arhgap29 (Novus Biologicals)

Novus Biologicals arhgap29

FIGURE 1 Characterization of <t>ARHGAP29</t> knockdown keratinocytes. (A) Western blot for ARHGAP29 (A29, top panel) and Ponceau red staining of the same membrane (bottom; one representative of three experiments) of keratinocytes transduced with CRISPR scrambled (sc), CRISPR ARHGAP29 (#1, #2), shRNA scramble, shRNA ARHGAP29 (#2, #3), and sh#3 transduced with ARHGAP29 (+A29) or GFP (+GFP). (B) Quantification of ARHGAP29 protein levels. Values are the means (N = 3) ± SEM, **p < .01 and ***p < .001 following ordinary one-way ANOVA test with Tukey's multiple comparisons post-hoc test (only relevant comparisons are shown). (C) Representative phase contrast micrographs of scramble, CRISPR knockdown, shRNA knockdown (sh#3) and shRNA knockdown keratinocytes transduced with ARHGAP29-GFP (sh#3 + A29), all grown in KSFM. Scale bar = 100 μm. (D) Quantification of keratinocyte area under the conditions shown in C. Boxes display the 25–75th percentiles where the line represents the median and whiskers display the minimum to maximum values, *p < .05, ***p < .001 and ****p < .0001 following Kruskal–Wallis test with Dunn's multiple comparisons post-hoc test (only relevant comparisons are shown). N = 200–400 cells per group. ns, non-significant.

Arhgap29, supplied by Novus Biologicals, 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/product/parg1+antibody/PARG1+Antibody/pm39560169-264-52-53
Average 93 stars, based on 1 article reviews

arhgap29 - by Bioz Stars, 2026-09

93/100 stars

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parg1 (arhgap29 maxpab polyclonal antibody) ab (Abnova)

Abnova parg1 (arhgap29 maxpab polyclonal antibody) ab

Identification of RCC antigen <t>PARG1</t> by SEREX and expression of PARG1 mRNA in normal kidney, RCC tissues, and RCC cell lines. (A) Presence of anti-PARG1 IgG from sera of RCC was detected by Western blot analysis with recombinant His-tagged PARG1 protein. Detection samples are shown in red. (B) Frequent detection of anti-PARG1 IgG in sera from patients with RCC was evaluated by ELISA. ELISA was done with the recombinant PARG1 protein. The horizontal line indicates the cutoff value for positivity (OD = 0.032: the average absorbance of the healthy individuals plus 2 SD). Positive sera were found in 13 of 24 (54.2%) patients with RCC but not in healthy donors. (C) Expression of PARG1 mRNA in normal kidney and RCC tissue in the same RCC patient sample was detected by qPCR analysis. GAPDH mRNA expression was used as an internal control. (D) Expression of PARG1 in human RCC cell lines was detected by qPCR analysis. GAPDH was used as an internal control. HEK293T was used as control sample for this assay.

Parg1 (Arhgap29 Maxpab Polyclonal Antibody) Ab, supplied by Abnova, 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/product/parg1+antibody/parg1++arhgap29+maxpab+polyclonal+antibody++ab/pmc05284488-110-0-8
Average 90 stars, based on 1 article reviews

parg1 (arhgap29 maxpab polyclonal antibody) ab - by Bioz Stars, 2026-09

90/100 stars

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parg1 antibody (biorbyt)

N/A

Rabbit Polyclonal to PARG1. Isotype Note: IgG Host Note: Rabbit Conjugation Note: Unconjugated Reactivity Note: Human, Mouse, Rat Application Note: WB, IHC-P, P-ELISA

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parg1 antibody [hrp] (Novus Biologicals)

N/A

The PARG1 Antibody [HRP] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody (Novus Biologicals)

N/A

The PARG1 Antibody from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human. The PARG1 antibody has been validated for the following applications: Western Blot, Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody [alexa fluor® 405] (Novus Biologicals)

N/A

The PARG1 Antibody [Alexa Fluor® 405] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody [alexa fluor® 488] (Novus Biologicals)

N/A

The PARG1 Antibody [Alexa Fluor® 488] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody [dylight 680] (Novus Biologicals)

N/A

The PARG1 Antibody [DyLight 680] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody [dylight 594] (Novus Biologicals)

N/A

The PARG1 Antibody [DyLight 594] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody [alexa fluor® 350] (Novus Biologicals)

N/A

The PARG1 Antibody [Alexa Fluor® 350] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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parg1 antibody [alexa fluor® 532] (Novus Biologicals)

N/A

The PARG1 Antibody [Alexa Fluor® 532] from Novus is a PARG1 antibody to PARG1. This antibody reacts with Human, Mouse. The PARG1 antibody has been validated for the following applications: Immunocytochemistry/ Immunofluorescence, Immunoprecipitation.

