Review

total pak1 (Cell Signaling Technology Inc)

Cell Signaling Technology Inc is a verified supplier

Cell Signaling Technology Inc manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cell Signaling Technology Inc total pak1
Total Pak1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pak1/pm41923641-784-16-19
Average 86 stars, based on 1 article reviews

total pak1 - by Bioz Stars, 2026-11

86/100 stars

Images

Aqueous Normal-phase Chromatography:

Article Title: Rational discovery of therapeutic PAK1 allosteric activators.
Article Snippet: .. The primary antibodies for ANP (ab180649, Abcam, 1:500), phosphorylated PAK1 (p-PAK1, 2601, Cell Signaling Technology, 1:300), total-PAK1 (t-PAK1, 2602, Cell Signaling Technology, 1:1000), phosphorylated-ERK (p-ERK, 4370, Cell Signaling Technology, 1:1000), total-ERK (tERK, 4695, Cell Signaling Technology, 1:1000), phosphorylated-JNK (p-JNK 9251, Cell Signaling Technology, 1:1000), total-JNK (t-JNK, 9252, Cell Signaling Technology, 1:1000), phosphorylated-MKK7 (p-MKK7, 4171, Cell Signaling Technology, 1:1000), total-MKK7 (t-MKK7, 4172, Cell Signaling Technology, 1:1000), phosphorylated-MKK4 (p-MKK4, 9151, Cell Signaling Technology, 1:1000), total-MKK4 (t-MKK4, 9152, Cell Signaling Technology, 1:1000) and GAPDH (Santa Cruz Biotechnology, 1:1000) as the internal control were used. .. The membrane was incubated with the secondary antibody (1:1000) Goat anti-mouse IgG HRP (BBI life sciences, China) or Goat anti-rabbit IgG HRP (BBI life sciences, China) for 1 h at room temperature.

Control:

