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rhoa biosensor gfp rgbd  (Addgene inc)


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    Addgene inc rhoa biosensor gfp rgbd
    ( A ) <t>GTP-RhoA</t> was significantly increased in PKD1 cystic cell lines compared with control cells ( n = 4) using a Rhotekin-GTP pulldown assay. ( B ) GTP-RhoA was significantly increased in Pkd1- knockout kidneys compared with controls ( n = 3). ( C ) Phosphorylation of myosin light chain (pMLC), a major downstream target of ROCK, was significantly upregulated in isogenic PKD1 -null cells ( n = 3). ( D ) Expression of dominant negative RhoA (T19N) in PKD1 cells resulted in a significant increase in cilia length compared with dominant negative Cdc42 (N17) or Rac1 (N17) ( n = 3 independent experiments, N = 81 cells). ( E ) Active RhoA was localized using a GTP-RhoA biosensor (R-GBD) in control and PKD1 cells. In ciliated cells, active RhoA (GFP) was visualized at the cilia base (arrows) and was significantly increased in PKD1 cells ( n = 3 independent experiments, N = 22 cells). Insets show cilia under higher magnification (original magnification, ×1000). ( F ) Rapamycin-inducible centrosomal targeted expression (arrow) of constitutively active RhoA (Q63L) was associated with a significant decrease in cilia length in control cells compared with uninduced cells ( n = 3 independent experiments, N = 70 cells) * P < 0.05, ** P < 0.01, **** P < 0.0001. Significance determined by 2-tailed Student’s t test ( A–C and E ). Significance determined by 1-way ANOVA corrected (Dunnett) for multiple comparison ( D and F ). ADPKD, autosomal dominant polycystic kidney disease.
    Rhoa Biosensor Gfp Rgbd, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rhoa biosensor gfp rgbd/product/Addgene inc
    Average 93 stars, based on 19 article reviews
    rhoa biosensor gfp rgbd - by Bioz Stars, 2026-05
    93/100 stars

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    1) Product Images from "Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling"

    Article Title: Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling

    Journal: JCI Insight

    doi: 10.1172/jci.insight.135385

    ( A ) GTP-RhoA was significantly increased in PKD1 cystic cell lines compared with control cells ( n = 4) using a Rhotekin-GTP pulldown assay. ( B ) GTP-RhoA was significantly increased in Pkd1- knockout kidneys compared with controls ( n = 3). ( C ) Phosphorylation of myosin light chain (pMLC), a major downstream target of ROCK, was significantly upregulated in isogenic PKD1 -null cells ( n = 3). ( D ) Expression of dominant negative RhoA (T19N) in PKD1 cells resulted in a significant increase in cilia length compared with dominant negative Cdc42 (N17) or Rac1 (N17) ( n = 3 independent experiments, N = 81 cells). ( E ) Active RhoA was localized using a GTP-RhoA biosensor (R-GBD) in control and PKD1 cells. In ciliated cells, active RhoA (GFP) was visualized at the cilia base (arrows) and was significantly increased in PKD1 cells ( n = 3 independent experiments, N = 22 cells). Insets show cilia under higher magnification (original magnification, ×1000). ( F ) Rapamycin-inducible centrosomal targeted expression (arrow) of constitutively active RhoA (Q63L) was associated with a significant decrease in cilia length in control cells compared with uninduced cells ( n = 3 independent experiments, N = 70 cells) * P < 0.05, ** P < 0.01, **** P < 0.0001. Significance determined by 2-tailed Student’s t test ( A–C and E ). Significance determined by 1-way ANOVA corrected (Dunnett) for multiple comparison ( D and F ). ADPKD, autosomal dominant polycystic kidney disease.
    Figure Legend Snippet: ( A ) GTP-RhoA was significantly increased in PKD1 cystic cell lines compared with control cells ( n = 4) using a Rhotekin-GTP pulldown assay. ( B ) GTP-RhoA was significantly increased in Pkd1- knockout kidneys compared with controls ( n = 3). ( C ) Phosphorylation of myosin light chain (pMLC), a major downstream target of ROCK, was significantly upregulated in isogenic PKD1 -null cells ( n = 3). ( D ) Expression of dominant negative RhoA (T19N) in PKD1 cells resulted in a significant increase in cilia length compared with dominant negative Cdc42 (N17) or Rac1 (N17) ( n = 3 independent experiments, N = 81 cells). ( E ) Active RhoA was localized using a GTP-RhoA biosensor (R-GBD) in control and PKD1 cells. In ciliated cells, active RhoA (GFP) was visualized at the cilia base (arrows) and was significantly increased in PKD1 cells ( n = 3 independent experiments, N = 22 cells). Insets show cilia under higher magnification (original magnification, ×1000). ( F ) Rapamycin-inducible centrosomal targeted expression (arrow) of constitutively active RhoA (Q63L) was associated with a significant decrease in cilia length in control cells compared with uninduced cells ( n = 3 independent experiments, N = 70 cells) * P < 0.05, ** P < 0.01, **** P < 0.0001. Significance determined by 2-tailed Student’s t test ( A–C and E ). Significance determined by 1-way ANOVA corrected (Dunnett) for multiple comparison ( D and F ). ADPKD, autosomal dominant polycystic kidney disease.

