend Snippet: Inhibition of Dsg2 binding resulted in increased p38MAPK activity which is critical for enterocyte cohesion. ( A ) Western blot analysis after incubation of DLD1 cells with a Dsg2-specific antibody for 30 min revealed increased phosphorylation of p38MAPK. Cropped blots are displayed and full-length blots are included in the supplementary information. ( B ) Band intensity of detected p-p38MAPK was quantified using ImageJ and normalized to control (shown is mean ± SE, n = 6, *p < 0,05 compared to control). ( C ) DLD1 cells were treated with the p38MAPK inhibitor SB202190 or the activator anisomycin and analysed in a dispase-based cell dissociation assay. Both resulted in increased cell monolayer fragmentation. (Shown is mean ± SE, n = 3, *p < 0,05 compared to control).

Techniques: Inhibition, Binding Assay, Activity Assay, Western Blot, Incubation, Phospho-proteomics, Control

Well-balanced p38MAPK activity is critical for intestinal barrier function. Ca 2+ -switch assay with confluent DLD1 cells. ( A ) TER values decrease during depletion with 4 mM EGTA for 1 h and increase to back to control values during 2 h of repletion with 8 mM CaCl 2 . ( B ) Immunostaining of Dsg2 and Cld4 shows reduced and fragmented staining as well as gaps after 1 h depletion and similar staining to control condition after 2 h repletion. ( C ) Barrier reformation is not disturbed after application of a Dsg2-specific antibody but is impaired after addition of an inhibitory anti E-cadherin antibody. ( D ) TER values decrease after inhibition of p38MAPK with SB202190 and also barrier reformation is impaired in the Ca 2+ -switch experiment. Activation of p38MAPK via anisomycin has no effect in the short run but also induces reduction of TER values after about 10 h. (shown are representative graphs for at least three independent experiments).

Journal: Scientific Reports

Article Title: Desmoglein 2 regulates the intestinal epithelial barrier via p38 mitogen-activated protein kinase

doi: 10.1038/s41598-017-06713-y

Figure Lengend Snippet: Well-balanced p38MAPK activity is critical for intestinal barrier function. Ca 2+ -switch assay with confluent DLD1 cells. ( A ) TER values decrease during depletion with 4 mM EGTA for 1 h and increase to back to control values during 2 h of repletion with 8 mM CaCl 2 . ( B ) Immunostaining of Dsg2 and Cld4 shows reduced and fragmented staining as well as gaps after 1 h depletion and similar staining to control condition after 2 h repletion. ( C ) Barrier reformation is not disturbed after application of a Dsg2-specific antibody but is impaired after addition of an inhibitory anti E-cadherin antibody. ( D ) TER values decrease after inhibition of p38MAPK with SB202190 and also barrier reformation is impaired in the Ca 2+ -switch experiment. Activation of p38MAPK via anisomycin has no effect in the short run but also induces reduction of TER values after about 10 h. (shown are representative graphs for at least three independent experiments).

Techniques: Activity Assay, Control, Immunostaining, Staining, Inhibition, Activation Assay

Dsg2 regulates p38MAPK activity which is required for barrier properties. ( A ) Comparison of baseline TER values between wildtype and knockout cells revealed reduced TER in DLD1 cells lacking Dsg2 (shown is mean ± SE, n ≥ 10, *p < 0,05 compared to control, n.s not significant). ( B ) During Ca 2+ depletion for 1 h TER values of Dsg2-deficient cells decreased stronger compared to wildtype cells. (Shown is mean ± SE, n ≥ 6, *p < 0,05 compared to control, n.s not significant). ( C ) Wildtype and knockout cells grown on coverslips were stained for Dsg2 and Dsc2 to confirm knockout. Scale bar, 10 µm ( D ). Level of p-p38MAPK in Dsg2 and Dsc2 knockout cells was analysed via Western blot. Loss of Dsg2 and Dsc2 resulted in reduced level of p-p38MAPK which was not restored by Dsc2 rescue. α-Tubulin served as loading control. Cropped blots are displayed and full-length blots are included in the supplementary information. ( E ) Band intensity of detected p-p38MAPK was quantified using ImageJ and normalized to control (shown is mean ± SE, n ≥ 3, *p < 0,05 compared to control, n.s not significant). ( F ) Time for complete repletion during Ca 2+ -switch experiments was compared between wildtype and double knockout of Dsg2 and Dsc2. Loss of desmosomal cadherins resulted in a prolonged repletion time which was rescued by activation of p38MAPK via anisomycin (shown is mean ± SE, n ≥ 6, *p < 0,05 compared to wildtype under control conditions, #p < 0,05 compared to ΔDsg2ΔDsc2 under control conditions, n.s not significant). ( G ) Treatment with anisomycin reduced repletion time in ΔDsg2ΔDsc2 knockout cells. Representative graph for at least four independent Ca 2+ -switch experiments is shown.