Image Search Results

PAK1 is activated during steatotic hepatic ischemia-reperfusion injury and is associated with reduced post-transplant liver injury. (A) Hepatic PAK1 mRNA in high-fat diet-fed mice after sham surgery or IR (n = 4 mice per group). (B) Representative immunoblot of P-PAK1 and PAK1 in AML12 cells with or without H/R; actin was the loading control. (C, D) Representative immunoblots and quantification of P-PAK1 and PAK1 in mouse livers after sham surgery or IR (n = 4 mice per group). (E, F) Representative PAK1 IHC and quantification in steatotic mouse livers after sham surgery or IR (n = 4 mice per group). Scale bar, 50 µm. (G, H) Representative immunoblots and quantification of P-PAK1 and PAK1 in human graft biopsies obtained during cold preservation (CP) and after reperfusion (PR) (n = 3 grafts per phase). (I) Association between graft PAK1 IHC score and log10-transformed serum ALT on postoperative day 3 (n = 74 recipients). (J) Serum ALT on postoperative day 3 in the PAK1-low (n = 31) and PAK1-high (n = 43) groups. (K) Association between graft PAK1 IHC score and log10-transformed serum AST on postoperative day 3. (n = 74 recipients). (L) Serum AST on postoperative day 3 in the PAK1-low (n = 31) and PAK1-high (n = 43) groups. (M) Representative graft IHC overview images and enlargements of the boxed regions, showing low and high PAK1 expression. Scale bar, 50 µm. (N) Kaplan-Meier graft survival analysis stratified by PAK1 expression (PAK1-high, n = 43; PAK1-low, n = 31). One in vivo experiment using the indicated numbers of mice. Data are shown as mean ± SD; Student's t test for A and F. Two-way ANOVA for D and H. Survival curves were compared by the log-rank test. n.s. P > 0.05; *P < 0.05; **P < 0.01; ***P < 0.001. PAK1, p21-activated kinase 1; NAFLD, nonalcoholic fatty liver disease; IRI, ischemia reperfusion injury; H/R, hypoxia/reoxygenation; CP, cold preservation; PR, postreperfusion; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; EAD, early allograft dysfunction.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: PAK1 is activated during steatotic hepatic ischemia-reperfusion injury and is associated with reduced post-transplant liver injury. (A) Hepatic PAK1 mRNA in high-fat diet-fed mice after sham surgery or IR (n = 4 mice per group). (B) Representative immunoblot of P-PAK1 and PAK1 in AML12 cells with or without H/R; actin was the loading control. (C, D) Representative immunoblots and quantification of P-PAK1 and PAK1 in mouse livers after sham surgery or IR (n = 4 mice per group). (E, F) Representative PAK1 IHC and quantification in steatotic mouse livers after sham surgery or IR (n = 4 mice per group). Scale bar, 50 µm. (G, H) Representative immunoblots and quantification of P-PAK1 and PAK1 in human graft biopsies obtained during cold preservation (CP) and after reperfusion (PR) (n = 3 grafts per phase). (I) Association between graft PAK1 IHC score and log10-transformed serum ALT on postoperative day 3 (n = 74 recipients). (J) Serum ALT on postoperative day 3 in the PAK1-low (n = 31) and PAK1-high (n = 43) groups. (K) Association between graft PAK1 IHC score and log10-transformed serum AST on postoperative day 3. (n = 74 recipients). (L) Serum AST on postoperative day 3 in the PAK1-low (n = 31) and PAK1-high (n = 43) groups. (M) Representative graft IHC overview images and enlargements of the boxed regions, showing low and high PAK1 expression. Scale bar, 50 µm. (N) Kaplan-Meier graft survival analysis stratified by PAK1 expression (PAK1-high, n = 43; PAK1-low, n = 31). One in vivo experiment using the indicated numbers of mice. Data are shown as mean ± SD; Student's t test for A and F. Two-way ANOVA for D and H. Survival curves were compared by the log-rank test. n.s. P > 0.05; *P < 0.05; **P < 0.01; ***P < 0.001. PAK1, p21-activated kinase 1; NAFLD, nonalcoholic fatty liver disease; IRI, ischemia reperfusion injury; H/R, hypoxia/reoxygenation; CP, cold preservation; PR, postreperfusion; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; EAD, early allograft dysfunction.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Western Blot, Control, Preserving, Transformation Assay, Expressing, Analysis, In Vivo, Immunohistochemistry

