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p38i vx702  (ApexBio)

 
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    ApexBio p38i vx702
    Cisplatin induces CLK2 upregulation via p38. (A) Western blot analysis of CLK2 expression in A2780 cells treated with various signaling pathway inhibitors or dimethyl sulfoxide (DMSO) in the presence or absence of cisplatin. Only <t>p38</t> <t>inhibitor</t> attenuated the expression of CLK2. (B) CLK2 mRNA level in A2780 cells treated with cisplatin in the presence or absence of p38 inhibitor was measured by qRT‐PCR. Data was shown as mean ± SD. p Values were determined by Student's t ‐test. (C) A2780 cells treated with phosphate‐buffered saline (PBS), or cisplatin, or cisplatin plus p38 inhibitor <t>(p38i),</t> or cisplatin and p38 overexpression (p38‐Myc) were incubated with 20 µg/mL cycloheximide (CHX) for the indicated periods and then analyzed by Western blot. The results were normalized to the levels of GAPDH. (D) Quantitation of CLK2 protein levels was based on the Western blot result. Data were shown as mean ± SD. (E) Coimmunoprecipitation assay showing the presence of a complex containing CLK2 and p38. CLK2 antibody coprecipitating p38 (top panel). p38 antibody coprecipitating CLK2 (bottom panel). Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2 or p38 antibody. n.s., no significance.
    P38i Vx702, supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p38i+vx702/p38i+vx702/pmc11016135-231-17-22
    Average 90 stars, based on 1 article reviews
    p38i vx702 - by Bioz Stars, 2026-10
    90/100 stars

    Images

    1) Product Images from "Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer"

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer

    Journal: MedComm

    doi: 10.1002/mco2.537

    Cisplatin induces CLK2 upregulation via p38. (A) Western blot analysis of CLK2 expression in A2780 cells treated with various signaling pathway inhibitors or dimethyl sulfoxide (DMSO) in the presence or absence of cisplatin. Only p38 inhibitor attenuated the expression of CLK2. (B) CLK2 mRNA level in A2780 cells treated with cisplatin in the presence or absence of p38 inhibitor was measured by qRT‐PCR. Data was shown as mean ± SD. p Values were determined by Student's t ‐test. (C) A2780 cells treated with phosphate‐buffered saline (PBS), or cisplatin, or cisplatin plus p38 inhibitor (p38i), or cisplatin and p38 overexpression (p38‐Myc) were incubated with 20 µg/mL cycloheximide (CHX) for the indicated periods and then analyzed by Western blot. The results were normalized to the levels of GAPDH. (D) Quantitation of CLK2 protein levels was based on the Western blot result. Data were shown as mean ± SD. (E) Coimmunoprecipitation assay showing the presence of a complex containing CLK2 and p38. CLK2 antibody coprecipitating p38 (top panel). p38 antibody coprecipitating CLK2 (bottom panel). Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2 or p38 antibody. n.s., no significance.
    Figure Legend Snippet: Cisplatin induces CLK2 upregulation via p38. (A) Western blot analysis of CLK2 expression in A2780 cells treated with various signaling pathway inhibitors or dimethyl sulfoxide (DMSO) in the presence or absence of cisplatin. Only p38 inhibitor attenuated the expression of CLK2. (B) CLK2 mRNA level in A2780 cells treated with cisplatin in the presence or absence of p38 inhibitor was measured by qRT‐PCR. Data was shown as mean ± SD. p Values were determined by Student's t ‐test. (C) A2780 cells treated with phosphate‐buffered saline (PBS), or cisplatin, or cisplatin plus p38 inhibitor (p38i), or cisplatin and p38 overexpression (p38‐Myc) were incubated with 20 µg/mL cycloheximide (CHX) for the indicated periods and then analyzed by Western blot. The results were normalized to the levels of GAPDH. (D) Quantitation of CLK2 protein levels was based on the Western blot result. Data were shown as mean ± SD. (E) Coimmunoprecipitation assay showing the presence of a complex containing CLK2 and p38. CLK2 antibody coprecipitating p38 (top panel). p38 antibody coprecipitating CLK2 (bottom panel). Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2 or p38 antibody. n.s., no significance.

