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rabbit anti pak1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti pak1
    Rabbit Anti Pak1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 778 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pak1/PAK1+Antibody/10__1038_slash_s41467___026___78499___5-321-31-34
    Average 96 stars, based on 778 article reviews
    rabbit anti pak1 - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    Western Blot:

    Article Title: Synergistic intragenic epigenetic deregulation by IDH2 and SRSF2 mutations causes mis-splicing of key transcriptional regulators
    Article Snippet: Thirty-five micrograms of protein lysate from each sample was loaded on 4 to 12% Bis-Tris gels (Invitrogen, NP0335BOX), transferred to polyvinylidene difluoride membrane using the iBlot 2 Gel Transfer Device (Invitrogen, #IB21001), and blocked with Intercept Blocking Buffer (LI-COR, #927-60003). .. The following antibodies were used for Western blot analysis: PAK1 (Cell Signaling Technology, #2602; RRID:AB_330222), CCM2 (Cell Signaling Technology, #32463), PPOX (Santa Cruz, #sc-271768; RRID:AB_10708546), and ACTIN (1:5000; Cell Signaling Technology, #3700s; RRID:AB_2242334 or #4970s; RRID:AB_2223172). .. All primary antibodies were diluted to a final concentration of 1:1000 in Intercept Antibody Diluent (LI-COR) unless otherwise noted.

    Article Title: Synergistic intragenic epigenetic deregulation by IDH2 and SRSF2 mutations causes mis-splicing of key transcriptional regulators.
    Article Snippet: Thirty- five micrograms of protein lysate from each sample was loaded on 4 to 12% Bis- Tris gels (Invitrogen, NP0335BOX), transferred to polyvinylidene difluoride membrane using the iBlot 2 Gel Transfer Device (Invitrogen, #IB21001), and blocked with Intercept Blocking Buffer (LI- COR, #927- 60003). .. The following antibodies were used for Western blot analysis: PAK1 (Cell Signaling Technology, #2602; RRID:AB_330222), CCM2 (Cell Signaling Technology, #32463), PPOX (Santa Cruz, #sc- 271768; RRID:AB_10708546), and ACTIN (1:5000; Cell Signaling Technology, #3700s; RRID:AB_2242334 or #4970s; RRID:AB_2223172). .. All primary antibodies were diluted to a final concentration of 1:1000 in Intercept Antibody Diluent (LI- COR) unless otherwise noted.

    Article Title: Rational discovery of therapeutic PAK1 allosteric activators.
    Article Snippet: Protein concentration was determined by Bio-Rad protein assay. .. Protein extracts (30 μg) were subject to immunoblot analyses with antibodies (all antibodies applied in this study were used as 1:1000 dilution) against PAK1 (Cell Signaling, 2602), CHOP (Cell Signaling, 2895), phospho-PAK1 (Cell signaling, 2601), phospho-PERK (Cell Signaling, 3179), ATF6 (Abcam, ab37149), BiP (Cell signaling, 3183), ATF4 (Abcam, ab85049), GADPH (Cell Signaling, 92310). ..

    Cell-Signaling:

    Article Title: DOCK10 Regulates Insulin Hypersecretion in Insulinoma and Serves as a Diagnostic and Therapeutic Target
    Article Snippet: Primary antibodies for Western blotting , , , . .. PAK1 , Cell Signaling Technology , 2602S , 1:100. .. phospho PAK1 , Cell Signaling Technology , 2601S , 1:10.

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST (50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20) and incubated with primary antibody solutions, such as PAK1 (1:1000), Rac1/Cdc42 (1:1000; Cell Signaling, Cat# 4651S), Igα−5 (1:1000; Cell Signaling, Cat# 4705S), or FLAG antibody (1:1000; Milipore-Sigma, Cat# F3165), diluted in a blocking buffer overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphor-paxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α−5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4°C. ..

    Membrane:

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST (50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20) and incubated with primary antibody solutions, such as PAK1 (1:1000), Rac1/Cdc42 (1:1000; Cell Signaling, Cat# 4651S), Igα−5 (1:1000; Cell Signaling, Cat# 4705S), or FLAG antibody (1:1000; Milipore-Sigma, Cat# F3165), diluted in a blocking buffer overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphor-paxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α−5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation.
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphopaxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α-5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4oC. ..

