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primary antibodies against arhgap29  (Novus Biologicals)


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    Novus Biologicals primary antibodies against arhgap29
    ( A ) Schematic representation of the overlap of microarray data of 223 genes upregulated by induced epithelial–mesenchymal transition (EMT) and 32 considered Rho GTPase-activating proteins. Microarray data from Ziegler et al. were re-analyzed to show the upregulated expression of selected genes. Gene expression data of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were compared. Among the genes examined were 32 genes that had previously been recognized as Rho GTPase-activating proteins. EMT-induced upregulation in MCF-7-EMT cells was found in 223 genes in comparison to MCF-7 wild-type cells. Only the Rho GTPase-activating protein 29 <t>(ARHGAP29)</t> was found to overlap. The relative change in expression (FC, fold change) of genes under consideration was 1.0–4.53. ( B ) Kaplan-Meier survival analysis of the luminal A breast cancer subtype (Threshold = 8 FPKM; ARHGAP29 low n = 271; ARHGAP29 high n = 209; Statistical test: Log-rank (Mantel-Cox) test; p = 0.0141). ( C ) Evidence of the significantly increased basal expression of ARHGAP29 in MCF-7-EMT cells was found. Basal expression (average expression) of ARHGAP29 in the cell lines MCF-7- and MCF-7-EMT was found. Microarray data from Ziegler et al., 2014 comparing the gene expression of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were examined to investigate ARHGAP29 gene expression. ( D ) Expression of ARHGAP29 in MCF-7, MCF-7-EMT, T-47D, T-47D-EMT, and HCC1806 breast cancer cells. Expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (*) p < 0.05.
    Primary Antibodies Against Arhgap29, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against arhgap29/product/Novus Biologicals
    Average 94 stars, based on 13 article reviews
    primary antibodies against arhgap29 - by Bioz Stars, 2026-04
    94/100 stars

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    1) Product Images from "Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells"

    Article Title: Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

    Journal: Cells

    doi: 10.3390/cells9122616

    ( A ) Schematic representation of the overlap of microarray data of 223 genes upregulated by induced epithelial–mesenchymal transition (EMT) and 32 considered Rho GTPase-activating proteins. Microarray data from Ziegler et al. were re-analyzed to show the upregulated expression of selected genes. Gene expression data of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were compared. Among the genes examined were 32 genes that had previously been recognized as Rho GTPase-activating proteins. EMT-induced upregulation in MCF-7-EMT cells was found in 223 genes in comparison to MCF-7 wild-type cells. Only the Rho GTPase-activating protein 29 (ARHGAP29) was found to overlap. The relative change in expression (FC, fold change) of genes under consideration was 1.0–4.53. ( B ) Kaplan-Meier survival analysis of the luminal A breast cancer subtype (Threshold = 8 FPKM; ARHGAP29 low n = 271; ARHGAP29 high n = 209; Statistical test: Log-rank (Mantel-Cox) test; p = 0.0141). ( C ) Evidence of the significantly increased basal expression of ARHGAP29 in MCF-7-EMT cells was found. Basal expression (average expression) of ARHGAP29 in the cell lines MCF-7- and MCF-7-EMT was found. Microarray data from Ziegler et al., 2014 comparing the gene expression of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were examined to investigate ARHGAP29 gene expression. ( D ) Expression of ARHGAP29 in MCF-7, MCF-7-EMT, T-47D, T-47D-EMT, and HCC1806 breast cancer cells. Expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (*) p < 0.05.
    Figure Legend Snippet: ( A ) Schematic representation of the overlap of microarray data of 223 genes upregulated by induced epithelial–mesenchymal transition (EMT) and 32 considered Rho GTPase-activating proteins. Microarray data from Ziegler et al. were re-analyzed to show the upregulated expression of selected genes. Gene expression data of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were compared. Among the genes examined were 32 genes that had previously been recognized as Rho GTPase-activating proteins. EMT-induced upregulation in MCF-7-EMT cells was found in 223 genes in comparison to MCF-7 wild-type cells. Only the Rho GTPase-activating protein 29 (ARHGAP29) was found to overlap. The relative change in expression (FC, fold change) of genes under consideration was 1.0–4.53. ( B ) Kaplan-Meier survival analysis of the luminal A breast cancer subtype (Threshold = 8 FPKM; ARHGAP29 low n = 271; ARHGAP29 high n = 209; Statistical test: Log-rank (Mantel-Cox) test; p = 0.0141). ( C ) Evidence of the significantly increased basal expression of ARHGAP29 in MCF-7-EMT cells was found. Basal expression (average expression) of ARHGAP29 in the cell lines MCF-7- and MCF-7-EMT was found. Microarray data from Ziegler et al., 2014 comparing the gene expression of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were examined to investigate ARHGAP29 gene expression. ( D ) Expression of ARHGAP29 in MCF-7, MCF-7-EMT, T-47D, T-47D-EMT, and HCC1806 breast cancer cells. Expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (*) p < 0.05.