    Techniques Used: Control, Knock-Out, Phospho-proteomics, Expressing, Dominant Negative Mutation, Comparison

    A model showing how mutation of PC1 could lead to reduced cilia/centrosomal localization or retention of ARHGAP35. Two possible scenarios are shown: (a) trafficking and delivery of PC1 and ARHGAP35 in the same vesicles to the centrosome compartment and (b) retention of cleaved PC1 C-terminus (CT1) bound to centrosomal ARHGAP35. The RhoA-dependent kinase, ROCK, has been previously shown to be localized to centrosomes . Loss of centrosomal ARHGAP35 leads to the accumulation of centrosomal “active” GTP-RhoA, the activation of ROCK and its downstream effectors (e.g., pMLC), leading to increased actin polymerization and shorter cilia. It is plausible that the local increase in centrosomal ROCK activity could lead in turn to a cascade of ROCK activation, which spreads throughout the cell. PC1, polycystin-1; ADPKD, autosomal dominant polycystic kidney disease.
    Figure Legend Snippet: A model showing how mutation of PC1 could lead to reduced cilia/centrosomal localization or retention of ARHGAP35. Two possible scenarios are shown: (a) trafficking and delivery of PC1 and ARHGAP35 in the same vesicles to the centrosome compartment and (b) retention of cleaved PC1 C-terminus (CT1) bound to centrosomal ARHGAP35. The RhoA-dependent kinase, ROCK, has been previously shown to be localized to centrosomes . Loss of centrosomal ARHGAP35 leads to the accumulation of centrosomal “active” GTP-RhoA, the activation of ROCK and its downstream effectors (e.g., pMLC), leading to increased actin polymerization and shorter cilia. It is plausible that the local increase in centrosomal ROCK activity could lead in turn to a cascade of ROCK activation, which spreads throughout the cell. PC1, polycystin-1; ADPKD, autosomal dominant polycystic kidney disease.

    Techniques Used: Mutagenesis, Activation Assay, Activity Assay



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    rhoa biosensor gfp rgbd  (Addgene inc)
    93
    Addgene inc rhoa biosensor gfp rgbd
    ( A ) <t>GTP-RhoA</t> was significantly increased in PKD1 cystic cell lines compared with control cells ( n = 4) using a Rhotekin-GTP pulldown assay. ( B ) GTP-RhoA was significantly increased in Pkd1- knockout kidneys compared with controls ( n = 3). ( C ) Phosphorylation of myosin light chain (pMLC), a major downstream target of ROCK, was significantly upregulated in isogenic PKD1 -null cells ( n = 3). ( D ) Expression of dominant negative RhoA (T19N) in PKD1 cells resulted in a significant increase in cilia length compared with dominant negative Cdc42 (N17) or Rac1 (N17) ( n = 3 independent experiments, N = 81 cells). ( E ) Active RhoA was localized using a GTP-RhoA biosensor (R-GBD) in control and PKD1 cells. In ciliated cells, active RhoA (GFP) was visualized at the cilia base (arrows) and was significantly increased in PKD1 cells ( n = 3 independent experiments, N = 22 cells). Insets show cilia under higher magnification (original magnification, ×1000). ( F ) Rapamycin-inducible centrosomal targeted expression (arrow) of constitutively active RhoA (Q63L) was associated with a significant decrease in cilia length in control cells compared with uninduced cells ( n = 3 independent experiments, N = 70 cells) * P < 0.05, ** P < 0.01, **** P < 0.0001. Significance determined by 2-tailed Student’s t test ( A–C and E ). Significance determined by 1-way ANOVA corrected (Dunnett) for multiple comparison ( D and F ). ADPKD, autosomal dominant polycystic kidney disease.
    Rhoa Biosensor Gfp Rgbd, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rhoa biosensor gfp rgbd/product/Addgene inc
    Average 93 stars, based on 1 article reviews
    rhoa biosensor gfp rgbd - by Bioz Stars, 2026-05
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    ( A ) GTP-RhoA was significantly increased in PKD1 cystic cell lines compared with control cells ( n = 4) using a Rhotekin-GTP pulldown assay. ( B ) GTP-RhoA was significantly increased in Pkd1- knockout kidneys compared with controls ( n = 3). ( C ) Phosphorylation of myosin light chain (pMLC), a major downstream target of ROCK, was significantly upregulated in isogenic PKD1 -null cells ( n = 3). ( D ) Expression of dominant negative RhoA (T19N) in PKD1 cells resulted in a significant increase in cilia length compared with dominant negative Cdc42 (N17) or Rac1 (N17) ( n = 3 independent experiments, N = 81 cells). ( E ) Active RhoA was localized using a GTP-RhoA biosensor (R-GBD) in control and PKD1 cells. In ciliated cells, active RhoA (GFP) was visualized at the cilia base (arrows) and was significantly increased in PKD1 cells ( n = 3 independent experiments, N = 22 cells). Insets show cilia under higher magnification (original magnification, ×1000). ( F ) Rapamycin-inducible centrosomal targeted expression (arrow) of constitutively active RhoA (Q63L) was associated with a significant decrease in cilia length in control cells compared with uninduced cells ( n = 3 independent experiments, N = 70 cells) * P < 0.05, ** P < 0.01, **** P < 0.0001. Significance determined by 2-tailed Student’s t test ( A–C and E ). Significance determined by 1-way ANOVA corrected (Dunnett) for multiple comparison ( D and F ). ADPKD, autosomal dominant polycystic kidney disease.