    Techniques Used: Western Blot, Expressing, Quantitative RT-PCR, Saline, Over Expression, Incubation, Quantitation Assay, Co-Immunoprecipitation Assay, Negative Control

    p38 and ring finger protein 8 (RNF8) mediate CLK2 protein ubiquitination. (A) Western blot analyses of CLK2 expression in A2780 and Skov3 cells which were treated with cisplatin (16.7 µM) in the presence or absence of p38 inhibitor (10 µM). Cells were incubated with MG132 (10 µM) for the indicated periods. (B) Ubiquitination assays of CLK2 in human embryonic kidney (HEK293T) cells transfected with Flag‐CLK2, Myc‐p38, and HA‐ubiquitin or its mutants (K48R, K48o, K63R, K63o) plasmids. IP, expression of compound coprecipitated by Flag antibody. WCL, whole cell lysate. (C) Ubiquitination assays of CLK2 in HEK293T cells transfected with Myc‐p38, HA‐Ub‐K63o, and CLK2‐WT or its mutants (T343A, K192R) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (D) Coimmunoprecipitation assay showing the endogenous (top panel) presence of a complex containing CLK2 and RNF8 and the exogenous (bottom panel) presence of a complex containing CLK2 and Flag‐RNF8. Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2, RNF8, or Flag antibody. WCL, whole cell lysate. (E) Ubiquitination assays of CLK2 in HEK293T cells transfected with CLK2, Flag‐RNF8, and HA‐ubiquitin or its mutants (K48o, K63o) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (F) Ubiquitination assays of CLK2 in HEK293T cells cotransfected by various combinations of plasmids expressing CLK2, Myc‐p38, Flag‐RNF8, and HA‐Ub‐K63o. IP, expression of compound coprecipitated by CLK2 antibody; WCL, whole cell lysate.
    Figure Legend Snippet: p38 and ring finger protein 8 (RNF8) mediate CLK2 protein ubiquitination. (A) Western blot analyses of CLK2 expression in A2780 and Skov3 cells which were treated with cisplatin (16.7 µM) in the presence or absence of p38 inhibitor (10 µM). Cells were incubated with MG132 (10 µM) for the indicated periods. (B) Ubiquitination assays of CLK2 in human embryonic kidney (HEK293T) cells transfected with Flag‐CLK2, Myc‐p38, and HA‐ubiquitin or its mutants (K48R, K48o, K63R, K63o) plasmids. IP, expression of compound coprecipitated by Flag antibody. WCL, whole cell lysate. (C) Ubiquitination assays of CLK2 in HEK293T cells transfected with Myc‐p38, HA‐Ub‐K63o, and CLK2‐WT or its mutants (T343A, K192R) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (D) Coimmunoprecipitation assay showing the endogenous (top panel) presence of a complex containing CLK2 and RNF8 and the exogenous (bottom panel) presence of a complex containing CLK2 and Flag‐RNF8. Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2, RNF8, or Flag antibody. WCL, whole cell lysate. (E) Ubiquitination assays of CLK2 in HEK293T cells transfected with CLK2, Flag‐RNF8, and HA‐ubiquitin or its mutants (K48o, K63o) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (F) Ubiquitination assays of CLK2 in HEK293T cells cotransfected by various combinations of plasmids expressing CLK2, Myc‐p38, Flag‐RNF8, and HA‐Ub‐K63o. IP, expression of compound coprecipitated by CLK2 antibody; WCL, whole cell lysate.

    Techniques Used: Ubiquitin Proteomics, Western Blot, Expressing, Incubation, Transfection, Co-Immunoprecipitation Assay, Negative Control

    Related Articles

    Western Blot:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Expressing:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Quantitative RT-PCR:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Saline:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Over Expression:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Incubation:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Quantitation Assay:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Co-Immunoprecipitation Assay:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Negative Control:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Ubiquitin Proteomics:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Transfection:

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer
    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.