    Incubation:

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST (50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20) and incubated with primary antibody solutions, such as PAK1 (1:1000), Rac1/Cdc42 (1:1000; Cell Signaling, Cat# 4651S), Igα−5 (1:1000; Cell Signaling, Cat# 4705S), or FLAG antibody (1:1000; Milipore-Sigma, Cat# F3165), diluted in a blocking buffer overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphor-paxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α−5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation.
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphopaxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α-5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4oC. ..

    Blocking Assay:

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST (50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20) and incubated with primary antibody solutions, such as PAK1 (1:1000), Rac1/Cdc42 (1:1000; Cell Signaling, Cat# 4651S), Igα−5 (1:1000; Cell Signaling, Cat# 4705S), or FLAG antibody (1:1000; Milipore-Sigma, Cat# F3165), diluted in a blocking buffer overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphor-paxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α−5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4°C. ..

    Article Title: Redox regulation of cell migration via Nischarin S-glutathionylation.
    Article Snippet: .. The membrane was blocked with 5 % BSA in TBST containing 50 mM Tris-HCl, 150 mM NaCl, and 0.1 % Tween-20, and incubated with primary antibody solution, containing phospho-PAK1 (p423) (1:1000; Cell Signaling, Cat# 2601S), PAK1 (1:1000; Cell Signaling, Cat# 2608S), phospho-cofilin-Ser-3 (Cell Signaling, Cat# 3311S), Cofilin (Cell Signaling, Cat# 3318S), phospho-LIMK-1 (Cell Signaling, Cat# 3841S), LIMK1 (Cell Signaling, Cat# 3842S), phosphopaxillin (Cell Signaling, Cat# 441026G), Paxillin (Cell Signaling, Cat# 2542S) NISCH (D6T4X) (Cell Signaling, Cat# 85124S), phospho-p38 MAPK (1:1000; Cell Signaling, Cat# 9211S), p38 MAPK (1:1000; Cell Signaling, Cat# 9212S), phospho-MEK1/2 (1:1000; Cell Signaling, Cat# 9154S), MEK1/2 (1:1000; Cell Signaling, Cat# 9122S), phospho-p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9101S), p44/42 MAPK (ERK1/2) (1:1000; Cell Signaling, Cat# 9102S), phospho-JNK (1:1000; Cell Signaling, Cat# 9251S), JNK (1:1000; Cell Signaling, Cat# 9252S), phospho-p38 (1:1000; Cell Signaling, Cat# 9211S), p38 (1:1000; Cell Signaling, Cat# 9212S), Integrin α-5 (Cell Signaling, Cat# 4705S), GSTO1/2 (1:1000; Santa Cruz, Cat# sc-166040), GSTP (1:1000; MBL Life Science, Cat# 311-H), Glrx3 (1:1000; Sigma, Cat# SAB1410104), or FLAG antibody (1:1000; Millipore-Sigma, Cat# F3165), diluted in a blocking buffer and incubated for overnight at 4oC. ..

    other:

    Article Title: CtBP1 sustains activity-dependent muscle properties and dampens synaptic, contractile and metabolic changes triggered by denervation.
    Article Snippet: AChR turnover was assessed by sequential injection of 25 pmoles of α-bungarotoxin-Alexa488 and -Alexa555 (Invitrogen), as previously done [28].



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    Image Search Results


    PAK1 expression is adversely associated with the overall survival of ovarian cancer patients. (A) Genetic alterations of PAK1 across different cancer types, as retrieved from the cBioPortal database. (B) PAK1 expression patterns across a variety of cancers. (C) Association between PAK1 expression levels and copy number variations. (D) Correlation of PAK1 expression with homologous recombination (HR) status. (E) Kaplan–Meier survival analysis comparing ovarian cancer patient outcomes with low ( n = 467) and high ( n = 188) PAK1 expression levels.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: PAK1 expression is adversely associated with the overall survival of ovarian cancer patients. (A) Genetic alterations of PAK1 across different cancer types, as retrieved from the cBioPortal database. (B) PAK1 expression patterns across a variety of cancers. (C) Association between PAK1 expression levels and copy number variations. (D) Correlation of PAK1 expression with homologous recombination (HR) status. (E) Kaplan–Meier survival analysis comparing ovarian cancer patient outcomes with low ( n = 467) and high ( n = 188) PAK1 expression levels.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Expressing, Homologous Recombination