Hepatocyte PAK1 overexpression attenuates apoptosis and inflammatory responses during hepatic ischemia-reperfusion. (A) Representative immunoblot of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 in OA-treated AML12-NC and AML12-PAK1-OE cells after H/R; actin was the loading control. (B) Representative reactive oxygen species fluorescence in AML12-NC and AML12-PAK1-OE cells after H/R, shown as overview images and enlargements of the boxed regions. (C) Representative flow-cytometry profiles of AML12-NC and AML12-PAK1-OE cells under basal conditions and after H/R. (D-F) Serum ALT, AST, and IL-6 in AAV8-NC and AAV8-PAK1-OE mice after sham surgery or IR (n = 4 mice per group). (G, H) Representative liver immunoblots and quantification of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 after IR (n = 3 mice per group); actin was the loading control. (I) Representative TUNEL staining of liver sections after sham surgery or IR, shown as overview images and enlargements of the boxed regions (n = 4 mice per group). Scale bar, 50 µm. (J) Representative H&E, F4/80, and Ly6G staining after sham surgery or IR (n = 4 mice per group). Scale bar, 50 µm. (K-M) Quantification of TUNEL-positive area, F4/80-positive cells, and Ly6G-positive cells in IR livers (n = 4 mice per group). Three independent cell experiments for A-C, one in vivo experiment using the indicated numbers of biologically independent mice. Data are mean ± SD. One-way ANOVA was used for D-F, two-way ANOVA for H, and unpaired two-sided Student's t tests for K-M. ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. OA, oleic acid; H/R, hypoxia/reoxygenation; IR, ischemia-reperfusion; AAV8, adeno-associated virus 8; OE, overexpression; NC, negative control; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling; H&E, hematoxylin and eosin; ROS, reactive oxygen species; ALT, alanine aminotransferase; AST, aspartate aminotransferase; IL-6, interleukin-6.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: Hepatocyte PAK1 overexpression attenuates apoptosis and inflammatory responses during hepatic ischemia-reperfusion. (A) Representative immunoblot of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 in OA-treated AML12-NC and AML12-PAK1-OE cells after H/R; actin was the loading control. (B) Representative reactive oxygen species fluorescence in AML12-NC and AML12-PAK1-OE cells after H/R, shown as overview images and enlargements of the boxed regions. (C) Representative flow-cytometry profiles of AML12-NC and AML12-PAK1-OE cells under basal conditions and after H/R. (D-F) Serum ALT, AST, and IL-6 in AAV8-NC and AAV8-PAK1-OE mice after sham surgery or IR (n = 4 mice per group). (G, H) Representative liver immunoblots and quantification of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 after IR (n = 3 mice per group); actin was the loading control. (I) Representative TUNEL staining of liver sections after sham surgery or IR, shown as overview images and enlargements of the boxed regions (n = 4 mice per group). Scale bar, 50 µm. (J) Representative H&E, F4/80, and Ly6G staining after sham surgery or IR (n = 4 mice per group). Scale bar, 50 µm. (K-M) Quantification of TUNEL-positive area, F4/80-positive cells, and Ly6G-positive cells in IR livers (n = 4 mice per group). Three independent cell experiments for A-C, one in vivo experiment using the indicated numbers of biologically independent mice. Data are mean ± SD. One-way ANOVA was used for D-F, two-way ANOVA for H, and unpaired two-sided Student's t tests for K-M. ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. OA, oleic acid; H/R, hypoxia/reoxygenation; IR, ischemia-reperfusion; AAV8, adeno-associated virus 8; OE, overexpression; NC, negative control; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling; H&E, hematoxylin and eosin; ROS, reactive oxygen species; ALT, alanine aminotransferase; AST, aspartate aminotransferase; IL-6, interleukin-6.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Over Expression, Western Blot, Control, Fluorescence, Flow Cytometry, TUNEL Assay, Staining, In Vivo, Virus, Negative Control

