Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
Article Abstract:
Primary mouse embryo fibroblasts (MEFs) are usually established as cell lines that grow unceasingly accompanied by loss of the p53 or p19ARF tumor suppressors. The suppressors perform in a common biochemical pathway. Myc signaling by way of the ARF tumor suppressor controls p53-dependent apoptosis and immortalizing. AFR controls a p53-dependent bottleneck that guards cells against signals that are oncogenic and hyperproliferative.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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The tumor suppressors Ink4c and p53 collaborate independently with Patched to suppress medulloblastoma formation
Article Abstract:
The genetic alternations in human medulloblastoma (MB) include mutations in the Sonic hedgehog (SHH) signaling pathway and TP53 inactivation. Studies revealed that in tumor cells purified from double heterozygotes, Ptc1 allele, but not Ink4c was inactivated and hence it was concluded that Ink4c combined with Ptc1 mutation is haploinsufficient for tumor suppression.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2005
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N-terminal polyubiquitination and degradation of the Arf tumor suppressor
Article Abstract:
The Arf tumor suppressor protein upsets the performance of the p53-negative regulator Mdm2, which results in the cell cycle arrest dependent on p53. The mouse p19(super Arf) and the human p14(super Arf) go through the N-terminal polyubiquitination technique, which is not thoroughly developed and it appears in proteins, which do not contain lysine.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2004
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