    Techniques Used: Microarray, Expressing, Gene Expression, Transformation Assay, Comparison, Real-time Polymerase Chain Reaction

    ( A ) Detection of reduced Rho GTPase activating protein 29 (ARHGAP29) expression after transient siRNA transfection of MCF-7-EMT, T-47D-EMT, and HCC1806 breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression. The effect of downregulation of ARHGAP29 on the invasion of MCF-7-EMT ( B ), T-47D-EMT, ( C ) and HCC1806 ( D ) breast cancer cells was investigated. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The invasion of transiently transfected breast cancer cells was analyzed after 96 h of coculture with MG63 osteosarcoma cells. The number of invaded cells in the treatment group was calibrated to the number of invaded cells in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t -tests; (****) p < 0.0001; (**) p < 0.01; (*) p < 0.05.
    Figure Legend Snippet: ( A ) Detection of reduced Rho GTPase activating protein 29 (ARHGAP29) expression after transient siRNA transfection of MCF-7-EMT, T-47D-EMT, and HCC1806 breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression. The effect of downregulation of ARHGAP29 on the invasion of MCF-7-EMT ( B ), T-47D-EMT, ( C ) and HCC1806 ( D ) breast cancer cells was investigated. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The invasion of transiently transfected breast cancer cells was analyzed after 96 h of coculture with MG63 osteosarcoma cells. The number of invaded cells in the treatment group was calibrated to the number of invaded cells in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t -tests; (****) p < 0.0001; (**) p < 0.01; (*) p < 0.05.

    Techniques Used: Expressing, Transfection, Control, Real-time Polymerase Chain Reaction

    Effect of the downregulation of Rho GTPase activating protein 29 (ARHGAP29) on the proliferation of MCF-7-EMT ( A ), T-47D-EMT ( B ), and HCC1806 ( C ) breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). After cell culture for 120 h, transiently transfected breast cancer cells were detached and counted using a Neubauer counting chamber. The number of cells in the treatment group was calibrated to the cell number in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (**) p < 0.01; (*) p < 0.05.
    Figure Legend Snippet: Effect of the downregulation of Rho GTPase activating protein 29 (ARHGAP29) on the proliferation of MCF-7-EMT ( A ), T-47D-EMT ( B ), and HCC1806 ( C ) breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). After cell culture for 120 h, transiently transfected breast cancer cells were detached and counted using a Neubauer counting chamber. The number of cells in the treatment group was calibrated to the cell number in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (**) p < 0.01; (*) p < 0.05.

