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The mTOR Independent Function of Tsc1 and FNIPs

Rebecca A Sager1, Mark R Woodford1, Mehdi Mollapour2

  • 1Department of Urology, SUNY Upstate Medical University, Syracuse, NY 13210, USA; Upstate Cancer Center, SUNY Upstate Medical University, Syracuse, NY 13210, USA; Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, NY 13210, USA; These authors contributed equally to this work.

Trends in Biochemical Sciences
|October 27, 2018
PubMed

Insights

New research reveals Tsc1 and FNIP1/2 regulate Hsp90, impacting cellular processes beyond the known AMPK-mTOR pathway. A holistic cellular view is essential for understanding these protein functions.

Area of Science:

  • Cellular Biology
  • Molecular Chaperones
  • Signal Transduction

Background:

  • Tsc1 and FNIP1/2 are known regulators in cellular signaling pathways.
  • The molecular chaperone Hsp90 plays critical roles in protein homeostasis.
  • Previous research primarily focused on AMPK-mTOR signaling.

Purpose of the Study:

  • To identify novel functions of Tsc1 and FNIP1/2.
  • To investigate the regulatory relationship between Tsc1, FNIP1/2, and Hsp90.
  • To explore the broader cellular implications of these interactions beyond established pathways.

Main Methods:

  • Biochemical assays to assess protein interactions.
  • Cellular imaging to observe protein localization and function.
  • Genetic manipulation to study the effects of Tsc1 and FNIP1/2 depletion or overexpression.

Main Results:

  • Tsc1 and FNIP1/2 were identified as novel regulators of Hsp90 activity.
  • These proteins influence Hsp90-dependent client protein stability.
  • The regulatory roles extend beyond the canonical AMPK-mTOR pathway, indicating a wider cellular impact.

Conclusions:

  • Tsc1 and FNIP1/2 possess functions beyond AMPK-mTOR signaling, acting as key regulators of Hsp90.
  • Understanding these proteins requires a comprehensive, holistic view of cellular networks.
  • This discovery broadens the scope of Hsp90 regulation and its cellular consequences.
Keywords:
Birt-Hogg-Dubé syndromeHsp90co-chaperonemTORtuberous sclerosis complex

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