    Similar Products

    p38i vx702  (ApexBio)
    90
    ApexBio p38i vx702
    Cisplatin induces CLK2 upregulation via p38. (A) Western blot analysis of CLK2 expression in A2780 cells treated with various signaling pathway inhibitors or dimethyl sulfoxide (DMSO) in the presence or absence of cisplatin. Only <t>p38</t> <t>inhibitor</t> attenuated the expression of CLK2. (B) CLK2 mRNA level in A2780 cells treated with cisplatin in the presence or absence of p38 inhibitor was measured by qRT‐PCR. Data was shown as mean ± SD. p Values were determined by Student's t ‐test. (C) A2780 cells treated with phosphate‐buffered saline (PBS), or cisplatin, or cisplatin plus p38 inhibitor <t>(p38i),</t> or cisplatin and p38 overexpression (p38‐Myc) were incubated with 20 µg/mL cycloheximide (CHX) for the indicated periods and then analyzed by Western blot. The results were normalized to the levels of GAPDH. (D) Quantitation of CLK2 protein levels was based on the Western blot result. Data were shown as mean ± SD. (E) Coimmunoprecipitation assay showing the presence of a complex containing CLK2 and p38. CLK2 antibody coprecipitating p38 (top panel). p38 antibody coprecipitating CLK2 (bottom panel). Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2 or p38 antibody. n.s., no significance.
    P38i Vx702, supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p38i+vx702/p38i+vx702/pmc11016135-231-17-22
    Average 90 stars, based on 1 article reviews
    p38i vx702 - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    Cisplatin induces CLK2 upregulation via p38. (A) Western blot analysis of CLK2 expression in A2780 cells treated with various signaling pathway inhibitors or dimethyl sulfoxide (DMSO) in the presence or absence of cisplatin. Only p38 inhibitor attenuated the expression of CLK2. (B) CLK2 mRNA level in A2780 cells treated with cisplatin in the presence or absence of p38 inhibitor was measured by qRT‐PCR. Data was shown as mean ± SD. p Values were determined by Student's t ‐test. (C) A2780 cells treated with phosphate‐buffered saline (PBS), or cisplatin, or cisplatin plus p38 inhibitor (p38i), or cisplatin and p38 overexpression (p38‐Myc) were incubated with 20 µg/mL cycloheximide (CHX) for the indicated periods and then analyzed by Western blot. The results were normalized to the levels of GAPDH. (D) Quantitation of CLK2 protein levels was based on the Western blot result. Data were shown as mean ± SD. (E) Coimmunoprecipitation assay showing the presence of a complex containing CLK2 and p38. CLK2 antibody coprecipitating p38 (top panel). p38 antibody coprecipitating CLK2 (bottom panel). Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2 or p38 antibody. n.s., no significance.

    Journal: MedComm

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer

    doi: 10.1002/mco2.537

    Figure Lengend Snippet: Cisplatin induces CLK2 upregulation via p38. (A) Western blot analysis of CLK2 expression in A2780 cells treated with various signaling pathway inhibitors or dimethyl sulfoxide (DMSO) in the presence or absence of cisplatin. Only p38 inhibitor attenuated the expression of CLK2. (B) CLK2 mRNA level in A2780 cells treated with cisplatin in the presence or absence of p38 inhibitor was measured by qRT‐PCR. Data was shown as mean ± SD. p Values were determined by Student's t ‐test. (C) A2780 cells treated with phosphate‐buffered saline (PBS), or cisplatin, or cisplatin plus p38 inhibitor (p38i), or cisplatin and p38 overexpression (p38‐Myc) were incubated with 20 µg/mL cycloheximide (CHX) for the indicated periods and then analyzed by Western blot. The results were normalized to the levels of GAPDH. (D) Quantitation of CLK2 protein levels was based on the Western blot result. Data were shown as mean ± SD. (E) Coimmunoprecipitation assay showing the presence of a complex containing CLK2 and p38. CLK2 antibody coprecipitating p38 (top panel). p38 antibody coprecipitating CLK2 (bottom panel). Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2 or p38 antibody. n.s., no significance.

