Journal: Cell Death Discovery

Article Title: Transcriptomic profiling reveals p53 as a key regulator of doxorubicin-induced cardiotoxicity

doi: 10.1038/s41420-019-0182-6

Figure Lengend Snippet: a The transcription factor encoded by TP53 increases or decreases the transcription of genes involved in apoptotic ( TNFRSF10A, TNFRSF10B, TNFRSF10C, TNFRSF10D, FAS, PMAIP1, BBC3, BAX ) and cell cycle progression pathways ( CDK1, GADD45A, CDKN1A ), respectively. Genes in gray depict overlap with Reyes et al., genes depicted in gray with red outline indicate diffirent isoforms of genes identified in Reyes et al.; Yellow = increased expression, Blue = decreased expression. b Damage caused by interaction of doxorubicin into the DNA activated p53, which then increases transcription of DRs and stalls cell cycle progression. If the damage is deemed irreparable by DNA repair mechanisms, apoptosis is triggered

Article Snippet: A 1:2000 dilution of anti-p53 antibody (R&D Systems, Minneapolis, MN, cat. no: HAF1355) was used and a 1:1000 of each of the following antibodies was used: anti-phosphorylated-S15-p53 (Cell Signaling Technology, Danvers, MA, cat. no: 9286); anti-DR4 (Cell Signaling Technology, Danvers, MA, cat. no: 42533); anti-DR5 (Cell Signaling Technology, Danvers, MA, cat. no: 8074); anti-Fas (Santa Cruz Biotechnology, Dallas, TX, cat. no: sc-715); anti-TNFR1 (Cell Signaling Technology, Danvers, MA, cat. no: 3736).

Techniques: Expressing

Journal: Cell Death Discovery

Article Title: Transcriptomic profiling reveals p53 as a key regulator of doxorubicin-induced cardiotoxicity

doi: 10.1038/s41420-019-0182-6

Figure Lengend Snippet: a Immunoblot and b densitometric quantification demonstrate after exposing cardiomyocytes to 150 nM or 500 nM of doxorubicin for 48 h the phosphorylation of p53 and total expression of p53, TNFR1, DR4, DR5, and Fas increase. TNFR1 protein expression increased only after exposure to 500 nM of doxorubicin. The protein expression of p53 targets, DR4 and DR5, decrease after a 7-day washout period. Fas remains slightly upregulated after 7-day washout

Article Snippet: A 1:2000 dilution of anti-p53 antibody (R&D Systems, Minneapolis, MN, cat. no: HAF1355) was used and a 1:1000 of each of the following antibodies was used: anti-phosphorylated-S15-p53 (Cell Signaling Technology, Danvers, MA, cat. no: 9286); anti-DR4 (Cell Signaling Technology, Danvers, MA, cat. no: 42533); anti-DR5 (Cell Signaling Technology, Danvers, MA, cat. no: 8074); anti-Fas (Santa Cruz Biotechnology, Dallas, TX, cat. no: sc-715); anti-TNFR1 (Cell Signaling Technology, Danvers, MA, cat. no: 3736).

Techniques: Western Blot, Phospho-proteomics, Expressing

Journal: Cell Death Discovery

Article Title: Transcriptomic profiling reveals p53 as a key regulator of doxorubicin-induced cardiotoxicity

doi: 10.1038/s41420-019-0182-6

Figure Lengend Snippet: Doxorubicin, a DNA intercalating agent, induces DNA strand breaks and triggers the activation of p53 to initiate DNA damage responses. Activation of p53 induces increased transcription of genes involved in the extrinsic and intrinsic apoptotic pathway. In the presence of circulating ligands, the extrinsic apoptotic pathway is activated

Article Snippet: A 1:2000 dilution of anti-p53 antibody (R&D Systems, Minneapolis, MN, cat. no: HAF1355) was used and a 1:1000 of each of the following antibodies was used: anti-phosphorylated-S15-p53 (Cell Signaling Technology, Danvers, MA, cat. no: 9286); anti-DR4 (Cell Signaling Technology, Danvers, MA, cat. no: 42533); anti-DR5 (Cell Signaling Technology, Danvers, MA, cat. no: 8074); anti-Fas (Santa Cruz Biotechnology, Dallas, TX, cat. no: sc-715); anti-TNFR1 (Cell Signaling Technology, Danvers, MA, cat. no: 3736).

Techniques: Activation Assay