    PAK1 regulates homologous recombination (HR) repair and olaparib sensitivity in ovarian cancer cells. (A, B) HR (A) and non-homologous end-joining (NHEJ) (B) repair efficiencies in control and PAK1-depleted HEK293T cells, evaluated using HR and NHEJ reporter systems. Data were presented as mean ± standard error of the mean from three independent experiments. (C) Western blotting analysis of PAK2 and PAK3 in control and PAK2/PAK3-depleted HEK293T cells. (D – G) HR (D, F) and NHEJ (E, G) repair efficiencies in control and PAK2/PAK3-depleted HEK293T cells, evaluated using HR and NHEJ reporter systems. (H, I) Cell cycle distribution in control and PAK1-depleted Ovcar8 cells, analyzed by flow cytometry. (J, K) RAD51 foci formation in Ovcar8 cells treated with 10 μM olaparib for 24 h: (J) representative images and (K) quantification. More than 200 cells were analyzed per experiment. (L, N) The survival of control or PAK1-depleted Ovcar8 (L) and SKOV-3 (N) cells, assessed by colony formation assay. (M, O) Phosphorylation of CHK1 in control or PAK1-depleted Ovcar8 (M) and SKOV-3 (O) cells, treated with 10 μM olaparib for 6 h. (P, Q) The survival of control, (P) PAK2-depleted, or (Q) PAK3-depleted Ovcar8 cells, assessed by colony formation assay. Error bars represent the standard error of the mean from three independent experiments. Scale bars = 50 μm.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: PAK1 regulates homologous recombination (HR) repair and olaparib sensitivity in ovarian cancer cells. (A, B) HR (A) and non-homologous end-joining (NHEJ) (B) repair efficiencies in control and PAK1-depleted HEK293T cells, evaluated using HR and NHEJ reporter systems. Data were presented as mean ± standard error of the mean from three independent experiments. (C) Western blotting analysis of PAK2 and PAK3 in control and PAK2/PAK3-depleted HEK293T cells. (D – G) HR (D, F) and NHEJ (E, G) repair efficiencies in control and PAK2/PAK3-depleted HEK293T cells, evaluated using HR and NHEJ reporter systems. (H, I) Cell cycle distribution in control and PAK1-depleted Ovcar8 cells, analyzed by flow cytometry. (J, K) RAD51 foci formation in Ovcar8 cells treated with 10 μM olaparib for 24 h: (J) representative images and (K) quantification. More than 200 cells were analyzed per experiment. (L, N) The survival of control or PAK1-depleted Ovcar8 (L) and SKOV-3 (N) cells, assessed by colony formation assay. (M, O) Phosphorylation of CHK1 in control or PAK1-depleted Ovcar8 (M) and SKOV-3 (O) cells, treated with 10 μM olaparib for 6 h. (P, Q) The survival of control, (P) PAK2-depleted, or (Q) PAK3-depleted Ovcar8 cells, assessed by colony formation assay. Error bars represent the standard error of the mean from three independent experiments. Scale bars = 50 μm.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Homologous Recombination, Non-Homologous End Joining, Control, Western Blot, Flow Cytometry, Colony Assay, Phospho-proteomics

    PAK1 regulates homologous recombination (HR) repair and olaparib sensitivity dependent on its kinase activity. PAK1-depleted cells were transfected with wild-type PAK1 or the K299R kinase mutant for 24 h. (A) Western blotting analysis of PAK1 and CHK1 phosphorylation in transfected Ovcar8 cells treated with 10 μM olaparib for 6 h. (B) The survival of transfected Ovcar8 cells treated with different concentrations of olaparib for 2 weeks, assessed by colony formation assay. (C) HR activity in transfected HEK293T cells co-transfected with HR reporter plasmids, followed by HR assay after 48 h. (D, E) RAD51 foci formation in transfected Ovcar8 cells treated with 10 μM olaparib for 24 h: (D) representative images and (E) quantification. Over 200 cells were analyzed in each experiment. Error bars represent the standard error of the mean from three independent experiments.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: PAK1 regulates homologous recombination (HR) repair and olaparib sensitivity dependent on its kinase activity. PAK1-depleted cells were transfected with wild-type PAK1 or the K299R kinase mutant for 24 h. (A) Western blotting analysis of PAK1 and CHK1 phosphorylation in transfected Ovcar8 cells treated with 10 μM olaparib for 6 h. (B) The survival of transfected Ovcar8 cells treated with different concentrations of olaparib for 2 weeks, assessed by colony formation assay. (C) HR activity in transfected HEK293T cells co-transfected with HR reporter plasmids, followed by HR assay after 48 h. (D, E) RAD51 foci formation in transfected Ovcar8 cells treated with 10 μM olaparib for 24 h: (D) representative images and (E) quantification. Over 200 cells were analyzed in each experiment. Error bars represent the standard error of the mean from three independent experiments.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Homologous Recombination, Activity Assay, Transfection, Mutagenesis, Western Blot, Phospho-proteomics, Colony Assay