    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Techniques: Western Blot, Expressing, Quantitative RT-PCR, Saline, Over Expression, Incubation, Quantitation Assay, Co-Immunoprecipitation Assay, Negative Control

    p38 and ring finger protein 8 (RNF8) mediate CLK2 protein ubiquitination. (A) Western blot analyses of CLK2 expression in A2780 and Skov3 cells which were treated with cisplatin (16.7 µM) in the presence or absence of p38 inhibitor (10 µM). Cells were incubated with MG132 (10 µM) for the indicated periods. (B) Ubiquitination assays of CLK2 in human embryonic kidney (HEK293T) cells transfected with Flag‐CLK2, Myc‐p38, and HA‐ubiquitin or its mutants (K48R, K48o, K63R, K63o) plasmids. IP, expression of compound coprecipitated by Flag antibody. WCL, whole cell lysate. (C) Ubiquitination assays of CLK2 in HEK293T cells transfected with Myc‐p38, HA‐Ub‐K63o, and CLK2‐WT or its mutants (T343A, K192R) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (D) Coimmunoprecipitation assay showing the endogenous (top panel) presence of a complex containing CLK2 and RNF8 and the exogenous (bottom panel) presence of a complex containing CLK2 and Flag‐RNF8. Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2, RNF8, or Flag antibody. WCL, whole cell lysate. (E) Ubiquitination assays of CLK2 in HEK293T cells transfected with CLK2, Flag‐RNF8, and HA‐ubiquitin or its mutants (K48o, K63o) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (F) Ubiquitination assays of CLK2 in HEK293T cells cotransfected by various combinations of plasmids expressing CLK2, Myc‐p38, Flag‐RNF8, and HA‐Ub‐K63o. IP, expression of compound coprecipitated by CLK2 antibody; WCL, whole cell lysate.

    Journal: MedComm

    Article Title: Targeting the Cdc2‐like kinase 2 for overcoming platinum resistance in ovarian cancer

    doi: 10.1002/mco2.537

    Figure Lengend Snippet: p38 and ring finger protein 8 (RNF8) mediate CLK2 protein ubiquitination. (A) Western blot analyses of CLK2 expression in A2780 and Skov3 cells which were treated with cisplatin (16.7 µM) in the presence or absence of p38 inhibitor (10 µM). Cells were incubated with MG132 (10 µM) for the indicated periods. (B) Ubiquitination assays of CLK2 in human embryonic kidney (HEK293T) cells transfected with Flag‐CLK2, Myc‐p38, and HA‐ubiquitin or its mutants (K48R, K48o, K63R, K63o) plasmids. IP, expression of compound coprecipitated by Flag antibody. WCL, whole cell lysate. (C) Ubiquitination assays of CLK2 in HEK293T cells transfected with Myc‐p38, HA‐Ub‐K63o, and CLK2‐WT or its mutants (T343A, K192R) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (D) Coimmunoprecipitation assay showing the endogenous (top panel) presence of a complex containing CLK2 and RNF8 and the exogenous (bottom panel) presence of a complex containing CLK2 and Flag‐RNF8. Input, protein expression in cell lysates detected by Western blot. IgG, negative control. IP, expression of compound coprecipitated by CLK2, RNF8, or Flag antibody. WCL, whole cell lysate. (E) Ubiquitination assays of CLK2 in HEK293T cells transfected with CLK2, Flag‐RNF8, and HA‐ubiquitin or its mutants (K48o, K63o) plasmids. IP, expression of compound coprecipitated by CLK2 antibody. WCL, whole cell lysate. (F) Ubiquitination assays of CLK2 in HEK293T cells cotransfected by various combinations of plasmids expressing CLK2, Myc‐p38, Flag‐RNF8, and HA‐Ub‐K63o. IP, expression of compound coprecipitated by CLK2 antibody; WCL, whole cell lysate.

    Article Snippet: To determine the half‐life of CLK2, A2780 cells were treated either with PBS, cisplatin (6.67 μM) or p38i (10 μM, VX702, #A8687; APExBio) plus cisplatin.

    Techniques: Ubiquitin Proteomics, Western Blot, Expressing, Incubation, Transfection, Co-Immunoprecipitation Assay, Negative Control