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Appears in Networks 4

In-Edges 6

p(HBP:HBP00071) increases p(HGNC:TP53) View Subject | View Object

For example, P53 expression, as well as p53-mediated apoptosis, can be enhanced by AICD (Alves da Costa et al. 2006; Ozaki et al. 2006) PubMed:22122372

p(HBP:HBP00071) increases act(p(HGNC:TP53)) View Subject | View Object

For example, P53 expression, as well as p53-mediated apoptosis, can be enhanced by AICD (Alves da Costa et al. 2006; Ozaki et al. 2006) PubMed:22122372

complex(p(HBP:HBP00071), p(HGNC:APBB1), p(HGNC:KAT5)) regulates p(HGNC:TP53) View Subject | View Object

Although Tip60 does not bind to AICD directly, an indirect interaction between AICD and Tip60 is mediated by Fe65. Upon forming this complex, AICD is stabilized and can be translocated into the nucleus to regulate expression of genes such as KAI1, Neprilysin, LRP1, p53, GSK-3b and EGF receptor (Baek et al. 2002; Kim et al. 2003; Cao and Sudhof 2004; Pardossi-Piquard et al. 2005; Alves da Costa et al. 2006; Liu et al. 2007; Zhang et al. 2007) PubMed:22122372

p(HGNC:HTT, var("?")) decreases deg(p(HGNC:TP53)) View Subject | View Object

A study in cultured mouse neuroblastoma cells showed that N-terminal mutant Huntingtin inhibited the 20S proteasome catalytic activity, in turn causing impaired proteasomal degradation of p53, subsequent loss of mitochondrial membrane potential, release of cytochrome c, caspase activation, and apoptosis (Jana et al., 2001) (Figure 2). PubMed:14556719

p(HBP:"UBB+1") increases act(p(HGNC:TP53)) View Subject | View Object

UBB+ 1-capped polyUb chains are resistant to deubiquitination and inhibit proteasomal activity, which may mediate neurodegeneration through mitochondrial stress and p53 activation in neurites (Tan et al., 2007). PubMed:23528736

Out-Edges 1

act(p(HGNC:TP53)) increases bp(GO:"apoptotic process") View Subject | View Object

For example, P53 expression, as well as p53-mediated apoptosis, can be enhanced by AICD (Alves da Costa et al. 2006; Ozaki et al. 2006) PubMed:22122372

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.