    Techniques Used: Transfection, Control, Cell Culture

    ( A ) Probability of interaction of Rho GTPase activating protein 29 (ARHGAP29) with AKT1, SIRT1, PTPN13, CDC42, MAGEA11, and RHOD. In silico analyses were carried out using the GIANT web server (Genome-wide Integrated Analysis of gene Networks in Tissues, provided by HumanBase, https://hb.flatironinstitute.org/ , last accessed on 26 July 2019). A value of 0.1 was chosen as a minimum confidence interval to investigate interactions. The maximum number of genes considered was seven. The color of the connecting lines between interaction partners reflects possible interactions from 0 (no interaction) to 1 (high probability of interaction). The expression of AKT1 and the pAKT1/AKT1 ratio in MCF-7-EMT ( B ), T-47D-EMT ( C ), and HCC1806 ( D ) breast cancer cells after knock-down of ARHGAP29 expression are shown. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of AKT1 was determined using Western blot analysis and normalized to GAPDH expression using at least three biological and technical replicates. The pAKT1/AKT1 ratio was analyzed as the quotient of pAKT1 versus AKT1 expression. Representative blots for ARHGAP29, AKT1 and pAKT1 are shown. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (***) p < 0.001; (**) p < 0.01; (*) p < 0.05.
    Figure Legend Snippet: ( A ) Probability of interaction of Rho GTPase activating protein 29 (ARHGAP29) with AKT1, SIRT1, PTPN13, CDC42, MAGEA11, and RHOD. In silico analyses were carried out using the GIANT web server (Genome-wide Integrated Analysis of gene Networks in Tissues, provided by HumanBase, https://hb.flatironinstitute.org/ , last accessed on 26 July 2019). A value of 0.1 was chosen as a minimum confidence interval to investigate interactions. The maximum number of genes considered was seven. The color of the connecting lines between interaction partners reflects possible interactions from 0 (no interaction) to 1 (high probability of interaction). The expression of AKT1 and the pAKT1/AKT1 ratio in MCF-7-EMT ( B ), T-47D-EMT ( C ), and HCC1806 ( D ) breast cancer cells after knock-down of ARHGAP29 expression are shown. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of AKT1 was determined using Western blot analysis and normalized to GAPDH expression using at least three biological and technical replicates. The pAKT1/AKT1 ratio was analyzed as the quotient of pAKT1 versus AKT1 expression. Representative blots for ARHGAP29, AKT1 and pAKT1 are shown. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (***) p < 0.001; (**) p < 0.01; (*) p < 0.05.

    Techniques Used: In Silico, Genome Wide, Expressing, Knockdown, Transfection, Control, Western Blot



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    primary antibodies against arhgap29  (Novus Biologicals)
    94
    Novus Biologicals primary antibodies against arhgap29
    ( A ) Schematic representation of the overlap of microarray data of 223 genes upregulated by induced epithelial–mesenchymal transition (EMT) and 32 considered Rho GTPase-activating proteins. Microarray data from Ziegler et al. were re-analyzed to show the upregulated expression of selected genes. Gene expression data of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were compared. Among the genes examined were 32 genes that had previously been recognized as Rho GTPase-activating proteins. EMT-induced upregulation in MCF-7-EMT cells was found in 223 genes in comparison to MCF-7 wild-type cells. Only the Rho GTPase-activating protein 29 <t>(ARHGAP29)</t> was found to overlap. The relative change in expression (FC, fold change) of genes under consideration was 1.0–4.53. ( B ) Kaplan-Meier survival analysis of the luminal A breast cancer subtype (Threshold = 8 FPKM; ARHGAP29 low n = 271; ARHGAP29 high n = 209; Statistical test: Log-rank (Mantel-Cox) test; p = 0.0141). ( C ) Evidence of the significantly increased basal expression of ARHGAP29 in MCF-7-EMT cells was found. Basal expression (average expression) of ARHGAP29 in the cell lines MCF-7- and MCF-7-EMT was found. Microarray data from Ziegler et al., 2014 comparing the gene expression of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were examined to investigate ARHGAP29 gene expression. ( D ) Expression of ARHGAP29 in MCF-7, MCF-7-EMT, T-47D, T-47D-EMT, and HCC1806 breast cancer cells. Expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (*) p < 0.05.
    Primary Antibodies Against Arhgap29, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against arhgap29/product/Novus Biologicals
    Average 94 stars, based on 1 article reviews
    primary antibodies against arhgap29 - by Bioz Stars, 2026-04
    94/100 stars
    		  Buy from Supplier
    primary anti arhgap29 antibody  (Novus Biologicals)
    94
    Novus Biologicals primary anti arhgap29 antibody
    Immunohistochemical staining of <t>ArhGAP29-RhoA/ROCK1</t> in human endometrium. ArhGAP29 staining in normal human endometrium was more obvious compared with endometrial tissue with severe IUAs; whereas, immunohistochemical staining of RhoA/ROCK1 in human endometrium with severe IUAs was more obvious compared with normal endometrial tissue. Scale bar, 50 µm. IUAs, intrauterine adhesions; ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1.
    Primary Anti Arhgap29 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary anti arhgap29 antibody/product/Novus Biologicals
    Average 94 stars, based on 1 article reviews
    primary anti arhgap29 antibody - by Bioz Stars, 2026-04
    94/100 stars
    		  Buy from Supplier

