Gene interactions and pathways from curated databases and text-mining

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HUWE1 — TP53

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: TP53 → HUWE1 (decreases, HUWE1 Activity, TP53 Activity)
    Evidence: It has been proposed that ARF is expressed only when an E2F signaling threshold is exceeded following oncogenic activation. The main activity of ARF is its ability to bind to p53 inhibitors and to control ribosome biogenesis. Human double minute (HDM2) [mouse double minute 2 (Mdm2) in mouse] and ARF protein binding 1 (BP1)/Mule are two specific E3 ubiquitin ligases that mediate p53 degradation through ubiquitination.
  • NCI Pathway Database p53 pathway: p53 (TP53) → ARF-BP1 (HUWE1) (proteasomal ubiquitin-dependent protein catabolic process, collaborate) Chen et al., Cell 2005*
    Evidence: mutant phenotype, assay, physical interaction

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Yoon et al., Biochem Biophys Res Commun 2005 (Colorectal Neoplasms) : Over-expression of human UREB1 in colorectal cancer : HECT domain of human UREB1 inhibits the activity of tumor suppressor p53 protein
Khoronenkova et al., FEBS Lett 2011 : Mule inhibition leads to p53 accumulation and activates cellular DNA damage responses
Kon et al., J Biol Chem 2012 (Diabetes Mellitus) : These findings underscore an important role of ARF-BP1 in maintaining ß-cell homeostasis in aging mice and reveal that the stability of p53 is critically regulated by ARF-BP1 in vivo
Hao et al., J Exp Med 2012 : The E3 ubiquitin ligase Mule acts through the ATM-p53 axis to maintain B lymphocyte homeostasis ... Loss of Mule in both MEFs and B cells at steady state resulted in increased levels of phospho-ataxia telangiectasia mutated (ATM) and the ATM substrate p53 ... Thus, Mule regulates the ATM-p53 axis to maintain B cell homeostasis under both steady-state and stress conditions
Qi et al., International journal of molecular sciences 2012 : Downregulation of ARF-BP1 resulted in elevated steady state levels of p53 , growth arrest and apoptosis