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p c jun antibodies  (Abmart Inc)

 
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    Abmart Inc p c jun antibodies
    P C Jun Antibodies, supplied by Abmart 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/p+c+jun+antibodies/anti+c+jun+p/pm41921290-68-4-0
    Average 86 stars, based on 1 article reviews
    p c jun antibodies - by Bioz Stars, 2026-09
    86/100 stars

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    other:

    Article Title: Dihydromyricetin attenuates LPS-induced liver injury in chicks through the JNK signaling pathway.
    Article Snippet: Recently, the incidence of liver injury in livestock and poultry caused by bacterial infections has been on the rise.. As a major pathogenic factor determining Gram-negative bacterial infections, lipopolysaccharide (LPS) frequently contributes to reduced performance and even mortality in poultry, thus inflicting substantial economic losses in the livestock industry.. It is imperative to develop safe and efficient protective drugs to mitigate liver damage and decrease susceptibility to chronic diseases in farm animals.



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    ULK2 modulated c-Jun phosphorylation in ovarian cancer organoids. (A) Immunoblot analysis of phospho-c-Jun <t>(Ser243)</t> and c-Jun expression, with β-actin as loading control. (B) In vitro kinase assay to test the phosphorylation of c-Jun protein by ULK2 protein. (C-D) Quantification of ULK2 and c-Jun immunofluorescence signals was performed using IPP 6.0 software. E. ULK2 and c-Jun were examined by immunofluorescence. (F) Co-IP analysis indicated an interaction between ULK2 and c-Jun in chemoresistant ovarian cancer organoid. (G) Analysis of protein stability by cycloheximide (CHX) chase assay. Western blot of organoid lysates following treatment with CHX (50 μg/mL) for the indicated durations. (H) c-Jun was immunoprecipitated from chemoresistant ovarian cancer organoids and subsequently probed with an antiubiquitin antibody by Western blot. (I) Analysis of c-Jun mRNA expression by qRT-PCR. (J) c-Jun silencing reduced the cell viability of chemo-resistant ovarian cancer organoid. Organoids were treated with 8 μg/L cisplatin in different time intervals. (K) Assessment of glucose uptake following the knockdown of c-Jun. (L) Analysis of lactate production subsequent to c-Jun silencing. (M) Effect of c-Jun overexpression was verified by qRT-PCR. (N) The overexpression of c-Jun counteracted the decrease in cell viability caused by the upregulation of ULK2 in chemo-resistant ovarian cancer organoid. (O) Glucose uptake assay. (P) Effects of ULK2 overexpression and c-Jun S243A mutation on cell viability in chemoresistant ovarian cancer organoids. Organoids were treated with 8 μg/L cisplatin in different time intervals. Q. ULK2 overexpression suppresses glucose uptake, which is rescued by the c-Jun S243A mutation in chemoresistant ovarian cancer organoids. * p < .05; ** p < .01.
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    ULK2 modulated c-Jun phosphorylation in ovarian cancer organoids. (A) Immunoblot analysis of phospho-c-Jun (Ser243) and c-Jun expression, with β-actin as loading control. (B) In vitro kinase assay to test the phosphorylation of c-Jun protein by ULK2 protein. (C-D) Quantification of ULK2 and c-Jun immunofluorescence signals was performed using IPP 6.0 software. E. ULK2 and c-Jun were examined by immunofluorescence. (F) Co-IP analysis indicated an interaction between ULK2 and c-Jun in chemoresistant ovarian cancer organoid. (G) Analysis of protein stability by cycloheximide (CHX) chase assay. Western blot of organoid lysates following treatment with CHX (50 μg/mL) for the indicated durations. (H) c-Jun was immunoprecipitated from chemoresistant ovarian cancer organoids and subsequently probed with an antiubiquitin antibody by Western blot. (I) Analysis of c-Jun mRNA expression by qRT-PCR. (J) c-Jun silencing reduced the cell viability of chemo-resistant ovarian cancer organoid. Organoids were treated with 8 μg/L cisplatin in different time intervals. (K) Assessment of glucose uptake following the knockdown of c-Jun. (L) Analysis of lactate production subsequent to c-Jun silencing. (M) Effect of c-Jun overexpression was verified by qRT-PCR. (N) The overexpression of c-Jun counteracted the decrease in cell viability caused by the upregulation of ULK2 in chemo-resistant ovarian cancer organoid. (O) Glucose uptake assay. (P) Effects of ULK2 overexpression and c-Jun S243A mutation on cell viability in chemoresistant ovarian cancer organoids. Organoids were treated with 8 μg/L cisplatin in different time intervals. Q. ULK2 overexpression suppresses glucose uptake, which is rescued by the c-Jun S243A mutation in chemoresistant ovarian cancer organoids. * p < .05; ** p < .01.