    PAK1 inhibition enhances the efficiency of olaparib in ovarian cancer cells. (A) Western blotting analysis of PAK1 and CHK1 phosphorylation in Ovcar8 cells treated with 10 μM olaparib, 10 μM IPA-3, or their combination for 6 h. (B) Homologous recombination (HR) efficiency in HEK293T cells transfected with HR reporter plasmids, treated with olaparib, IPA-3, or both, followed by HR assay. (C, D) RAD51 foci formation in Ovcar8 cells treated with olaparib, IPA-3, or their combination for 24 h: (C) representative images and (D) quantification. More than 200 cells were analyzed per experiment. (E, F) The survival of Ovcar8 (E) and SKOV-3 (F) cells treated with olaparib alone or in combination with IPA-3, assessed by colony formation assay. Error bars represent the standard error of the mean from three independent experiments. Statistical significance was determined by a two-tailed t -test, with P -values < 0.05 considered significant.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: PAK1 inhibition enhances the efficiency of olaparib in ovarian cancer cells. (A) Western blotting analysis of PAK1 and CHK1 phosphorylation in Ovcar8 cells treated with 10 μM olaparib, 10 μM IPA-3, or their combination for 6 h. (B) Homologous recombination (HR) efficiency in HEK293T cells transfected with HR reporter plasmids, treated with olaparib, IPA-3, or both, followed by HR assay. (C, D) RAD51 foci formation in Ovcar8 cells treated with olaparib, IPA-3, or their combination for 24 h: (C) representative images and (D) quantification. More than 200 cells were analyzed per experiment. (E, F) The survival of Ovcar8 (E) and SKOV-3 (F) cells treated with olaparib alone or in combination with IPA-3, assessed by colony formation assay. Error bars represent the standard error of the mean from three independent experiments. Statistical significance was determined by a two-tailed t -test, with P -values < 0.05 considered significant.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Inhibition, Western Blot, Phospho-proteomics, Homologous Recombination, Transfection, Colony Assay, Two Tailed Test

    PAK1 inhibition promotes olaparib-induced replication stress and DNA damage. (A, B) DNA fiber assay for the length of CIdU (red) tracks in Ovcar8 cells treated with olaparib, IPA-3, or their combination for 6 h: (A) representative images and (B) quantification. Data were expressed as mean ± standard deviation, analyzed by a two-tailed unpaired t -test. (C, D) Immunoblot analysis of chromatin and soluble fractions of Ovcar8 cells treated with olaparib, IPA-3, or both for 6 h, probing for the indicated antibodies (C), or IPOND (isolation of proteins on nascent DNA) analysis of RPA1 and RPA2 at replication forks (D). (E, F) γ-H2AX foci formation in Ovcar8 cells treated with olaparib, IPA-3, or their combination for 24 h: (E) representative images and (F) quantification. More than 100 cells were counted per experiment. (G) RNA sequencing analysis of Ovcar8 cells treated with olaparib and IPA-3. Differentially expressed genes were classified based on fold change ≥ 1.5 or ≤ 0.5, with P < 0.05. (H) Biological process analysis of up- and down-regulated genes in the combination treatment compared with IPA-3 alone. (I, J) GSEA of up- and down-regulated genes in the combination treatment compared with IPA-3 alone. (K) The heatmap displaying up-regulated genes associated with DNA repair. (L) The quantitative real-time PCR showed the up-regulated genes associated with DNA repair. Error bars represent the standard error of the mean from three independent experiments. Statistical significance was determined by a two-tailed t -test. Two-sided P -values < 0.05 were considered significant. Scale bars = 50 μm.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: PAK1 inhibition promotes olaparib-induced replication stress and DNA damage. (A, B) DNA fiber assay for the length of CIdU (red) tracks in Ovcar8 cells treated with olaparib, IPA-3, or their combination for 6 h: (A) representative images and (B) quantification. Data were expressed as mean ± standard deviation, analyzed by a two-tailed unpaired t -test. (C, D) Immunoblot analysis of chromatin and soluble fractions of Ovcar8 cells treated with olaparib, IPA-3, or both for 6 h, probing for the indicated antibodies (C), or IPOND (isolation of proteins on nascent DNA) analysis of RPA1 and RPA2 at replication forks (D). (E, F) γ-H2AX foci formation in Ovcar8 cells treated with olaparib, IPA-3, or their combination for 24 h: (E) representative images and (F) quantification. More than 100 cells were counted per experiment. (G) RNA sequencing analysis of Ovcar8 cells treated with olaparib and IPA-3. Differentially expressed genes were classified based on fold change ≥ 1.5 or ≤ 0.5, with P < 0.05. (H) Biological process analysis of up- and down-regulated genes in the combination treatment compared with IPA-3 alone. (I, J) GSEA of up- and down-regulated genes in the combination treatment compared with IPA-3 alone. (K) The heatmap displaying up-regulated genes associated with DNA repair. (L) The quantitative real-time PCR showed the up-regulated genes associated with DNA repair. Error bars represent the standard error of the mean from three independent experiments. Statistical significance was determined by a two-tailed t -test. Two-sided P -values < 0.05 were considered significant. Scale bars = 50 μm.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Inhibition, Standard Deviation, Two Tailed Test, Western Blot, Isolation, RNA Sequencing, Real-time Polymerase Chain Reaction