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Image Search Results

FIGURE 1 Characterization of ARHGAP29 knockdown keratinocytes. (A) Western blot for ARHGAP29 (A29, top panel) and Ponceau red staining of the same membrane (bottom; one representative of three experiments) of keratinocytes transduced with CRISPR scrambled (sc), CRISPR ARHGAP29 (#1, #2), shRNA scramble, shRNA ARHGAP29 (#2, #3), and sh#3 transduced with ARHGAP29 (+A29) or GFP (+GFP). (B) Quantification of ARHGAP29 protein levels. Values are the means (N = 3) ± SEM, **p < .01 and ***p < .001 following ordinary one-way ANOVA test with Tukey's multiple comparisons post-hoc test (only relevant comparisons are shown). (C) Representative phase contrast micrographs of scramble, CRISPR knockdown, shRNA knockdown (sh#3) and shRNA knockdown keratinocytes transduced with ARHGAP29-GFP (sh#3 + A29), all grown in KSFM. Scale bar = 100 μm. (D) Quantification of keratinocyte area under the conditions shown in C. Boxes display the 25–75th percentiles where the line represents the median and whiskers display the minimum to maximum values, *p < .05, ***p < .001 and ****p < .0001 following Kruskal–Wallis test with Dunn's multiple comparisons post-hoc test (only relevant comparisons are shown). N = 200–400 cells per group. ns, non-significant.

Journal: Developmental dynamics : an official publication of the American Association of Anatomists

Article Title: ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing.

doi: 10.1002/dvdy.759

Figure Lengend Snippet: FIGURE 1 Characterization of ARHGAP29 knockdown keratinocytes. (A) Western blot for ARHGAP29 (A29, top panel) and Ponceau red staining of the same membrane (bottom; one representative of three experiments) of keratinocytes transduced with CRISPR scrambled (sc), CRISPR ARHGAP29 (#1, #2), shRNA scramble, shRNA ARHGAP29 (#2, #3), and sh#3 transduced with ARHGAP29 (+A29) or GFP (+GFP). (B) Quantification of ARHGAP29 protein levels. Values are the means (N = 3) ± SEM, **p < .01 and ***p < .001 following ordinary one-way ANOVA test with Tukey's multiple comparisons post-hoc test (only relevant comparisons are shown). (C) Representative phase contrast micrographs of scramble, CRISPR knockdown, shRNA knockdown (sh#3) and shRNA knockdown keratinocytes transduced with ARHGAP29-GFP (sh#3 + A29), all grown in KSFM. Scale bar = 100 μm. (D) Quantification of keratinocyte area under the conditions shown in C. Boxes display the 25–75th percentiles where the line represents the median and whiskers display the minimum to maximum values, *p < .05, ***p < .001 and ****p < .0001 following Kruskal–Wallis test with Dunn's multiple comparisons post-hoc test (only relevant comparisons are shown). N = 200–400 cells per group. ns, non-significant.

Article Snippet: The following antibodies were used for immunofluorescence: Phalloidin-TRITC (Sigma-Aldrich, St Louis, MO; catalog #P1951) was used at 1/10,000; rabbit polyclonal against phospho-Myosin regulatory light chain 2 at position Ser19 (Cell Signaling, Danvers, MA; catalog #3671) was used at 1/100 (in Figure 2, used with Alexa Fluor 488 goat anti-mouse); rabbit polyclonal against ARHGAP29 (Novus Biologicals, catalog #NBP1-05989) was used at 1/150; mouse monoclonal against Keratin 14 (Santa Cruz Biotechnology, catalog #sc-53253) was used at 1/20; Alexa Fluor 488 goat anti-mouse and antirabbit IgG (Invitrogen, Waltham, MA; catalog #A-11001 (mouse) and A-11008 (rabbit)) and Alexa Fluor 568 goat anti-mouse and anti-rabbit IgG (Invitrogen, catalog #A11004 (mouse) and A-11011 (rabbit)) were used at 1/200.

