hy-p0121 Search Results


reacp53  (MedChemExpress)
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MedChemExpress reacp53
Acetylation halts aggregation and reactivates missense mutant p53 (A) Western blot analysis detected the solubility of p53 in indicated NSCLC cells. GAPDH served as a loading control. (B) Western blot analysis showed the solubility of ectopic p53 and R175H in H1299 cells. (C) Western blot analysis detected the effect of acetylation simulation on p53 solubility. The lower panel showed the quantitative of solubility ratio between the indicated groups (mean ± SD and determined using Student’s t tests, n = 3, ∗∗p < 0.01). (D) Western blot assay demonstrated the expression of p53 and acetylated p53 in the indicated cells treated with increased concentrations of <t>ReAcp53</t> for 20 h. The lower panel displays the trend of the indicated protein alteration. Data were expressed as mean ± SD. (E) IP analysis detected the overall p53 acetylation in the indicated cells treated with ReAcp53 (5 μM) for 20 h. Cell lysates were obtained by IP using p53 antibody followed by Western blot assay using the indicated antibodies. (F) Western blot analysis detected the effect of ReAcp53 on p53 solubility in the indicated cells treated with ReAcp53 (5 μM) for 20 h. The lower panel shows the quantitative solubility ratio between the indicated groups (mean ± SD and determined using Student’s t tests, n = 3, ∗∗p < 0.01). (G) Schematic illustration of the evaluation of in vivo tumor growth derived from H1299-R175H cells responding to ReAcp53 treatment. Mice bearing tumors with volume of 200 m3 were randomly grouped and received intraperitoneal injections of DMSO or ReAcp53 (15 mg/kg) every day for 14 days. Tumor volume was monitored as indicated from the first treatment. Tumors were collected on the 15th day post-first treatment. (H) Growth curve of subcutaneous xenografts. (Mean ± SD and determined using Student’s t tests, n = 5, ∗p < 0.05, ∗∗p < 0.01). (I) Representative images of subcutaneous xenografts collected at the 15th day after first treatment. The right panel shows the tumor weight statistics (mean ± SD and determined using Student’s t tests, n = 5, ∗∗p < 0.01).
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Acetylation halts aggregation and reactivates missense mutant p53 (A) Western blot analysis detected the solubility of p53 in indicated NSCLC cells. GAPDH served as a loading control. (B) Western blot analysis showed the solubility of ectopic p53 and R175H in H1299 cells. (C) Western blot analysis detected the effect of acetylation simulation on p53 solubility. The lower panel showed the quantitative of solubility ratio between the indicated groups (mean ± SD and determined using Student’s t tests, n = 3, ∗∗p < 0.01). (D) Western blot assay demonstrated the expression of p53 and acetylated p53 in the indicated cells treated with increased concentrations of ReAcp53 for 20 h. The lower panel displays the trend of the indicated protein alteration. Data were expressed as mean ± SD. (E) IP analysis detected the overall p53 acetylation in the indicated cells treated with ReAcp53 (5 μM) for 20 h. Cell lysates were obtained by IP using p53 antibody followed by Western blot assay using the indicated antibodies. (F) Western blot analysis detected the effect of ReAcp53 on p53 solubility in the indicated cells treated with ReAcp53 (5 μM) for 20 h. The lower panel shows the quantitative solubility ratio between the indicated groups (mean ± SD and determined using Student’s t tests, n = 3, ∗∗p < 0.01). (G) Schematic illustration of the evaluation of in vivo tumor growth derived from H1299-R175H cells responding to ReAcp53 treatment. Mice bearing tumors with volume of 200 m3 were randomly grouped and received intraperitoneal injections of DMSO or ReAcp53 (15 mg/kg) every day for 14 days. Tumor volume was monitored as indicated from the first treatment. Tumors were collected on the 15th day post-first treatment. (H) Growth curve of subcutaneous xenografts. (Mean ± SD and determined using Student’s t tests, n = 5, ∗p < 0.05, ∗∗p < 0.01). (I) Representative images of subcutaneous xenografts collected at the 15th day after first treatment. The right panel shows the tumor weight statistics (mean ± SD and determined using Student’s t tests, n = 5, ∗∗p < 0.01).

Journal: iScience

Article Title: Acetylation halts missense mutant p53 aggregation and rescues tumor suppression in non-small cell lung cancers

doi: 10.1016/j.isci.2023.107003

Figure Lengend Snippet: Acetylation halts aggregation and reactivates missense mutant p53 (A) Western blot analysis detected the solubility of p53 in indicated NSCLC cells. GAPDH served as a loading control. (B) Western blot analysis showed the solubility of ectopic p53 and R175H in H1299 cells. (C) Western blot analysis detected the effect of acetylation simulation on p53 solubility. The lower panel showed the quantitative of solubility ratio between the indicated groups (mean ± SD and determined using Student’s t tests, n = 3, ∗∗p < 0.01). (D) Western blot assay demonstrated the expression of p53 and acetylated p53 in the indicated cells treated with increased concentrations of ReAcp53 for 20 h. The lower panel displays the trend of the indicated protein alteration. Data were expressed as mean ± SD. (E) IP analysis detected the overall p53 acetylation in the indicated cells treated with ReAcp53 (5 μM) for 20 h. Cell lysates were obtained by IP using p53 antibody followed by Western blot assay using the indicated antibodies. (F) Western blot analysis detected the effect of ReAcp53 on p53 solubility in the indicated cells treated with ReAcp53 (5 μM) for 20 h. The lower panel shows the quantitative solubility ratio between the indicated groups (mean ± SD and determined using Student’s t tests, n = 3, ∗∗p < 0.01). (G) Schematic illustration of the evaluation of in vivo tumor growth derived from H1299-R175H cells responding to ReAcp53 treatment. Mice bearing tumors with volume of 200 m3 were randomly grouped and received intraperitoneal injections of DMSO or ReAcp53 (15 mg/kg) every day for 14 days. Tumor volume was monitored as indicated from the first treatment. Tumors were collected on the 15th day post-first treatment. (H) Growth curve of subcutaneous xenografts. (Mean ± SD and determined using Student’s t tests, n = 5, ∗p < 0.05, ∗∗p < 0.01). (I) Representative images of subcutaneous xenografts collected at the 15th day after first treatment. The right panel shows the tumor weight statistics (mean ± SD and determined using Student’s t tests, n = 5, ∗∗p < 0.01).

Article Snippet: ReAcp53 , MedChemExpress , Cat# HY-P0121.

Techniques: Mutagenesis, Western Blot, Solubility, Control, Expressing, In Vivo, Derivative Assay

Journal: iScience

Article Title: Acetylation halts missense mutant p53 aggregation and rescues tumor suppression in non-small cell lung cancers

doi: 10.1016/j.isci.2023.107003

Figure Lengend Snippet:

Article Snippet: ReAcp53 , MedChemExpress , Cat# HY-P0121.

Techniques: Ubiquitin Proteomics, Virus, Recombinant, Chromatin Immunoprecipitation, cDNA Synthesis, Sequencing, Software