Journal: Scientific Reports

Article Title: Desmoglein 2 regulates the intestinal epithelial barrier via p38 mitogen-activated protein kinase

doi: 10.1038/s41598-017-06713-y

Figure Lengend Snippet: Dsg2 regulates p38MAPK activity which is required for barrier properties. ( A ) Comparison of baseline TER values between wildtype and knockout cells revealed reduced TER in DLD1 cells lacking Dsg2 (shown is mean ± SE, n ≥ 10, *p < 0,05 compared to control, n.s not significant). ( B ) During Ca 2+ depletion for 1 h TER values of Dsg2-deficient cells decreased stronger compared to wildtype cells. (Shown is mean ± SE, n ≥ 6, *p < 0,05 compared to control, n.s not significant). ( C ) Wildtype and knockout cells grown on coverslips were stained for Dsg2 and Dsc2 to confirm knockout. Scale bar, 10 µm ( D ). Level of p-p38MAPK in Dsg2 and Dsc2 knockout cells was analysed via Western blot. Loss of Dsg2 and Dsc2 resulted in reduced level of p-p38MAPK which was not restored by Dsc2 rescue. α-Tubulin served as loading control. Cropped blots are displayed and full-length blots are included in the supplementary information. ( E ) Band intensity of detected p-p38MAPK was quantified using ImageJ and normalized to control (shown is mean ± SE, n ≥ 3, *p < 0,05 compared to control, n.s not significant). ( F ) Time for complete repletion during Ca 2+ -switch experiments was compared between wildtype and double knockout of Dsg2 and Dsc2. Loss of desmosomal cadherins resulted in a prolonged repletion time which was rescued by activation of p38MAPK via anisomycin (shown is mean ± SE, n ≥ 6, *p < 0,05 compared to wildtype under control conditions, #p < 0,05 compared to ΔDsg2ΔDsc2 under control conditions, n.s not significant). ( G ) Treatment with anisomycin reduced repletion time in ΔDsg2ΔDsc2 knockout cells. Representative graph for at least four independent Ca 2+ -switch experiments is shown.

Techniques: Activity Assay, Comparison, Knock-Out, Control, Staining, Western Blot, Double Knockout, Activation Assay

(A) Clear expression of mRNA can be detected for most desmogleins, with the exception of DSG1 which shows only faint expression. ( B–C ) Representative immunofluorescence analyses of DSG2 (B) and DSG4 (C) at the cell border of normal human prostatic glandular epithelium. Original magnification: 200X. Scale bars correspond to 100 µm.

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: (A) Clear expression of mRNA can be detected for most desmogleins, with the exception of DSG1 which shows only faint expression. ( B–C ) Representative immunofluorescence analyses of DSG2 (B) and DSG4 (C) at the cell border of normal human prostatic glandular epithelium. Original magnification: 200X. Scale bars correspond to 100 µm.

Article Snippet: Anti-DSG2 mouse monoclonal antibody (clone 10G11) was purchased from ARP, Inc (Belmont, MA) and used at a dilution of 1∶50 for immunofluorescence analysis of normal prostate tissue and cell lines; anti-DSG1/2 mouse monoclonal antibody (clone DG3.10) was purchased from Fitzgerald (Acton, MA) and used at a dilution of 1∶20 for TMAs.