Techniques: Knockdown, Western Blot, Staining, Membrane, Transduction, CRISPR, shRNA

FIGURE 3 ARHGAP29 promotes keratinocyte proliferation. (A) Quantification of population doubling time. Values are the means ± SEM, *p < .05 following Brown–Forsythe test and Welch ANOVA test with Dunnett's T3 multiple comparisons post-hoc test. N = 6–8 per group. (B) Representative images of colony forming efficiency dishes with CRISPR scramble (CRISPRsc), CRISPR ARHGAP29 (CRISPR#1), shRNA scramble (shSc) and shRNA ARHGAP29 (sh#3) keratinocytes. (C) Quantification of colony area for all cell lines (including those represented in B). N = 752–1639 per group. Values are the means ± SEM, ****p < .0001 following Kruskal–Wallis test with Dunn's multiple comparisons post-hoc test (only comparisons to scrambled are shown). (D) Quantification of number of cells per colony for all cell lines (N = 9–12). Values are the means ± SEM, **p < .01, ****p < .0001 following ordinary one-way ANOVA with Tukey's multiple comparisons post-hoc test (only comparisons to scrambled are shown). (E) Quantification of number of cells per colony area (“cell density”) for all cell lines (N = 9–12). Values are the means ± SEM, *p < .05, ****p < .0001 following ordinary one-way ANOVA with Tukey's multiple comparisons post-hoc test. Only comparisons to scrambled are shown.

Journal: Developmental dynamics : an official publication of the American Association of Anatomists

Article Title: ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing.

doi: 10.1002/dvdy.759

Figure Lengend Snippet: FIGURE 3 ARHGAP29 promotes keratinocyte proliferation. (A) Quantification of population doubling time. Values are the means ± SEM, *p < .05 following Brown–Forsythe test and Welch ANOVA test with Dunnett's T3 multiple comparisons post-hoc test. N = 6–8 per group. (B) Representative images of colony forming efficiency dishes with CRISPR scramble (CRISPRsc), CRISPR ARHGAP29 (CRISPR#1), shRNA scramble (shSc) and shRNA ARHGAP29 (sh#3) keratinocytes. (C) Quantification of colony area for all cell lines (including those represented in B). N = 752–1639 per group. Values are the means ± SEM, ****p < .0001 following Kruskal–Wallis test with Dunn's multiple comparisons post-hoc test (only comparisons to scrambled are shown). (D) Quantification of number of cells per colony for all cell lines (N = 9–12). Values are the means ± SEM, **p < .01, ****p < .0001 following ordinary one-way ANOVA with Tukey's multiple comparisons post-hoc test (only comparisons to scrambled are shown). (E) Quantification of number of cells per colony area (“cell density”) for all cell lines (N = 9–12). Values are the means ± SEM, *p < .05, ****p < .0001 following ordinary one-way ANOVA with Tukey's multiple comparisons post-hoc test. Only comparisons to scrambled are shown.

Techniques: CRISPR, shRNA

FIGURE 5 ARHGAP29 promotes collective cell migration. (A) Phase contrast micrographs of in vitro scratch wounds in confluent monolayers of shRNA scramble (shSc), shRNA ARHGAP29 (sh#3), and sh#3 transduced with ARHGAP29 (sh#3 + A29) keratinocytes grown in DMEM:HAM. Scale bar = 100 μm. T0 = 0 h after scratch and T 12 = 12 h after scratch. (B) Quantifications of the percentage of scratch closure over a 12-h period in all CRISPR and shRNA cell lines compared to their respective scrambled controls. Values are the means ± SEM, *p < .05 and **p < .01 after two-way ANOVA with Tukey's multiple comparisons post-hoc test. N = 6 per group.

Journal: Developmental dynamics : an official publication of the American Association of Anatomists

Article Title: ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing.

doi: 10.1002/dvdy.759

Figure Lengend Snippet: FIGURE 5 ARHGAP29 promotes collective cell migration. (A) Phase contrast micrographs of in vitro scratch wounds in confluent monolayers of shRNA scramble (shSc), shRNA ARHGAP29 (sh#3), and sh#3 transduced with ARHGAP29 (sh#3 + A29) keratinocytes grown in DMEM:HAM. Scale bar = 100 μm. T0 = 0 h after scratch and T 12 = 12 h after scratch. (B) Quantifications of the percentage of scratch closure over a 12-h period in all CRISPR and shRNA cell lines compared to their respective scrambled controls. Values are the means ± SEM, *p < .05 and **p < .01 after two-way ANOVA with Tukey's multiple comparisons post-hoc test. N = 6 per group.

