DEPTOR ubiquitination and destruction by SCF(β-TrCP)

Am J Physiol Endocrinol Metab. 2012 Jul 15;303(2):E163-9. doi: 10.1152/ajpendo.00105.2012. Epub 2012 Mar 27.

Abstract

β-Transducin repeats-containing protein (β-TrCP) is the substrate recognition subunit of the SCF (SKP1, CUL1, and F-box protein)-type E3 ubiquitin ligase complex. SCF(β-TrCP) ubiquitinates specifically phosphorylated substrates to promote their subsequent destruction by the 26S proteasome and plays a critical role in various human diseases including tumorigenesis. We and others (Duan S et al. Mol Cell 44: 317-324, 2011; Gao D et al. Mol Cell 44: 290-303, 2011; Zhao Y et al. Mol Cell 44: 304-316, 2011) recently reported that SCF(β-TrCP) regulates cell growth and autophagy by controlling the ubiquitination and destruction of DEPTOR, an endogenous mammalian target of rapamycin inhibitor, in a phosphorylation-dependent manner. In this review, we discuss β-TrCP's new downstream substrate, DEPTOR, as well as summarize the novel functional aspects of β-TrCP in controlling cell growth and regulating autophagy, in part through governing the stability of DEPTOR.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Autophagy
  • Enzyme Stability
  • Humans
  • Intracellular Signaling Peptides and Proteins
  • SKP Cullin F-Box Protein Ligases / metabolism*
  • Signal Transduction
  • Substrate Specificity
  • TOR Serine-Threonine Kinases / metabolism*
  • Ubiquitination*

Substances

  • Intracellular Signaling Peptides and Proteins
  • SKP Cullin F-Box Protein Ligases
  • DEPTOR protein, human
  • MTOR protein, human
  • TOR Serine-Threonine Kinases