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    ( A ) Schematic representation of the overlap of microarray data of 223 genes upregulated by induced epithelial–mesenchymal transition (EMT) and 32 considered Rho GTPase-activating proteins. Microarray data from Ziegler et al. were re-analyzed to show the upregulated expression of selected genes. Gene expression data of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were compared. Among the genes examined were 32 genes that had previously been recognized as Rho GTPase-activating proteins. EMT-induced upregulation in MCF-7-EMT cells was found in 223 genes in comparison to MCF-7 wild-type cells. Only the Rho GTPase-activating protein 29 (ARHGAP29) was found to overlap. The relative change in expression (FC, fold change) of genes under consideration was 1.0–4.53. ( B ) Kaplan-Meier survival analysis of the luminal A breast cancer subtype (Threshold = 8 FPKM; ARHGAP29 low n = 271; ARHGAP29 high n = 209; Statistical test: Log-rank (Mantel-Cox) test; p = 0.0141). ( C ) Evidence of the significantly increased basal expression of ARHGAP29 in MCF-7-EMT cells was found. Basal expression (average expression) of ARHGAP29 in the cell lines MCF-7- and MCF-7-EMT was found. Microarray data from Ziegler et al., 2014 comparing the gene expression of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were examined to investigate ARHGAP29 gene expression. ( D ) Expression of ARHGAP29 in MCF-7, MCF-7-EMT, T-47D, T-47D-EMT, and HCC1806 breast cancer cells. Expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (*) p < 0.05.

    Journal: Cells

    Article Title: Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

    doi: 10.3390/cells9122616

    Figure Lengend Snippet: ( A ) Schematic representation of the overlap of microarray data of 223 genes upregulated by induced epithelial–mesenchymal transition (EMT) and 32 considered Rho GTPase-activating proteins. Microarray data from Ziegler et al. were re-analyzed to show the upregulated expression of selected genes. Gene expression data of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were compared. Among the genes examined were 32 genes that had previously been recognized as Rho GTPase-activating proteins. EMT-induced upregulation in MCF-7-EMT cells was found in 223 genes in comparison to MCF-7 wild-type cells. Only the Rho GTPase-activating protein 29 (ARHGAP29) was found to overlap. The relative change in expression (FC, fold change) of genes under consideration was 1.0–4.53. ( B ) Kaplan-Meier survival analysis of the luminal A breast cancer subtype (Threshold = 8 FPKM; ARHGAP29 low n = 271; ARHGAP29 high n = 209; Statistical test: Log-rank (Mantel-Cox) test; p = 0.0141). ( C ) Evidence of the significantly increased basal expression of ARHGAP29 in MCF-7-EMT cells was found. Basal expression (average expression) of ARHGAP29 in the cell lines MCF-7- and MCF-7-EMT was found. Microarray data from Ziegler et al., 2014 comparing the gene expression of MCF-7 wild-type cells and mesenchymal-transformed MCF-7-EMT cells were examined to investigate ARHGAP29 gene expression. ( D ) Expression of ARHGAP29 in MCF-7, MCF-7-EMT, T-47D, T-47D-EMT, and HCC1806 breast cancer cells. Expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (*) p < 0.05.

    Article Snippet: Primary antibodies against ARHGAP29 1:2000 (#NBP1-05989, Novus Biologicals, Centennial, CO, USA), AKT1 1:1000 (#9272, Cell Signaling, Danvers, MA, USA), pAKT1 1:1000 (#4058, Cell Signaling), and GAPDH 1:2000 (#5174S, Cell Signaling) were used.

