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Large tumor suppressor 2, LATS2, activates JNK in a kinase-independent mechanism through ASK1

Lauren Rusnak1,2, Cong Tang2,3, Qi Qi2

  • 1Graduate Program in Cancer Biology, Emory University, Atlanta, GA, USA.

Journal of Molecular Cell Biology
|November 30, 2018
PubMed

Insights

Large tumor suppressor 2 (LATS2) binds to apoptosis signal-regulating kinase 1 (ASK1), enhancing cell death signaling. This interaction reveals a new kinase-independent role for LATS2 in stress response pathways.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • Apoptosis signal-regulating kinase 1 (ASK1) is crucial for cellular stress response and cell death.
  • ASK1 activity is tightly regulated by interactions and modifications, with deregulation linked to cancer and neurological disorders.
  • Large tumor suppressor 2 (LATS2) is a key kinase in the Hippo pathway, often downregulated in cancer.

Purpose of the Study:

  • To identify novel binding partners of ASK1.
  • To characterize the functional interaction between LATS2 and ASK1.
  • To elucidate the role of LATS2 in ASK1-mediated signaling pathways.

Main Methods:

  • Co-immunoprecipitation assays to confirm LATS2-ASK1 interaction.
  • Western blotting to assess JNK MAPK activation.
  • Kinase activity assays to evaluate the role of LATS2 and ASK1 catalytic activity.

Main Results:

  • LATS2 was identified as a novel binding partner for ASK1.
  • LATS2 enhances ASK1-mediated apoptosis and JNK MAPK activation.
  • This enhancement is dependent on ASK1 catalytic activity but not LATS2 kinase activity.

Conclusions:

  • LATS2 acts as a positive regulator of the ASK1-MKK-JNK signaling pathway.
  • LATS2 possesses a kinase-independent function in regulating cellular stress responses.
  • This discovery highlights a novel regulatory mechanism in stress signaling.

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