    Journal: JCI Insight

    Article Title: Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling

    doi: 10.1172/jci.insight.135385

    Figure Lengend Snippet: ( A ) GTP-RhoA was significantly increased in PKD1 cystic cell lines compared with control cells ( n = 4) using a Rhotekin-GTP pulldown assay. ( B ) GTP-RhoA was significantly increased in Pkd1- knockout kidneys compared with controls ( n = 3). ( C ) Phosphorylation of myosin light chain (pMLC), a major downstream target of ROCK, was significantly upregulated in isogenic PKD1 -null cells ( n = 3). ( D ) Expression of dominant negative RhoA (T19N) in PKD1 cells resulted in a significant increase in cilia length compared with dominant negative Cdc42 (N17) or Rac1 (N17) ( n = 3 independent experiments, N = 81 cells). ( E ) Active RhoA was localized using a GTP-RhoA biosensor (R-GBD) in control and PKD1 cells. In ciliated cells, active RhoA (GFP) was visualized at the cilia base (arrows) and was significantly increased in PKD1 cells ( n = 3 independent experiments, N = 22 cells). Insets show cilia under higher magnification (original magnification, ×1000). ( F ) Rapamycin-inducible centrosomal targeted expression (arrow) of constitutively active RhoA (Q63L) was associated with a significant decrease in cilia length in control cells compared with uninduced cells ( n = 3 independent experiments, N = 70 cells) * P < 0.05, ** P < 0.01, **** P < 0.0001. Significance determined by 2-tailed Student’s t test ( A–C and E ). Significance determined by 1-way ANOVA corrected (Dunnett) for multiple comparison ( D and F ). ADPKD, autosomal dominant polycystic kidney disease.

    Article Snippet: The active RhoA biosensor GFP-rGBD (gift of William Bement, University of Wisconsin–Madison, Madison, Wisconsin, USA; Addgene plasmid 26732) ( ) was transfected into UCL93 or OX161 cells.

    Techniques: Control, Knock-Out, Phospho-proteomics, Expressing, Dominant Negative Mutation, Comparison

    A model showing how mutation of PC1 could lead to reduced cilia/centrosomal localization or retention of ARHGAP35. Two possible scenarios are shown: (a) trafficking and delivery of PC1 and ARHGAP35 in the same vesicles to the centrosome compartment and (b) retention of cleaved PC1 C-terminus (CT1) bound to centrosomal ARHGAP35. The RhoA-dependent kinase, ROCK, has been previously shown to be localized to centrosomes . Loss of centrosomal ARHGAP35 leads to the accumulation of centrosomal “active” GTP-RhoA, the activation of ROCK and its downstream effectors (e.g., pMLC), leading to increased actin polymerization and shorter cilia. It is plausible that the local increase in centrosomal ROCK activity could lead in turn to a cascade of ROCK activation, which spreads throughout the cell. PC1, polycystin-1; ADPKD, autosomal dominant polycystic kidney disease.

    Journal: JCI Insight

    Article Title: Polycystin-1 regulates ARHGAP35-dependent centrosomal RhoA activation and ROCK signaling

    doi: 10.1172/jci.insight.135385

    Figure Lengend Snippet: A model showing how mutation of PC1 could lead to reduced cilia/centrosomal localization or retention of ARHGAP35. Two possible scenarios are shown: (a) trafficking and delivery of PC1 and ARHGAP35 in the same vesicles to the centrosome compartment and (b) retention of cleaved PC1 C-terminus (CT1) bound to centrosomal ARHGAP35. The RhoA-dependent kinase, ROCK, has been previously shown to be localized to centrosomes . Loss of centrosomal ARHGAP35 leads to the accumulation of centrosomal “active” GTP-RhoA, the activation of ROCK and its downstream effectors (e.g., pMLC), leading to increased actin polymerization and shorter cilia. It is plausible that the local increase in centrosomal ROCK activity could lead in turn to a cascade of ROCK activation, which spreads throughout the cell. PC1, polycystin-1; ADPKD, autosomal dominant polycystic kidney disease.

    Article Snippet: The active RhoA biosensor GFP-rGBD (gift of William Bement, University of Wisconsin–Madison, Madison, Wisconsin, USA; Addgene plasmid 26732) ( ) was transfected into UCL93 or OX161 cells.

    Techniques: Mutagenesis, Activation Assay, Activity Assay