Hepatic PAK1 knockdown aggravates hepatocellular apoptosis and inflammation during hepatic ischemia-reperfusion. (A) Representative immunoblot of PAK1, Bcl-2, Bax, and cleaved caspase-3 in OA-treated AML12-NC and AML12-shPAK1 cells after H/R; actin was the loading control. (B) Representative reactive oxygen species fluorescence in AML12-NC and AML12-shPAK1 cells after H/R, shown as overview images and enlargements of the boxed regions. (C) Representative flow-cytometry profiles of AML12-NC and AML12-shPAK1 cells under basal conditions and after H/R. (D-F) Serum ALT, AST, and IL-6 in AAV8-NC and AAV8-shPAK1 mice after sham surgery or IR (n = 4 mice per group). (G, H) Representative liver immunoblots and quantification of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 after IR (n = 3 mice per group); actin was the loading control. (I) Representative TUNEL staining of IR liver sections from AAV8-NC and AAV8-shPAK1 mice, shown as overview images and enlargements of the boxed regions (n = 4 mice per group). Scale bar, 50 µm. (J) Representative H&E, F4/80, and Ly6G staining of IR liver sections (n = 4 mice per group). Scale bar, 50 µm. (K-M) Quantification of TUNEL-positive area, F4/80-positive cells, and Ly6G-positive cells in IR livers (n = 4 mice per group). Three independent cell experiments for A-C, one in vivo experiment using the indicated numbers of biologically independent mice. Data are mean ± SD. One-way ANOVA was used for D-F, two-way ANOVA for H, and unpaired two-sided Student's t tests for K-M. ns, not significant; *P < 0.05; **P < 0.01. OA, oleic acid; H/R, hypoxia/reoxygenation; IR, ischemia-reperfusion; AAV8, adeno-associated virus 8; shPAK1, short hairpin RNA targeting PAK1; NC, negative control; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling; H&E, hematoxylin and eosin; ROS, reactive oxygen species; ALT, alanine aminotransferase; AST, aspartate aminotransferase; IL-6, interleukin-6.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: Hepatic PAK1 knockdown aggravates hepatocellular apoptosis and inflammation during hepatic ischemia-reperfusion. (A) Representative immunoblot of PAK1, Bcl-2, Bax, and cleaved caspase-3 in OA-treated AML12-NC and AML12-shPAK1 cells after H/R; actin was the loading control. (B) Representative reactive oxygen species fluorescence in AML12-NC and AML12-shPAK1 cells after H/R, shown as overview images and enlargements of the boxed regions. (C) Representative flow-cytometry profiles of AML12-NC and AML12-shPAK1 cells under basal conditions and after H/R. (D-F) Serum ALT, AST, and IL-6 in AAV8-NC and AAV8-shPAK1 mice after sham surgery or IR (n = 4 mice per group). (G, H) Representative liver immunoblots and quantification of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 after IR (n = 3 mice per group); actin was the loading control. (I) Representative TUNEL staining of IR liver sections from AAV8-NC and AAV8-shPAK1 mice, shown as overview images and enlargements of the boxed regions (n = 4 mice per group). Scale bar, 50 µm. (J) Representative H&E, F4/80, and Ly6G staining of IR liver sections (n = 4 mice per group). Scale bar, 50 µm. (K-M) Quantification of TUNEL-positive area, F4/80-positive cells, and Ly6G-positive cells in IR livers (n = 4 mice per group). Three independent cell experiments for A-C, one in vivo experiment using the indicated numbers of biologically independent mice. Data are mean ± SD. One-way ANOVA was used for D-F, two-way ANOVA for H, and unpaired two-sided Student's t tests for K-M. ns, not significant; *P < 0.05; **P < 0.01. OA, oleic acid; H/R, hypoxia/reoxygenation; IR, ischemia-reperfusion; AAV8, adeno-associated virus 8; shPAK1, short hairpin RNA targeting PAK1; NC, negative control; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling; H&E, hematoxylin and eosin; ROS, reactive oxygen species; ALT, alanine aminotransferase; AST, aspartate aminotransferase; IL-6, interleukin-6.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Knockdown, Western Blot, Control, Fluorescence, Flow Cytometry, TUNEL Assay, Staining, In Vivo, Virus, shRNA, Negative Control