    Techniques: Microarray, Expressing, Gene Expression, Transformation Assay, Comparison, Real-time Polymerase Chain Reaction

    ( A ) Detection of reduced Rho GTPase activating protein 29 (ARHGAP29) expression after transient siRNA transfection of MCF-7-EMT, T-47D-EMT, and HCC1806 breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression. The effect of downregulation of ARHGAP29 on the invasion of MCF-7-EMT ( B ), T-47D-EMT, ( C ) and HCC1806 ( D ) breast cancer cells was investigated. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The invasion of transiently transfected breast cancer cells was analyzed after 96 h of coculture with MG63 osteosarcoma cells. The number of invaded cells in the treatment group was calibrated to the number of invaded cells in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t -tests; (****) p < 0.0001; (**) p < 0.01; (*) p < 0.05.

    Journal: Cells

    Article Title: Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

    doi: 10.3390/cells9122616

    Figure Lengend Snippet: ( A ) Detection of reduced Rho GTPase activating protein 29 (ARHGAP29) expression after transient siRNA transfection of MCF-7-EMT, T-47D-EMT, and HCC1806 breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of ARHGAP29 was analyzed by quantitative real-time PCR and normalized to GAPDH expression. The effect of downregulation of ARHGAP29 on the invasion of MCF-7-EMT ( B ), T-47D-EMT, ( C ) and HCC1806 ( D ) breast cancer cells was investigated. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The invasion of transiently transfected breast cancer cells was analyzed after 96 h of coculture with MG63 osteosarcoma cells. The number of invaded cells in the treatment group was calibrated to the number of invaded cells in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t -tests; (****) p < 0.0001; (**) p < 0.01; (*) p < 0.05.

    Article Snippet: Primary antibodies against ARHGAP29 1:2000 (#NBP1-05989, Novus Biologicals, Centennial, CO, USA), AKT1 1:1000 (#9272, Cell Signaling, Danvers, MA, USA), pAKT1 1:1000 (#4058, Cell Signaling), and GAPDH 1:2000 (#5174S, Cell Signaling) were used.

    Techniques: Expressing, Transfection, Control, Real-time Polymerase Chain Reaction

    Effect of the downregulation of Rho GTPase activating protein 29 (ARHGAP29) on the proliferation of MCF-7-EMT ( A ), T-47D-EMT ( B ), and HCC1806 ( C ) breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). After cell culture for 120 h, transiently transfected breast cancer cells were detached and counted using a Neubauer counting chamber. The number of cells in the treatment group was calibrated to the cell number in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (**) p < 0.01; (*) p < 0.05.

    Journal: Cells

    Article Title: Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

    doi: 10.3390/cells9122616

    Figure Lengend Snippet: Effect of the downregulation of Rho GTPase activating protein 29 (ARHGAP29) on the proliferation of MCF-7-EMT ( A ), T-47D-EMT ( B ), and HCC1806 ( C ) breast cancer cells. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). After cell culture for 120 h, transiently transfected breast cancer cells were detached and counted using a Neubauer counting chamber. The number of cells in the treatment group was calibrated to the cell number in the control group using at least three biological and technical replicates. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (**) p < 0.01; (*) p < 0.05.

    Article Snippet: Primary antibodies against ARHGAP29 1:2000 (#NBP1-05989, Novus Biologicals, Centennial, CO, USA), AKT1 1:1000 (#9272, Cell Signaling, Danvers, MA, USA), pAKT1 1:1000 (#4058, Cell Signaling), and GAPDH 1:2000 (#5174S, Cell Signaling) were used.