Techniques: Migration, In Vitro, shRNA, Transduction, CRISPR

FIGURE 6 ARHGAP29 is present in embryonic, but not in adult keratinocytes, and is upregulated following wounding. (A)– (F) Immunofluorescent staining for ARHGAP29 (cyan) of murine wild-type skin of an unwounded E14.5 embryo (A), E18.5 embryo (B), adult (C), and of a 2-day (D), 4-day (E), and 7-day (F) wound. Nuclear DNA is stained with Hoechst (magenta). Scale bar = 50 μm; yellow arrow heads indicate the leading edge of the epidermis in open wounds and white dotted lines indicate the epidermal–dermal junction. HF, hair follicle. One representative image of N = 3 per time point. (G) Western blot analysis for ARHGAP29 and GAPDH protein levels of E14.5, E17.5 and adult unwounded skin extracts. (H) Quantification of ARHGAP29 levels shown in panel G normalized to GAPDH (loading) and to E14.5 values used as the reference developmental time point. Values are the means ± SEM, *p < .05 and after ordinary one-way ANOVA with Tukey's multiple comparisons post-hoc test. N = 3 per group. (I) Quantification of ARHGAP29 levels (using immunofluorescent signal) in keratinocytes at different time points during wound healing. Values are the means ± SEM, *p < .05 and **p < .01 after ordinary one-way ANOVA with Dunnett's multiple comparisons post-hoc test. N = 3 per group.

Journal: Developmental dynamics : an official publication of the American Association of Anatomists

Article Title: ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing.

doi: 10.1002/dvdy.759

Figure Lengend Snippet: FIGURE 6 ARHGAP29 is present in embryonic, but not in adult keratinocytes, and is upregulated following wounding. (A)– (F) Immunofluorescent staining for ARHGAP29 (cyan) of murine wild-type skin of an unwounded E14.5 embryo (A), E18.5 embryo (B), adult (C), and of a 2-day (D), 4-day (E), and 7-day (F) wound. Nuclear DNA is stained with Hoechst (magenta). Scale bar = 50 μm; yellow arrow heads indicate the leading edge of the epidermis in open wounds and white dotted lines indicate the epidermal–dermal junction. HF, hair follicle. One representative image of N = 3 per time point. (G) Western blot analysis for ARHGAP29 and GAPDH protein levels of E14.5, E17.5 and adult unwounded skin extracts. (H) Quantification of ARHGAP29 levels shown in panel G normalized to GAPDH (loading) and to E14.5 values used as the reference developmental time point. Values are the means ± SEM, *p < .05 and after ordinary one-way ANOVA with Tukey's multiple comparisons post-hoc test. N = 3 per group. (I) Quantification of ARHGAP29 levels (using immunofluorescent signal) in keratinocytes at different time points during wound healing. Values are the means ± SEM, *p < .05 and **p < .01 after ordinary one-way ANOVA with Dunnett's multiple comparisons post-hoc test. N = 3 per group.

Techniques: Staining, Western Blot

Identification of RCC antigen PARG1 by SEREX and expression of PARG1 mRNA in normal kidney, RCC tissues, and RCC cell lines. (A) Presence of anti-PARG1 IgG from sera of RCC was detected by Western blot analysis with recombinant His-tagged PARG1 protein. Detection samples are shown in red. (B) Frequent detection of anti-PARG1 IgG in sera from patients with RCC was evaluated by ELISA. ELISA was done with the recombinant PARG1 protein. The horizontal line indicates the cutoff value for positivity (OD = 0.032: the average absorbance of the healthy individuals plus 2 SD). Positive sera were found in 13 of 24 (54.2%) patients with RCC but not in healthy donors. (C) Expression of PARG1 mRNA in normal kidney and RCC tissue in the same RCC patient sample was detected by qPCR analysis. GAPDH mRNA expression was used as an internal control. (D) Expression of PARG1 in human RCC cell lines was detected by qPCR analysis. GAPDH was used as an internal control. HEK293T was used as control sample for this assay.