    Combination of IPA-3 and olaparib synergistically suppresses ovarian cancer xenograft tumor growth. OVCAR8 and SKOV-3 cells were subcutaneously implanted into NOD-SCID mice, and the animals were treated with control (DMSO), IPA-3 (10 mg/kg), olaparib (50 mg/kg), or their combination (intraperitoneally, 3 days × 6 times). (A, B, L, M) Serum AST and ALT were measured for Ovcar8 (A, B) and SKOV-3 (L, M) xenografts. (C, D, N, O) Tumor images and growth curves for Ovcar8 (C, D) and SKOV-3 (N, O) xenografts. Data were expressed as mean ± standard error of the mean from five independent samples. Statistical significance was assessed by a two-tailed unpaired t -test. (E–K, P – V ) Hematoxylin-eosin, Ki-67, γ-H2AX, and cleaved caspase-3 staining in tumor tissues, evaluated by immunohistochemistry for Ovcar8 (E–K) and SKOV-3 (P–V) xenografts. Quantification is shown in the corresponding panels. Images of 10 random fields per section were analyzed using ImageJ software. Scale bars = 50 μm. Statistical analysis was performed using a two-tailed t -test and two-way ANOVA. P -values < 0.05 were considered significant.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: Combination of IPA-3 and olaparib synergistically suppresses ovarian cancer xenograft tumor growth. OVCAR8 and SKOV-3 cells were subcutaneously implanted into NOD-SCID mice, and the animals were treated with control (DMSO), IPA-3 (10 mg/kg), olaparib (50 mg/kg), or their combination (intraperitoneally, 3 days × 6 times). (A, B, L, M) Serum AST and ALT were measured for Ovcar8 (A, B) and SKOV-3 (L, M) xenografts. (C, D, N, O) Tumor images and growth curves for Ovcar8 (C, D) and SKOV-3 (N, O) xenografts. Data were expressed as mean ± standard error of the mean from five independent samples. Statistical significance was assessed by a two-tailed unpaired t -test. (E–K, P – V ) Hematoxylin-eosin, Ki-67, γ-H2AX, and cleaved caspase-3 staining in tumor tissues, evaluated by immunohistochemistry for Ovcar8 (E–K) and SKOV-3 (P–V) xenografts. Quantification is shown in the corresponding panels. Images of 10 random fields per section were analyzed using ImageJ software. Scale bars = 50 μm. Statistical analysis was performed using a two-tailed t -test and two-way ANOVA. P -values < 0.05 were considered significant.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Control, Two Tailed Test, Staining, Immunohistochemistry, Software