Techniques: Expressing, Immunofluorescence

(A–C) DSG2 is expressed in the luminal cells of the prostatic glands and this expression rarely co-localizes with basal cell CK14 expression. ( D–F ) DSG2 co-localizes with PSA expression in the luminal compartment of the gland. ( G–I ) DSG4 is also expressed in the luminal cells and rarely co-localizes with basal cell CK14 expression. ( J–L ) DSG4 expression co-localizes with luminal cell PSA expression. ( M–O ) The expression of DSG4 also shows almost complete co-localization with that of DSG2 in the luminal cells. Original magnification: 200X. Scale bars correspond to 100 µm.

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: (A–C) DSG2 is expressed in the luminal cells of the prostatic glands and this expression rarely co-localizes with basal cell CK14 expression. ( D–F ) DSG2 co-localizes with PSA expression in the luminal compartment of the gland. ( G–I ) DSG4 is also expressed in the luminal cells and rarely co-localizes with basal cell CK14 expression. ( J–L ) DSG4 expression co-localizes with luminal cell PSA expression. ( M–O ) The expression of DSG4 also shows almost complete co-localization with that of DSG2 in the luminal cells. Original magnification: 200X. Scale bars correspond to 100 µm.

Techniques: Expressing

(A) DSG2 expression is detected in all cell lines examined, including the normal immortalized prostate cell line BPH-1. Data is represented as mean ± SD. **P<0.01; *** P<0.001. ( B–E ) DSG2 is expressed at the cell border of LNCaP and DU145 cells; however, cell border expression is not detected in PC3 cells with only some cells showing faint, punctate, and diffuse staining (insert magnification; shown at 2.5X). Original magnification: 200X. Scale bars correspond to 100 µm.

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: (A) DSG2 expression is detected in all cell lines examined, including the normal immortalized prostate cell line BPH-1. Data is represented as mean ± SD. **P<0.01; *** P<0.001. ( B–E ) DSG2 is expressed at the cell border of LNCaP and DU145 cells; however, cell border expression is not detected in PC3 cells with only some cells showing faint, punctate, and diffuse staining (insert magnification; shown at 2.5X). Original magnification: 200X. Scale bars correspond to 100 µm.

Techniques: Expressing, Staining

Expression of DSG2 in prostate cancer as compared to normal prostate.

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: Expression of DSG2 in prostate cancer as compared to normal prostate.

Techniques: Expressing, Standard Deviation

(A–L) Representative immunofluorescence analysis of DSG2 and CK8/18 in prostate cancer. ( D, E–H ) TMAs showing high DSG2 expression in the cell border of well differentiated areas of the tumor (panel D, inside yellow dashed line). ( D, I–L ) TMAs showing low DSG2 expression in poorly differentiated areas of the tumor (panel D, shown in the remainder of the tumor outside of the yellow dashed line). Original magnification: 200X. Scale bars correspond to 100 µm. ( M ) Patients expressing higher levels of DSG2 had a significantly longer recurrence free survival than those expressing lower levels of DSG2 ( P = 0.01).

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: (A–L) Representative immunofluorescence analysis of DSG2 and CK8/18 in prostate cancer. ( D, E–H ) TMAs showing high DSG2 expression in the cell border of well differentiated areas of the tumor (panel D, inside yellow dashed line). ( D, I–L ) TMAs showing low DSG2 expression in poorly differentiated areas of the tumor (panel D, shown in the remainder of the tumor outside of the yellow dashed line). Original magnification: 200X. Scale bars correspond to 100 µm. ( M ) Patients expressing higher levels of DSG2 had a significantly longer recurrence free survival than those expressing lower levels of DSG2 ( P = 0.01).

Techniques: Immunofluorescence, Expressing

Correlation between DSG2 and clinico-pathological characteristics.

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: Correlation between DSG2 and clinico-pathological characteristics.

Techniques:

Multivariate analyses in the 414 patient cohort.

Journal: PLoS ONE

Article Title: Characterization of Desmoglein Expression in the Normal Prostatic Gland. Desmoglein 2 Is an Independent Prognostic Factor for Aggressive Prostate Cancer

doi: 10.1371/journal.pone.0098786

Figure Lengend Snippet: Multivariate analyses in the 414 patient cohort.

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