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: Identification of RCC antigen PARG1 by SEREX and expression of PARG1 mRNA in normal kidney, RCC tissues, and RCC cell lines. (A) Presence of anti-PARG1 IgG from sera of RCC was detected by Western blot analysis with recombinant His-tagged PARG1 protein. Detection samples are shown in red. (B) Frequent detection of anti-PARG1 IgG in sera from patients with RCC was evaluated by ELISA. ELISA was done with the recombinant PARG1 protein. The horizontal line indicates the cutoff value for positivity (OD = 0.032: the average absorbance of the healthy individuals plus 2 SD). Positive sera were found in 13 of 24 (54.2%) patients with RCC but not in healthy donors. (C) Expression of PARG1 mRNA in normal kidney and RCC tissue in the same RCC patient sample was detected by qPCR analysis. GAPDH mRNA expression was used as an internal control. (D) Expression of PARG1 in human RCC cell lines was detected by qPCR analysis. GAPDH was used as an internal control. HEK293T was used as control sample for this assay.

Article Snippet: PARG1 (ARHGAP29 MaxPab polyclonal antibody) Ab was from Abnova (Taiwan, Taipei), p21 Cip1/Waf1 Ab was from Carbioche (Germany), p53 (DO-1) Ab was from Santa Cruz Biotechnology (Delaware Avenue, CA), and phosphor-p53 (ser15) Ab was from Cell Signaling Technology.

Techniques: Expressing, Western Blot, Recombinant, Enzyme-linked Immunosorbent Assay, Control

Expression of PARG1 and survival analysis in patients with RCC. (A) Representative immunohistochemical analysis of PARG1 protein in paraffin-embedded tissues. (a) Normal proximal tubules (magnification, ×40), (b) RCC tissues (level 1), (c) RCC tissues (level 2), (d) RCC tissues (level 3), (e) pancreatic metastasis region, (f) lymph node metastasis legion, (g) microvascular invasion (magnification, ×10), and (h) microvascular invasion (high magnification, ×40). (B) RCC tissues were stained with anti–Ki-67 Ab, and Ki-67–positive cells (indicated by arrows) in high-powered field (HPF; magnification, ×40) were counted. The right graph shows the number of Ki-67–positive cells in each PARG1 expression level. (C) Kaplan-Meier overall survival curve with respect to low expression level ( n = 51) and high expression level ( n = 23) of PARG1. Five-year survival rate; P = .035. (D) Kaplan-Meier recurrence-free survival curve with respect to low expression level ( n = 40) and high expression level ( n = 13) of PARG1 in N0M0 patients with RCC. Five-year recurrence-free survival rate; P = .0084.

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: Expression of PARG1 and survival analysis in patients with RCC. (A) Representative immunohistochemical analysis of PARG1 protein in paraffin-embedded tissues. (a) Normal proximal tubules (magnification, ×40), (b) RCC tissues (level 1), (c) RCC tissues (level 2), (d) RCC tissues (level 3), (e) pancreatic metastasis region, (f) lymph node metastasis legion, (g) microvascular invasion (magnification, ×10), and (h) microvascular invasion (high magnification, ×40). (B) RCC tissues were stained with anti–Ki-67 Ab, and Ki-67–positive cells (indicated by arrows) in high-powered field (HPF; magnification, ×40) were counted. The right graph shows the number of Ki-67–positive cells in each PARG1 expression level. (C) Kaplan-Meier overall survival curve with respect to low expression level ( n = 51) and high expression level ( n = 23) of PARG1. Five-year survival rate; P = .035. (D) Kaplan-Meier recurrence-free survival curve with respect to low expression level ( n = 40) and high expression level ( n = 13) of PARG1 in N0M0 patients with RCC. Five-year recurrence-free survival rate; P = .0084.

