Gene interactions and pathways from curated databases and text-mining

◀ Back to TP53

APAF1 — TP53

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Moroni et al., Nat Cell Biol 2001 : Apaf-1 is a transcriptional target for E2F and p53
Robles et al., Cancer Res 2001 (Colorectal Neoplasms) : Consistently, p53 directly induced APAF-1 gene expression
Fortin et al., J Cell Biol 2001 (Brain Ischemia) : APAF1 is a key transcriptional target for p53 in the regulation of neuronal cell death ... In the present study, we demonstrate that p53 directly upregulates Apaf1 transcription as a critical step in the induction of neuronal cell death ... We addressed whether p53 directly regulates Apaf1 transcription via the two p53 consensus binding sites in the Apaf1 promoter ... In transient transfections in a neuronal cell line with p53 and Apaf1 promoter-luciferase constructs, p53 directly activated the Apaf1 promoter via both p53 sites ... Together, these results demonstrate that Apaf1 is a key transcriptional target for p53 that plays a pivotal role in the regulation of apoptosis after neuronal injury
Shinoura et al., Br J Cancer 2002 (Brain Neoplasms...) : To determine which gene is activated by wild type p53 induction and, in turn, activates Apaf-1 and caspase-9, we transduced the Bax, p21/WAF1 or Fas gene via adenovirus vector to U251 cells to achieve a similar expression level as that induced by the Adv for p53 in U251 cells
Rozenfeld-Granot et al., Oncogene 2002 : A positive feedback mechanism in the transcriptional activation of Apaf-1 by p53 and the coactivator Zac-1
Qin et al., Oncogene 2002 (Psoriasis) : Using normal human skin organ cultures and living epidermal equivalents, we demonstrate that in the proliferative basal layer, removal of KCs via apoptosis had a rapid onset ( beginning within 2 h ) following UV-light exposure generating progressively greater numbers of KCs with thymine dimers as the dose of UV-light was increased ; involved induction of Apaf-1 , activation of caspase-3, and was dependent on p53 activation as addition of a p53 chemical inhibitor blocked the apoptotic response
Li et al., Proc Natl Acad Sci U S A 2002 : These results indicate that p53 status is an important modulator of NO ( * ) -induced mutagenesis and apoptosis, and suggest that levels of the Apaf-1 and XIAP proteins, but not mitochondrial depolarization and cytochrome c release, are regulated by p53 in these human lymphoblastoid cells
Ho et al., Oncol Rep 2003 : Tissue-specific regulation of Apaf-1 expression by p53 ... Similarly, we detected a lower Apaf-1 mRNA level in the heart and spleen of p53-/- mice compared with the p53+/+ controls, supporting a transcriptional upregulation of Apaf-1 by p53 ... Taken together, these results demonstrate that p53 regulation of Apaf-1 expression is tissue-specific
Khan et al., Mol Cell Neurosci 2005 : We found that gp120 stimulates p53 activity and induces expression of the p53 pro-apoptotic target Apaf-1 in cultured neurons
Vaughn et al., Cell Death Differ 2007 : NGF deprivation relieves XIAP by selectively degrading it, whereas DNA damage overcomes XIAP via a p53 mediated induction of Apaf-1