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MedChemExpress erk inhibitor pd98059
SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors <t>PD98059/SCH772984.</t> Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
Erk Inhibitor Pd98059, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress pd98059
SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors <t>PD98059/SCH772984.</t> Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
Pd98059, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress erk signaling
SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors <t>PD98059/SCH772984.</t> Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
Erk Signaling, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress pretreatment
SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors <t>PD98059/SCH772984.</t> Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
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MedChemExpress mek erk pathway
SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors <t>PD98059/SCH772984.</t> Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.
Mek Erk Pathway, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress inhibitor pd98059
a Volcano plot of differentially expressed genes (DEGs) between CNTNAP2 ‑high and CNTNAP2 ‑low glioma samples. b Top 10 KEGG pathways enriched in DEGs from a . c Top 10 genes most positively and negatively correlated with CNTNAP2 expression in glioma. d Top 10 KEGG pathways enriched among CNTNAP2 ‑correlated genes from c . e Schematic of the ERK signaling pathway. f, g Western blot f and quantification g of p‑ERK and t‑ERK in U118MG cells after CNTNAP2 modulation. The protein expression was normalized with control as the standard. n = 3. h Schematic of ERK signaling in vivo. i, j Western blot i and quantification j of p‑ERK and t‑ERK in hippocampal tissues from WT vs. CNTNAP2 -/- mice. The protein expression was normalized with control as the standard. n = 6. k Schematic of PD98059‑mediated ERK inhibition. l, m Western blot l and quantification m showing <t>PD98059</t> reverses p‑ERK elevation induced by CNTNAP2 knockdown. The protein expression was normalized with control as the standard. n = 3. n CCK‑8 assay: PD98059 rescues CNTNAP2 knockdown‑induced proliferation. n = 3. o, p Wound‑healing schematic o and quantitation p : PD98059 blocks CNTNAP2 knockdown‑enhanced migration. n = 3. q, r Colony formation assay schematic q and quantitation r : PD98059 suppresses CNTNAP2 knockdown‑driven proliferation. n = 3. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.
Inhibitor Pd98059, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Pharmatech controls pd98059
a Volcano plot of differentially expressed genes (DEGs) between CNTNAP2 ‑high and CNTNAP2 ‑low glioma samples. b Top 10 KEGG pathways enriched in DEGs from a . c Top 10 genes most positively and negatively correlated with CNTNAP2 expression in glioma. d Top 10 KEGG pathways enriched among CNTNAP2 ‑correlated genes from c . e Schematic of the ERK signaling pathway. f, g Western blot f and quantification g of p‑ERK and t‑ERK in U118MG cells after CNTNAP2 modulation. The protein expression was normalized with control as the standard. n = 3. h Schematic of ERK signaling in vivo. i, j Western blot i and quantification j of p‑ERK and t‑ERK in hippocampal tissues from WT vs. CNTNAP2 -/- mice. The protein expression was normalized with control as the standard. n = 6. k Schematic of PD98059‑mediated ERK inhibition. l, m Western blot l and quantification m showing <t>PD98059</t> reverses p‑ERK elevation induced by CNTNAP2 knockdown. The protein expression was normalized with control as the standard. n = 3. n CCK‑8 assay: PD98059 rescues CNTNAP2 knockdown‑induced proliferation. n = 3. o, p Wound‑healing schematic o and quantitation p : PD98059 blocks CNTNAP2 knockdown‑enhanced migration. n = 3. q, r Colony formation assay schematic q and quantitation r : PD98059 suppresses CNTNAP2 knockdown‑driven proliferation. n = 3. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.
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SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors PD98059/SCH772984. Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Journal: iScience

Article Title: Downregulation of SPRED1 drives keratinocyte hyperproliferation in psoriasis via activation of the ERK-RSK1 signaling axis