Techniques: Expressing, Immunohistochemical staining, Staining

Correlation between PARG1 Expression and Clinicopathological Features in RCC Patients

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: Correlation between PARG1 Expression and Clinicopathological Features in RCC Patients

Techniques: Expressing

Correlation between Clinicopathological Features and Overall Survival in 74 RCC Patients

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: Correlation between Clinicopathological Features and Overall Survival in 74 RCC Patients

Techniques:

High PARG1 Expression Is an Independent Factor Correlating with 53 RCC Recurrence in N0M0 Patients

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: High PARG1 Expression Is an Independent Factor Correlating with 53 RCC Recurrence in N0M0 Patients

Techniques: Expressing

PARG1 was involved in cell proliferation and cell cycle progression through regulation of p53 and p21 Cip1/Waf1 in RCC cell lines. (A) Decrease of PARG1 mRNA and protein was observed after 2 days of incubation with two PARG1-specific siRNAs (si#2 and si#3) in SW839 and 769-p, whereas increase of PARG1 mRNA and protein was observed after 2 days of incubation with pcDNA3.1-PARG1 vector in HEK293T. (B) The inhibition of cell proliferation of SW839 and 769-p after 3 days of incubation with PARG1 siRNAs was observed in WST-1 assay (left graph) or trypan blue cell count (right graph); however, cell proliferation of HEK293T was increased by transfection with pcDNA3.1-PARG1. ** P < .01; data are presented as the mean ± SD of three independent experiments. (C) Cell cycle analysis confirmed that treating SW839 and 769-p cells with PARG1 siRNA blocked the cell cycle in G1 phase at day 3 after transfection. (D) PARG1 siRNA upregulated p53, p-p53(Ser15), and p21 Cip1/Waf1 protein expression by Western blotting in SW839 and 769-p. GAPDH was used as control. Representative results from three independent experiments (C, D).

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: PARG1 was involved in cell proliferation and cell cycle progression through regulation of p53 and p21 Cip1/Waf1 in RCC cell lines. (A) Decrease of PARG1 mRNA and protein was observed after 2 days of incubation with two PARG1-specific siRNAs (si#2 and si#3) in SW839 and 769-p, whereas increase of PARG1 mRNA and protein was observed after 2 days of incubation with pcDNA3.1-PARG1 vector in HEK293T. (B) The inhibition of cell proliferation of SW839 and 769-p after 3 days of incubation with PARG1 siRNAs was observed in WST-1 assay (left graph) or trypan blue cell count (right graph); however, cell proliferation of HEK293T was increased by transfection with pcDNA3.1-PARG1. ** P < .01; data are presented as the mean ± SD of three independent experiments. (C) Cell cycle analysis confirmed that treating SW839 and 769-p cells with PARG1 siRNA blocked the cell cycle in G1 phase at day 3 after transfection. (D) PARG1 siRNA upregulated p53, p-p53(Ser15), and p21 Cip1/Waf1 protein expression by Western blotting in SW839 and 769-p. GAPDH was used as control. Representative results from three independent experiments (C, D).

Techniques: Incubation, Plasmid Preparation, Inhibition, WST-1 Assay, Cell Counting, Transfection, Cell Cycle Assay, Expressing, Western Blot, Control

The role of PARG1 involved in cell invasion and migration through inhibition of RhoA activity. (A) Cell invasion ability was evaluated by Matrigel invasion assay in RCC cell lines and HEK293T. Invasion ability was decreased in PARG1 siRNA-transfected SW839 and 769-p cells, but invasion ability was increased in PARG1 expression vector–transfected HEK293T cells. * P < .05, ** P < .01; data are presented as the mean ± SD of three independent experiments. (B) Cell migration ability was performed by wound healing assay. Migration ability was decreased in PARG1 siRNA-transfected SW839 and 769-p cells at 10 hours of incubation; however, migration ability was increased in PARG1 expression vector–transfected HEK293T cells at 24 hours of incubation. * P < .05; data are presented as the mean ± SD of three independent experiments. (C) Effect of PARG1 on RhoA activity was determined using RhoA activation kit (pull-down assay and Western blotting). PARG1 siRNAs induced RhoA-GTP in RCC cell lines, but PARG1 expression vector reduced RhoA-GTP in HEK293T cells. (D) Scramble and PARG1 siRNAs-transfected SW839 cells were stained with PARG1 (FITC), F-actin (Texas red), and DAPI. Downregulation of PARG1 by siRNA induced actin stress fiber formation. Representative results from three independent experiments (C, D).