PAK1 promotes PCK1 lactylation and gluconeogenic reprogramming during steatotic hepatic ischemia-reperfusion. (A, B) GSVA pathway scores for GO positive regulation of gluconeogenesis and KEGG glycolysis/gluconeogenesis in OA-treated control and PAK1-OE AML12 cells after H/R (n = 3 samples per group). (C) GSVA pathway-score heatmap for four gluconeogenesis-related gene sets across the same samples. (D) Representative PAS staining of human graft sections with high or low PAS signals. Scale bar, 50 µm. (E) PAS scores in the PAK1-low and PAK1-high graft groups. (F) Representative PAS staining of IR livers from AAV8-NC and AAV8-PAK1-OE mice. Scale bars, 200 µm and 50 µm. (G, H) Hepatic PCK1 activity and glucose production in AAV8-NC+PBS, AAV8-NC+sodium lactate, and AAV8-PAK1-OE+PBS mice after IR (n = 4 mice per group). (I, J) PCK1 activity and glucose production in AML12 cells treated with control, sodium lactate, or PAK1 overexpression (n = 4 samples per group). (K) PCK1 immunoprecipitation followed by pan-Kla immunoblotting in control and PAK1-OE AML12 cells after H/R. (L) PCK1 immunoprecipitation and pan-Kla immunoblotting in IR livers from AAV8-NC and AAV8-PAK1-OE mice. (M) PCK1 immunoprecipitation and pan-Kla immunoblotting in control and shPAK1 AML12 cells after H/R; IgG was the negative control. (N) Structural superposition of native and K547-lactylated PCK1, with the modified region enlarged (RMSD = 1.388). (O) Representative Bcl-2 and cleaved caspase-3 immunoblots in OA-treated, H/R-exposed cells expressing Flag-PCK1 wild type, K547R, or K551R; actin was the loading control. One RNA-seq/GSVA analysis using n = 3 samples per group. Bar-graph data are mean ± SD. Unpaired two-sided Student's t tests were used for A, B, and E, and one-way ANOVA for G-J. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. GSVA, gene set variation analysis; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; PAS, periodic acid-Schiff; PCK1, phosphoenolpyruvate carboxykinase 1; Kla, lysine lactylation; pan-Kla, pan-lysine lactylation; IP, immunoprecipitation; RMSD, root-mean-square deviation.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: PAK1 promotes PCK1 lactylation and gluconeogenic reprogramming during steatotic hepatic ischemia-reperfusion. (A, B) GSVA pathway scores for GO positive regulation of gluconeogenesis and KEGG glycolysis/gluconeogenesis in OA-treated control and PAK1-OE AML12 cells after H/R (n = 3 samples per group). (C) GSVA pathway-score heatmap for four gluconeogenesis-related gene sets across the same samples. (D) Representative PAS staining of human graft sections with high or low PAS signals. Scale bar, 50 µm. (E) PAS scores in the PAK1-low and PAK1-high graft groups. (F) Representative PAS staining of IR livers from AAV8-NC and AAV8-PAK1-OE mice. Scale bars, 200 µm and 50 µm. (G, H) Hepatic PCK1 activity and glucose production in AAV8-NC+PBS, AAV8-NC+sodium lactate, and AAV8-PAK1-OE+PBS mice after IR (n = 4 mice per group). (I, J) PCK1 activity and glucose production in AML12 cells treated with control, sodium lactate, or PAK1 overexpression (n = 4 samples per group). (K) PCK1 immunoprecipitation followed by pan-Kla immunoblotting in control and PAK1-OE AML12 cells after H/R. (L) PCK1 immunoprecipitation and pan-Kla immunoblotting in IR livers from AAV8-NC and AAV8-PAK1-OE mice. (M) PCK1 immunoprecipitation and pan-Kla immunoblotting in control and shPAK1 AML12 cells after H/R; IgG was the negative control. (N) Structural superposition of native and K547-lactylated PCK1, with the modified region enlarged (RMSD = 1.388). (O) Representative Bcl-2 and cleaved caspase-3 immunoblots in OA-treated, H/R-exposed cells expressing Flag-PCK1 wild type, K547R, or K551R; actin was the loading control. One RNA-seq/GSVA analysis using n = 3 samples per group. Bar-graph data are mean ± SD. Unpaired two-sided Student's t tests were used for A, B, and E, and one-way ANOVA for G-J. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. GSVA, gene set variation analysis; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; PAS, periodic acid-Schiff; PCK1, phosphoenolpyruvate carboxykinase 1; Kla, lysine lactylation; pan-Kla, pan-lysine lactylation; IP, immunoprecipitation; RMSD, root-mean-square deviation.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Control, Staining, Activity Assay, Over Expression, Immunoprecipitation, Western Blot, Negative Control, Modification, Expressing, RNA Sequencing, Analysis, T-Test