    Journal: Science Progress

    Article Title: ULK2 suppresses glycolysis to attenuate cisplatin resistance in ovarian cancer organoid via c-Jun phosphorylation

    doi: 10.1177/00368504261421695

    Figure Lengend Snippet: ULK2 modulated c-Jun phosphorylation in ovarian cancer organoids. (A) Immunoblot analysis of phospho-c-Jun (Ser243) and c-Jun expression, with β-actin as loading control. (B) In vitro kinase assay to test the phosphorylation of c-Jun protein by ULK2 protein. (C-D) Quantification of ULK2 and c-Jun immunofluorescence signals was performed using IPP 6.0 software. E. ULK2 and c-Jun were examined by immunofluorescence. (F) Co-IP analysis indicated an interaction between ULK2 and c-Jun in chemoresistant ovarian cancer organoid. (G) Analysis of protein stability by cycloheximide (CHX) chase assay. Western blot of organoid lysates following treatment with CHX (50 μg/mL) for the indicated durations. (H) c-Jun was immunoprecipitated from chemoresistant ovarian cancer organoids and subsequently probed with an antiubiquitin antibody by Western blot. (I) Analysis of c-Jun mRNA expression by qRT-PCR. (J) c-Jun silencing reduced the cell viability of chemo-resistant ovarian cancer organoid. Organoids were treated with 8 μg/L cisplatin in different time intervals. (K) Assessment of glucose uptake following the knockdown of c-Jun. (L) Analysis of lactate production subsequent to c-Jun silencing. (M) Effect of c-Jun overexpression was verified by qRT-PCR. (N) The overexpression of c-Jun counteracted the decrease in cell viability caused by the upregulation of ULK2 in chemo-resistant ovarian cancer organoid. (O) Glucose uptake assay. (P) Effects of ULK2 overexpression and c-Jun S243A mutation on cell viability in chemoresistant ovarian cancer organoids. Organoids were treated with 8 μg/L cisplatin in different time intervals. Q. ULK2 overexpression suppresses glucose uptake, which is rescued by the c-Jun S243A mutation in chemoresistant ovarian cancer organoids. * p < .05; ** p < .01.

    Article Snippet: P-c-Jun (Ser243) antibody was obtained from Absin (abs148022, Shanghai, China), and c-Jun (9165) antibody was sourced from Cell Signaling Technology (Boston, MA, USA).

    Techniques: Phospho-proteomics, Western Blot, Expressing, Control, In Vitro, Kinase Assay, Immunofluorescence, Software, Co-Immunoprecipitation Assay, Immunoprecipitation, Quantitative RT-PCR, Knockdown, Over Expression, Mutagenesis

    ULK2 overexpression potentiated cisplatin sensitivity in ovarian cancer in xenograft models. (A) Images of subcutaneous xenograft tumor models established in nude mice. (B) The graph displayed the tumor growth progression observed in the nude mouse subjects. (C) Evaluation of tumor weights was conducted. ** p < .01. (D) Immunohistochemistry was performed to assess the association of ULK2, c-Jun and its phosphorylation at Ser243 site. (E) Immunofluorescence analysis was executed to confirm the interaction between ULK2 and p-c-Jun (Ser243) within the subcutaneous xenograft tumors. (F) Quantification of p-c-Jun (Ser243) immunofluorescence signal was performed using IPP 6.0 software. (G) Association between ULK2 and c-Jun was tested by immunofluorescence in the mice models. (H) The immunofluorescence intensity of c-Jun was quantified in ovarian cancer organoids using IPP 6.0 software.

    Journal: Science Progress

    Article Title: ULK2 suppresses glycolysis to attenuate cisplatin resistance in ovarian cancer organoid via c-Jun phosphorylation

    doi: 10.1177/00368504261421695

    Figure Lengend Snippet: ULK2 overexpression potentiated cisplatin sensitivity in ovarian cancer in xenograft models. (A) Images of subcutaneous xenograft tumor models established in nude mice. (B) The graph displayed the tumor growth progression observed in the nude mouse subjects. (C) Evaluation of tumor weights was conducted. ** p < .01. (D) Immunohistochemistry was performed to assess the association of ULK2, c-Jun and its phosphorylation at Ser243 site. (E) Immunofluorescence analysis was executed to confirm the interaction between ULK2 and p-c-Jun (Ser243) within the subcutaneous xenograft tumors. (F) Quantification of p-c-Jun (Ser243) immunofluorescence signal was performed using IPP 6.0 software. (G) Association between ULK2 and c-Jun was tested by immunofluorescence in the mice models. (H) The immunofluorescence intensity of c-Jun was quantified in ovarian cancer organoids using IPP 6.0 software.

    Article Snippet: P-c-Jun (Ser243) antibody was obtained from Absin (abs148022, Shanghai, China), and c-Jun (9165) antibody was sourced from Cell Signaling Technology (Boston, MA, USA).

    Techniques: Over Expression, Immunohistochemistry, Phospho-proteomics, Immunofluorescence, Software