    Techniques: Transfection, Control, Cell Culture

    ( A ) Probability of interaction of Rho GTPase activating protein 29 (ARHGAP29) with AKT1, SIRT1, PTPN13, CDC42, MAGEA11, and RHOD. In silico analyses were carried out using the GIANT web server (Genome-wide Integrated Analysis of gene Networks in Tissues, provided by HumanBase, https://hb.flatironinstitute.org/ , last accessed on 26 July 2019). A value of 0.1 was chosen as a minimum confidence interval to investigate interactions. The maximum number of genes considered was seven. The color of the connecting lines between interaction partners reflects possible interactions from 0 (no interaction) to 1 (high probability of interaction). The expression of AKT1 and the pAKT1/AKT1 ratio in MCF-7-EMT ( B ), T-47D-EMT ( C ), and HCC1806 ( D ) breast cancer cells after knock-down of ARHGAP29 expression are shown. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of AKT1 was determined using Western blot analysis and normalized to GAPDH expression using at least three biological and technical replicates. The pAKT1/AKT1 ratio was analyzed as the quotient of pAKT1 versus AKT1 expression. Representative blots for ARHGAP29, AKT1 and pAKT1 are shown. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (***) p < 0.001; (**) p < 0.01; (*) p < 0.05.

    Journal: Cells

    Article Title: Influence of ARHGAP29 on the Invasion of Mesenchymal-Transformed Breast Cancer Cells

    doi: 10.3390/cells9122616

    Figure Lengend Snippet: ( A ) Probability of interaction of Rho GTPase activating protein 29 (ARHGAP29) with AKT1, SIRT1, PTPN13, CDC42, MAGEA11, and RHOD. In silico analyses were carried out using the GIANT web server (Genome-wide Integrated Analysis of gene Networks in Tissues, provided by HumanBase, https://hb.flatironinstitute.org/ , last accessed on 26 July 2019). A value of 0.1 was chosen as a minimum confidence interval to investigate interactions. The maximum number of genes considered was seven. The color of the connecting lines between interaction partners reflects possible interactions from 0 (no interaction) to 1 (high probability of interaction). The expression of AKT1 and the pAKT1/AKT1 ratio in MCF-7-EMT ( B ), T-47D-EMT ( C ), and HCC1806 ( D ) breast cancer cells after knock-down of ARHGAP29 expression are shown. Breast cancer cells were transiently transfected with ARHGAP29-specific siRNA or non-targeting control siRNA (control). The expression of AKT1 was determined using Western blot analysis and normalized to GAPDH expression using at least three biological and technical replicates. The pAKT1/AKT1 ratio was analyzed as the quotient of pAKT1 versus AKT1 expression. Representative blots for ARHGAP29, AKT1 and pAKT1 are shown. Mean ± SEM values are given. Significance was determined with the help of unpaired t-tests; (***) p < 0.001; (**) p < 0.01; (*) p < 0.05.

    Article Snippet: Primary antibodies against ARHGAP29 1:2000 (#NBP1-05989, Novus Biologicals, Centennial, CO, USA), AKT1 1:1000 (#9272, Cell Signaling, Danvers, MA, USA), pAKT1 1:1000 (#4058, Cell Signaling), and GAPDH 1:2000 (#5174S, Cell Signaling) were used.

    Techniques: In Silico, Genome Wide, Expressing, Knockdown, Transfection, Control, Western Blot

    Immunohistochemical staining of ArhGAP29-RhoA/ROCK1 in human endometrium. ArhGAP29 staining in normal human endometrium was more obvious compared with endometrial tissue with severe IUAs; whereas, immunohistochemical staining of RhoA/ROCK1 in human endometrium with severe IUAs was more obvious compared with normal endometrial tissue. Scale bar, 50 µm. IUAs, intrauterine adhesions; ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1.

    Journal: Molecular Medicine Reports

    Article Title: MicroRNA-1291 promotes endometrial fibrosis by regulating the ArhGAP29-RhoA/ROCK1 signaling pathway in a murine model

    doi: 10.3892/mmr.2017.7210

    Figure Lengend Snippet: Immunohistochemical staining of ArhGAP29-RhoA/ROCK1 in human endometrium. ArhGAP29 staining in normal human endometrium was more obvious compared with endometrial tissue with severe IUAs; whereas, immunohistochemical staining of RhoA/ROCK1 in human endometrium with severe IUAs was more obvious compared with normal endometrial tissue. Scale bar, 50 µm. IUAs, intrauterine adhesions; ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1.