PAK1-dependent phosphorylation of ACSS2 facilitates ACSS2-KAT2A-PCK1 complex formation, thereby promoting PCK1 lactylation. (A) Reciprocal co-immunoprecipitation of Flag-PCK1 and HA-KAT2A; IgG and input controls are shown. (B) Representative confocal images of HA-PCK1 (green) and Flag-KAT2A (red), with DAPI nuclear counterstaining (blue). Scale bar, 10 µm. (C) Representative confocal images of HA-ACSS2 (green) and Flag-KAT2A (red). Scale bar, 10 µm. (D) Reciprocal co-immunoprecipitation of Flag-KAT2A and HA-ACSS2; IgG and input controls are shown. (E) ACSS2 immunoprecipitation followed by pan-phospho immunoblotting in control and PAK1-OE cells after H/R; IgG and input controls are shown. (F) Reciprocal co-immunoprecipitation of Flag-PAK1 and HA-ACSS2; IgG and input controls are shown. (G) Representative confocal images of HA-ACSS2 (green) and Flag-PAK1 (red). Scale bar, 10 µm. (H) Representative immunoblots of ACSS2, Bcl-2, Bax, and pan-Kla in control cells and cells expressing ACSS2 wild type, S659A, or S267A after OA treatment and H/R; actin was the loading control. PAK1, p21-activated kinase 1; ACSS2, acyl-CoA synthetase short-chain family member 2; KAT2A, lysine acetyltransferase 2A; PCK1, phosphoenolpyruvate carboxykinase 1; Kla, lysine lactylation; IP, immunoprecipitation; H/R, hypoxia/reoxygenation; WT, wild type.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: PAK1-dependent phosphorylation of ACSS2 facilitates ACSS2-KAT2A-PCK1 complex formation, thereby promoting PCK1 lactylation. (A) Reciprocal co-immunoprecipitation of Flag-PCK1 and HA-KAT2A; IgG and input controls are shown. (B) Representative confocal images of HA-PCK1 (green) and Flag-KAT2A (red), with DAPI nuclear counterstaining (blue). Scale bar, 10 µm. (C) Representative confocal images of HA-ACSS2 (green) and Flag-KAT2A (red). Scale bar, 10 µm. (D) Reciprocal co-immunoprecipitation of Flag-KAT2A and HA-ACSS2; IgG and input controls are shown. (E) ACSS2 immunoprecipitation followed by pan-phospho immunoblotting in control and PAK1-OE cells after H/R; IgG and input controls are shown. (F) Reciprocal co-immunoprecipitation of Flag-PAK1 and HA-ACSS2; IgG and input controls are shown. (G) Representative confocal images of HA-ACSS2 (green) and Flag-PAK1 (red). Scale bar, 10 µm. (H) Representative immunoblots of ACSS2, Bcl-2, Bax, and pan-Kla in control cells and cells expressing ACSS2 wild type, S659A, or S267A after OA treatment and H/R; actin was the loading control. PAK1, p21-activated kinase 1; ACSS2, acyl-CoA synthetase short-chain family member 2; KAT2A, lysine acetyltransferase 2A; PCK1, phosphoenolpyruvate carboxykinase 1; Kla, lysine lactylation; IP, immunoprecipitation; H/R, hypoxia/reoxygenation; WT, wild type.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Phospho-proteomics, Co-Immunoprecipitation Assay, Confocal, Immunoprecipitation, Western Blot, Control, Expressing