    Combination of IPA-3 and olaparib synergistically suppresses ovarian cancer cells' growth in patient-derived organoid and patient-derived xenograft models. (A, B, D, E) Ovarian cancer organoids were treated with IPA-3 (200 nM), olaparib (200 nM), or both for 3 days. Representative bright-field images and quantitative analysis are shown. (C, F) Western blotting analysis of CHK1 phosphorylation and cleaved caspase-3 in ovarian cancer organoids treated with IPA-3 (200 nM), olaparib (200 nM), or both for 3 days. (G, H) Patient-derived xenograft models were established by transplanting tumor tissues into 6-week-old female BALB/c nude mice. Mice were treated with DMSO, IPA-3 (10 mg/kg), olaparib (50 mg/kg), or their combination. Tumor images (G) and growth curves (H) are shown. (I–O) Immunohistochemical analysis of hematoxylin-eosin, cleaved caspase-3, γ-H2AX, and Ki-67 levels in tumor tissues. Quantification of staining is shown in (K), (M), and (O). Data were represented as mean ± standard deviation. Images of 10 random fields per section were recorded for analysis. Statistical significance was assessed using a two-tailed t -test and a two-way ANOVA. P -values < 0.05 were considered significant. Scale bars = 50 μm.

    Journal: Genes & Diseases

    Article Title: PAK1 inhibition synergistically enhances the anti-tumor efficacy of PARP inhibitors in ovarian cancers

    doi: 10.1016/j.gendis.2025.101887

    Figure Lengend Snippet: Combination of IPA-3 and olaparib synergistically suppresses ovarian cancer cells' growth in patient-derived organoid and patient-derived xenograft models. (A, B, D, E) Ovarian cancer organoids were treated with IPA-3 (200 nM), olaparib (200 nM), or both for 3 days. Representative bright-field images and quantitative analysis are shown. (C, F) Western blotting analysis of CHK1 phosphorylation and cleaved caspase-3 in ovarian cancer organoids treated with IPA-3 (200 nM), olaparib (200 nM), or both for 3 days. (G, H) Patient-derived xenograft models were established by transplanting tumor tissues into 6-week-old female BALB/c nude mice. Mice were treated with DMSO, IPA-3 (10 mg/kg), olaparib (50 mg/kg), or their combination. Tumor images (G) and growth curves (H) are shown. (I–O) Immunohistochemical analysis of hematoxylin-eosin, cleaved caspase-3, γ-H2AX, and Ki-67 levels in tumor tissues. Quantification of staining is shown in (K), (M), and (O). Data were represented as mean ± standard deviation. Images of 10 random fields per section were recorded for analysis. Statistical significance was assessed using a two-tailed t -test and a two-way ANOVA. P -values < 0.05 were considered significant. Scale bars = 50 μm.

    Article Snippet: Chlorodeoxyuridine (Cidu), 5-iodo-2′-deoxyuridine (Idu), and the PAK1 inhibitor IPA-3 were sourced from MedChemExpress, while the PARP inhibitor olaparib was acquired from TargetMol.

    Techniques: Derivative Assay, Western Blot, Phospho-proteomics, Immunohistochemical staining, Staining, Standard Deviation, Two Tailed Test

    Diagram of PAK1 structure and available chemical tools. (a) Schematic displaying various domains and known disease-associated mutations on PAK1, including the gain-of-function mutations at residues 131 and 429. (b) Chemical structure of the Novartis PAK1 probe, NVS-PAK1-1, and the PAK1 PROTAC, BJG-05-039.

    Journal: bioRxiv

    Article Title: Development of NanoBRET cellular target engagement assays in primary neurons for activating mutants of p21-activated kinase 1

    doi: 10.64898/2026.05.03.722513

    Figure Lengend Snippet: Diagram of PAK1 structure and available chemical tools. (a) Schematic displaying various domains and known disease-associated mutations on PAK1, including the gain-of-function mutations at residues 131 and 429. (b) Chemical structure of the Novartis PAK1 probe, NVS-PAK1-1, and the PAK1 PROTAC, BJG-05-039.

    Article Snippet: As an alternative strategy, Novartis developed an allosteric, ATP-competitive dibenzodiazepine compound, NVS-PAK1-1, that potently inhibited PAK1, with excellent kinome-wide selectivity .