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: The role of PARG1 involved in cell invasion and migration through inhibition of RhoA activity. (A) Cell invasion ability was evaluated by Matrigel invasion assay in RCC cell lines and HEK293T. Invasion ability was decreased in PARG1 siRNA-transfected SW839 and 769-p cells, but invasion ability was increased in PARG1 expression vector–transfected HEK293T cells. * P < .05, ** P < .01; data are presented as the mean ± SD of three independent experiments. (B) Cell migration ability was performed by wound healing assay. Migration ability was decreased in PARG1 siRNA-transfected SW839 and 769-p cells at 10 hours of incubation; however, migration ability was increased in PARG1 expression vector–transfected HEK293T cells at 24 hours of incubation. * P < .05; data are presented as the mean ± SD of three independent experiments. (C) Effect of PARG1 on RhoA activity was determined using RhoA activation kit (pull-down assay and Western blotting). PARG1 siRNAs induced RhoA-GTP in RCC cell lines, but PARG1 expression vector reduced RhoA-GTP in HEK293T cells. (D) Scramble and PARG1 siRNAs-transfected SW839 cells were stained with PARG1 (FITC), F-actin (Texas red), and DAPI. Downregulation of PARG1 by siRNA induced actin stress fiber formation. Representative results from three independent experiments (C, D).

Techniques: Migration, Inhibition, Activity Assay, Invasion Assay, Transfection, Expressing, Plasmid Preparation, Wound Healing Assay, Incubation, Activation Assay, Pull Down Assay, Western Blot, Staining

PARG1 promoted cell proliferation and invasion through inhibition of RhoA-ROCK signaling. (A) Dependency of cell proliferation ability on RhoA-ROCK signaling was evaluated by WST-1 assay with Rho-ROCK inhibitor Y27632 (1 μM) on PARG1-silenced SW839 RCC cells. Cell proliferation was restored in PARG1 siRNA transfected SW839 cell line by addition of Y27632 at day 2, compared with PBS treatment. * P < .05, ** P < .01; data are presented as the mean ± SD of three independent experiments. (B) Dependency of cell invasion ability on RhoA-ROCK signaling was evaluated by xCELLigence system analysis as described in Materials and Methods with Y27632 (1 μM) on PARG1-silenced SW839 cells by siRNA. PBS was used as control. Cell invasion ability was rescued by treatment with Y27632 in PARG1 siRNA transfected. SW839 cells transfected with scrambled or PARG1 siRNAs were treated with PBS or Y27632. * P < .05, ** P < .01; data are presented as the mean ± SD of three independent experiments. (C) The impact of Rho-ROCK inhibition on expressions of p53, p-p53 (Ser15), and p21 Cip1/Waf1 was evaluated by Western blotting in SW839 cells treated with scrambled or PARG1 siRNAs. Representative results from three independent experiments. PBS was used as control. (D) Schematic representation of the functional role of PARG1 involved in cell proliferation, migration, and invasion through regulation of RhoA-ROCK signaling pathway.

Journal: Translational Oncology

Article Title: Progression of Human Renal Cell Carcinoma via Inhibition of RhoA-ROCK Axis by PARG1 1 2

doi: 10.1016/j.tranon.2016.12.004

Figure Lengend Snippet: PARG1 promoted cell proliferation and invasion through inhibition of RhoA-ROCK signaling. (A) Dependency of cell proliferation ability on RhoA-ROCK signaling was evaluated by WST-1 assay with Rho-ROCK inhibitor Y27632 (1 μM) on PARG1-silenced SW839 RCC cells. Cell proliferation was restored in PARG1 siRNA transfected SW839 cell line by addition of Y27632 at day 2, compared with PBS treatment. * P < .05, ** P < .01; data are presented as the mean ± SD of three independent experiments. (B) Dependency of cell invasion ability on RhoA-ROCK signaling was evaluated by xCELLigence system analysis as described in Materials and Methods with Y27632 (1 μM) on PARG1-silenced SW839 cells by siRNA. PBS was used as control. Cell invasion ability was rescued by treatment with Y27632 in PARG1 siRNA transfected. SW839 cells transfected with scrambled or PARG1 siRNAs were treated with PBS or Y27632. * P < .05, ** P < .01; data are presented as the mean ± SD of three independent experiments. (C) The impact of Rho-ROCK inhibition on expressions of p53, p-p53 (Ser15), and p21 Cip1/Waf1 was evaluated by Western blotting in SW839 cells treated with scrambled or PARG1 siRNAs. Representative results from three independent experiments. PBS was used as control. (D) Schematic representation of the functional role of PARG1 involved in cell proliferation, migration, and invasion through regulation of RhoA-ROCK signaling pathway.

Techniques: Inhibition, WST-1 Assay, Transfection, Control, Western Blot, Functional Assay, Migration

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