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Literature summary for 2.1.1.366 extracted from

  • Ogawa, S.; Fukuda, A.; Matsumoto, Y.; Hanyu, Y.; Sono, M.; Fukunaga, Y.; Masuda, T.; Araki, O.; Nagao, M.; Yoshikawa, T.; Goto, N.; Hiramatsu, Y.; Tsuda, M.; Maruno, T.; Nakanishi, Y.; Hussein, M.S.; Tsuruyama, T.; Takaori, K.; Uemoto, S.; Seno, H.
    SETDB1 inhibits p53-mediated apoptosis and is required for formation of pancreatic ductal adenocarcinomas in mice (2020), Gastroenterology, 159, 682-696.e13.
    View publication on PubMed
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Application

Application Comment Organism
medicine loss of SETDB1 from pancreas accelerates formation of premalignant lesions in mice with pancreata that express activated KRAS. Expression of genes in the apoptotic pathway is upregulated and genes are regulated by p53 in SETDB1-deficient pancreata. Deletion of Setdb1 from pancreas prevents formation of pancreatic ductal adenocarcinoma, concomitant with increased apoptosis and upregulated expression of Trp53 in mice heterozygous for disruption of Trp53. Pancreata of mice with homozygous disruption of Trp53 have no increased apoptosis, and pancreatic ductal adenocarcinomas develop. SETDB1 binds to the Trp53 promoter to regulate its expression Mus musculus
medicine expression of an inactivated form of SETDB1 in human pancreatic ductal adenocarcinoma cells with wild-type TP53 results in TP53-induced apoptosis Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q15047
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Mus musculus O88974
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Source Tissue

Source Tissue Comment Organism Textmining
pancreas
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 Mus musculus
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pancreas
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 Homo sapiens
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pancreatic ductal adenocarcinoma cell
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 Mus musculus
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pancreatic ductal adenocarcinoma cell
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 Homo sapiens
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