    Techniques:

    BRET probe linker optimization and resulting BRET signal. (a) Structure of our NanoBRET tracer with NVS-PAK1-1 highlighted in blue, NanoBRET 590 dye highlighted in purple, and the varied linker structures shown on the right with the corresponding tracer name. (b) BRET signal elicited by each tracer at 0.25, 0.5, and 1 μM for both the full-length and truncated WT PAK1 constructs. (n=1, performed in technical duplicate)

    Journal: bioRxiv

    Article Title: Development of NanoBRET cellular target engagement assays in primary neurons for activating mutants of p21-activated kinase 1

    doi: 10.64898/2026.05.03.722513

    Figure Lengend Snippet: BRET probe linker optimization and resulting BRET signal. (a) Structure of our NanoBRET tracer with NVS-PAK1-1 highlighted in blue, NanoBRET 590 dye highlighted in purple, and the varied linker structures shown on the right with the corresponding tracer name. (b) BRET signal elicited by each tracer at 0.25, 0.5, and 1 μM for both the full-length and truncated WT PAK1 constructs. (n=1, performed in technical duplicate)

    Article Snippet: As an alternative strategy, Novartis developed an allosteric, ATP-competitive dibenzodiazepine compound, NVS-PAK1-1, that potently inhibited PAK1, with excellent kinome-wide selectivity .

    Techniques: Construct

    Development of the NanoBRET assay for PAK1(248–545), PAK1(248–545) Y429C, and full-length PAK1 Y429C. (a) Tracer titration experiments for tracer EC 50 determination with an 11-point tracer titration study for tracer 10 with and without NVS-PAK1-1. (b) Competition experiments with varying doses of tracer 10 and IC 50 determination of NVS-PAK1-1 at each tracer concentration. The table reports the NVS-PAK1-1 IC 50 at each tracer concentration, along with the standard error of the mean (SEM). The data are not background-subtracted, and the horizontal dotted line indicates the background level. All data is reported as n=3 ± SEM as indicated.

    Journal: bioRxiv

    Article Title: Development of NanoBRET cellular target engagement assays in primary neurons for activating mutants of p21-activated kinase 1

    doi: 10.64898/2026.05.03.722513

    Figure Lengend Snippet: Development of the NanoBRET assay for PAK1(248–545), PAK1(248–545) Y429C, and full-length PAK1 Y429C. (a) Tracer titration experiments for tracer EC 50 determination with an 11-point tracer titration study for tracer 10 with and without NVS-PAK1-1. (b) Competition experiments with varying doses of tracer 10 and IC 50 determination of NVS-PAK1-1 at each tracer concentration. The table reports the NVS-PAK1-1 IC 50 at each tracer concentration, along with the standard error of the mean (SEM). The data are not background-subtracted, and the horizontal dotted line indicates the background level. All data is reported as n=3 ± SEM as indicated.

    Article Snippet: As an alternative strategy, Novartis developed an allosteric, ATP-competitive dibenzodiazepine compound, NVS-PAK1-1, that potently inhibited PAK1, with excellent kinome-wide selectivity .

    Techniques: Titration, Concentration Assay

    Screening of literature inhibitors in HEK293 cells and primary hippocampal neurons. (a) Normalized NanoBRET curves for literature inhibitors MRIA-9, G5555, NVS-PAK1-1, and AZ13705339.(b) Calculated cellular K i,app comparison between truncated WT PAK1, truncated Y429C PAK1, and full-length Y429C PAK1. The statistical significance was assessed using a one-way ANOVA and Tukey’s post hoc analysis. For all quantifications of significance: **** p < 0.0001, *** p < 0.001, ** p < 0.01, and * p < 0.05. (c) NanoBRET curves for literature inhibitors in primary neurons (n=2 ± SEM).

    Journal: bioRxiv

    Article Title: Development of NanoBRET cellular target engagement assays in primary neurons for activating mutants of p21-activated kinase 1

    doi: 10.64898/2026.05.03.722513

    Figure Lengend Snippet: Screening of literature inhibitors in HEK293 cells and primary hippocampal neurons. (a) Normalized NanoBRET curves for literature inhibitors MRIA-9, G5555, NVS-PAK1-1, and AZ13705339.(b) Calculated cellular K i,app comparison between truncated WT PAK1, truncated Y429C PAK1, and full-length Y429C PAK1. The statistical significance was assessed using a one-way ANOVA and Tukey’s post hoc analysis. For all quantifications of significance: **** p < 0.0001, *** p < 0.001, ** p < 0.01, and * p < 0.05. (c) NanoBRET curves for literature inhibitors in primary neurons (n=2 ± SEM).

    Article Snippet: As an alternative strategy, Novartis developed an allosteric, ATP-competitive dibenzodiazepine compound, NVS-PAK1-1, that potently inhibited PAK1, with excellent kinome-wide selectivity .

    Techniques: Comparison