FTY720 mitigates steatotic hepatic ischemia-reperfusion injury by suppressing apoptosis, inflammation, and oxidative stress. (A) Chemical structure of FTY720. (B-D) Serum ALT, AST, and total bilirubin in mice after hepatic IR with vehicle or FTY720 treatment (n = 5 mice per group). (E, F) Representative liver immunoblots and quantification of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 after IR with vehicle or FTY720 (n = 4 mice per group); actin was the loading control. (G) Representative H&E, F4/80, and Ly6G staining after IR with vehicle or FTY720 (n = 4 mice per group). Scale bar, 50 µm. (H) Representative TUNEL staining after IR with vehicle or FTY720 (n = 4 mice per group). Scale bar, 50 µm. (I) Representative PAS staining after IR with vehicle or FTY720. Scale bars, 200 µm and 50 µm. (J-L) Hepatic malondialdehyde, superoxide dismutase, and glutathione levels after IR with vehicle or FTY720 (n = 4 mice per group). One in vivo experiment using the indicated numbers of biologically independent mice. Data are mean ± SD. Unpaired two-sided Student's t tests were used for B-D and J-L, and two-way ANOVA for F. ns, not significant; *P < 0.05; **P < 0.01; ****P < 0.0001. FTY720, fingolimod; IR, ischemia-reperfusion; ALT, alanine aminotransferase; AST, aspartate aminotransferase; PAK1, p21-activated kinase 1; P-PAK1, phosphorylated PAK1; PAS, periodic acid-Schiff.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: FTY720 mitigates steatotic hepatic ischemia-reperfusion injury by suppressing apoptosis, inflammation, and oxidative stress. (A) Chemical structure of FTY720. (B-D) Serum ALT, AST, and total bilirubin in mice after hepatic IR with vehicle or FTY720 treatment (n = 5 mice per group). (E, F) Representative liver immunoblots and quantification of P-PAK1, PAK1, Bcl-2, Bax, and cleaved caspase-3 after IR with vehicle or FTY720 (n = 4 mice per group); actin was the loading control. (G) Representative H&E, F4/80, and Ly6G staining after IR with vehicle or FTY720 (n = 4 mice per group). Scale bar, 50 µm. (H) Representative TUNEL staining after IR with vehicle or FTY720 (n = 4 mice per group). Scale bar, 50 µm. (I) Representative PAS staining after IR with vehicle or FTY720. Scale bars, 200 µm and 50 µm. (J-L) Hepatic malondialdehyde, superoxide dismutase, and glutathione levels after IR with vehicle or FTY720 (n = 4 mice per group). One in vivo experiment using the indicated numbers of biologically independent mice. Data are mean ± SD. Unpaired two-sided Student's t tests were used for B-D and J-L, and two-way ANOVA for F. ns, not significant; *P < 0.05; **P < 0.01; ****P < 0.0001. FTY720, fingolimod; IR, ischemia-reperfusion; ALT, alanine aminotransferase; AST, aspartate aminotransferase; PAK1, p21-activated kinase 1; P-PAK1, phosphorylated PAK1; PAS, periodic acid-Schiff.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Western Blot, Control, Staining, TUNEL Assay, In Vivo

Proposed model linking PAK1-ACSS2-KAT2A signaling to PCK1 lactylation and hepatoprotection. Schematic illustrating that PAK1 interacts with ACSS2 and cooperates with KAT2A to facilitate lactate-derived lactyl-CoA generation and local protein lactylation, thereby enhancing PCK1 lactylation and gluconeogenesis/glycogen production and ultimately alleviating hepatic injury in fatty liver IR injury. PAK1, p21-activated kinase 1; ACSS2, acyl-CoA synthetase short-chain family member 2; KAT2A, lysine acetyltransferase 2A; PCK1, phosphoenolpyruvate carboxykinase 1; IR, ischemia reperfusion.

Journal: International Journal of Biological Sciences

Article Title: PAK1 Promotes Gluconeogenesis Via the ACSS2/KAT2A/PCK1 Complex to Attenuate Steatotic Liver Ischemia-Reperfusion Injury

doi: 10.7150/ijbs.132770

Figure Lengend Snippet: Proposed model linking PAK1-ACSS2-KAT2A signaling to PCK1 lactylation and hepatoprotection. Schematic illustrating that PAK1 interacts with ACSS2 and cooperates with KAT2A to facilitate lactate-derived lactyl-CoA generation and local protein lactylation, thereby enhancing PCK1 lactylation and gluconeogenesis/glycogen production and ultimately alleviating hepatic injury in fatty liver IR injury. PAK1, p21-activated kinase 1; ACSS2, acyl-CoA synthetase short-chain family member 2; KAT2A, lysine acetyltransferase 2A; PCK1, phosphoenolpyruvate carboxykinase 1; IR, ischemia reperfusion.

Article Snippet: Immunohistochemistry (IHC) was carried out to detect the expression of PAK1 (21401-1-AP; Proteintech), Ly-6G (GB11229; Servicebio) and F4/80 (ab300421; Abcam).

Techniques: Derivative Assay

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.

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.

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.

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.

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.

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.

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

Review

total pak1 (Cell Signaling Technology Inc)

Structured Review

Images

Related Articles

Aqueous Normal-phase Chromatography:

Control:

Similar Products

Image Search Results