doi: 10.1016/j.isci.2026.116812

Figure Lengend Snippet: SPRED1 regulates NHEK cell proliferation via indirect interaction with ERK (A) Co-immunoprecipitation (CoIP) analysis of SPRED1-ERK interaction in NHEK cells transfected with pLVX-Flag-spred1. (B) qRT-PCR analysis of ERK mRNA expression in five experimental groups treated with ERK agonist Ro67-7476 or inhibitors PD98059/SCH772984. Statistical significance was assessed by one-way analysis of variance (ANOVA). (C and D) Western blot analysis of p -ERK protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (E and F) Immunofluorescence staining of p -ERK. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 20 μm. (G and H) CCK-8 assays for keratinocyte viability in five groups. Statistical significance was assessed by one-way ANOVA followed by Bonferroni correction. (I and J) EdU staining for keratinocyte proliferation. Statistical significance was assessed by one-way analysis of variance (ANOVA). Scale bars, 200 μm. (K) qRT-PCR analysis of PCNA mRNA expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (L and M) Western blot analysis of PCNA protein expression. Statistical significance was assessed by one-way analysis of variance (ANOVA). (N and O) Immunofluorescence staining of PCNA. Statistical significance was assessed by Brown-Forsythe corrected ANOVA. Scale bars, 40 μm. All experiments were performed in triplicate. N = 6 for all. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Article Snippet: ERK inhibitor PD98059 , MCE , Cat No. HY-12028.

Techniques: Immunoprecipitation, Transfection, Quantitative RT-PCR, Expressing, Western Blot, Immunofluorescence, Staining, CCK-8 Assay

a Volcano plot of differentially expressed genes (DEGs) between CNTNAP2 ‑high and CNTNAP2 ‑low glioma samples. b Top 10 KEGG pathways enriched in DEGs from a . c Top 10 genes most positively and negatively correlated with CNTNAP2 expression in glioma. d Top 10 KEGG pathways enriched among CNTNAP2 ‑correlated genes from c . e Schematic of the ERK signaling pathway. f, g Western blot f and quantification g of p‑ERK and t‑ERK in U118MG cells after CNTNAP2 modulation. The protein expression was normalized with control as the standard. n = 3. h Schematic of ERK signaling in vivo. i, j Western blot i and quantification j of p‑ERK and t‑ERK in hippocampal tissues from WT vs. CNTNAP2 -/- mice. The protein expression was normalized with control as the standard. n = 6. k Schematic of PD98059‑mediated ERK inhibition. l, m Western blot l and quantification m showing PD98059 reverses p‑ERK elevation induced by CNTNAP2 knockdown. The protein expression was normalized with control as the standard. n = 3. n CCK‑8 assay: PD98059 rescues CNTNAP2 knockdown‑induced proliferation. n = 3. o, p Wound‑healing schematic o and quantitation p : PD98059 blocks CNTNAP2 knockdown‑enhanced migration. n = 3. q, r Colony formation assay schematic q and quantitation r : PD98059 suppresses CNTNAP2 knockdown‑driven proliferation. n = 3. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Cancer Gene Therapy

Article Title: The Tumor-suppressive role of CNTNAP2 in glioma: Dual regulation of the NDN-ERK axis and M2 macrophage polarization

doi: 10.1038/s41417-026-01046-3

Figure Lengend Snippet: a Volcano plot of differentially expressed genes (DEGs) between CNTNAP2 ‑high and CNTNAP2 ‑low glioma samples. b Top 10 KEGG pathways enriched in DEGs from a . c Top 10 genes most positively and negatively correlated with CNTNAP2 expression in glioma. d Top 10 KEGG pathways enriched among CNTNAP2 ‑correlated genes from c . e Schematic of the ERK signaling pathway. f, g Western blot f and quantification g of p‑ERK and t‑ERK in U118MG cells after CNTNAP2 modulation. The protein expression was normalized with control as the standard. n = 3. h Schematic of ERK signaling in vivo. i, j Western blot i and quantification j of p‑ERK and t‑ERK in hippocampal tissues from WT vs. CNTNAP2 -/- mice. The protein expression was normalized with control as the standard. n = 6. k Schematic of PD98059‑mediated ERK inhibition. l, m Western blot l and quantification m showing PD98059 reverses p‑ERK elevation induced by CNTNAP2 knockdown. The protein expression was normalized with control as the standard. n = 3. n CCK‑8 assay: PD98059 rescues CNTNAP2 knockdown‑induced proliferation. n = 3. o, p Wound‑healing schematic o and quantitation p : PD98059 blocks CNTNAP2 knockdown‑enhanced migration. n = 3. q, r Colony formation assay schematic q and quantitation r : PD98059 suppresses CNTNAP2 knockdown‑driven proliferation. n = 3. ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The pharmacological inhibitor PD98059 was purchased from MedChemExpress (USA).

Techniques: Expressing, Western Blot, Control, In Vivo, Inhibition, Knockdown, Quantitation Assay, Migration, Colony Assay