    Article Snippet: Immunohistochemistry, using a commercial primary anti-ArhGAP29 antibody (NBP1-05989; Novus Biologicals Canada ULC, Oakville, ON, Canada), RhoA (sc179; 1:50; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) and ROCK1 (ab45171; 1:200; Abcam, Cambridge, MA, USA) were used to investigate the differential expression of ArhGAP29 and RhoA/ROCK1 in severe IUAs compared with normal endometrial tissue.

    Techniques: Immunohistochemical staining, Staining

    Effect of miR-1291 antagomir on ArhGAP29-RhoA/ROCK1 pathway in murine uterine tissue. Immunofluorescence staining for ArhGAP29, RhoA and ROCK1 (green) and nuclear DNA (DAPI, blue) in murine uterine tissue from the IUAs group, miR-1291 antagomir group and the negative control group. Scale bar, 50 µm. ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1; IUAs, intrauterine adhesions; miR, microRNA.

    Journal: Molecular Medicine Reports

    Article Title: MicroRNA-1291 promotes endometrial fibrosis by regulating the ArhGAP29-RhoA/ROCK1 signaling pathway in a murine model

    doi: 10.3892/mmr.2017.7210

    Figure Lengend Snippet: Effect of miR-1291 antagomir on ArhGAP29-RhoA/ROCK1 pathway in murine uterine tissue. Immunofluorescence staining for ArhGAP29, RhoA and ROCK1 (green) and nuclear DNA (DAPI, blue) in murine uterine tissue from the IUAs group, miR-1291 antagomir group and the negative control group. Scale bar, 50 µm. ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1; IUAs, intrauterine adhesions; miR, microRNA.

    Article Snippet: Immunohistochemistry, using a commercial primary anti-ArhGAP29 antibody (NBP1-05989; Novus Biologicals Canada ULC, Oakville, ON, Canada), RhoA (sc179; 1:50; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) and ROCK1 (ab45171; 1:200; Abcam, Cambridge, MA, USA) were used to investigate the differential expression of ArhGAP29 and RhoA/ROCK1 in severe IUAs compared with normal endometrial tissue.

    Techniques: Immunofluorescence, Staining, Negative Control

    Effect of miR-1291 antagomir on ArhGAP29-RhoA/ROCK1 expression. (A) The expression levels of ArhGAP29, RhoA and ROCK1 were examined by reverse transcription-quantitative polymerase chain reaction. (B) Representative western-blot images and (C) densitometry of expression of ArhGAP29, RhoA and ROCK1 following western blotting analysis. ★ P<0.05, ★★ P<0.01 vs. the IUAs group; **P<0.01, ***P<0.001 vs. miR-1291 antagomir group. ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1; IUAs, intrauterine adhesions; miR, microRNA.

    Journal: Molecular Medicine Reports

    Article Title: MicroRNA-1291 promotes endometrial fibrosis by regulating the ArhGAP29-RhoA/ROCK1 signaling pathway in a murine model

    doi: 10.3892/mmr.2017.7210

    Figure Lengend Snippet: Effect of miR-1291 antagomir on ArhGAP29-RhoA/ROCK1 expression. (A) The expression levels of ArhGAP29, RhoA and ROCK1 were examined by reverse transcription-quantitative polymerase chain reaction. (B) Representative western-blot images and (C) densitometry of expression of ArhGAP29, RhoA and ROCK1 following western blotting analysis. ★ P<0.05, ★★ P<0.01 vs. the IUAs group; **P<0.01, ***P<0.001 vs. miR-1291 antagomir group. ArhGAP29, Rho GTPase activating protein 29; ROCK1, Rho-associated coiled-coil containing protein kinase 1; IUAs, intrauterine adhesions; miR, microRNA.

    Article Snippet: Immunohistochemistry, using a commercial primary anti-ArhGAP29 antibody (NBP1-05989; Novus Biologicals Canada ULC, Oakville, ON, Canada), RhoA (sc179; 1:50; Santa Cruz Biotechnology, Inc., Dallas, TX, USA) and ROCK1 (ab45171; 1:200; Abcam, Cambridge, MA, USA) were used to investigate the differential expression of ArhGAP29 and RhoA/ROCK1 in severe IUAs compared with normal endometrial tissue.

    Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot