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The KSHV K1 Protein Modulates AMPK Function to Enhance Cell Survival
Penny M Anders1,2, Zhigang Zhang1,2, Prasana M Bhende1,2
1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Plos Pathogens
|November 10, 2016
Summary
Kaposi's sarcoma herpesvirus K1 protein enhances cell survival during nutrient deprivation by interacting with AMPKγ1. This interaction is crucial for KSHV pathogenesis and offers potential therapeutic targets.
Area of Science:
- Virology
- Molecular Biology
- Cancer Research
Background:
- Kaposi's sarcoma herpesvirus (KSHV) causes Kaposi's sarcoma and other cancers.
- KSHV protein K1 is implicated in KSHV pathogenesis and cell transformation.
- Cellular energy homeostasis pathways, like AMPK, are critical for cancer cell survival.
Purpose of the Study:
- To investigate the role of KSHV K1 protein in cell survival under nutrient stress.
- To identify cellular proteins interacting with KSHV K1.
- To elucidate the mechanism by which K1 promotes cell survival.
Main Methods:
- Infection of cells with wild-type and mutant KSHV viruses.
- Assessment of cell survival under nutrient deprivation and AMPK inhibition.
- Tandem affinity purification and mass spectrometry to identify K1-interacting proteins.
- Co-immunoprecipitation assays to confirm protein interactions.
Main Results:
- KSHV-infected cells expressing wild-type K1 showed enhanced survival during nutrient deprivation.
- KSHV K1 protein was found to associate with AMPKγ1.
- The N-terminus of K1 is essential for its interaction with AMPKγ1.
- K1-AMPKγ1 interaction conferred a survival advantage even under AMPK inhibition.
Conclusions:
- KSHV K1 protein promotes cell survival by associating with AMPKγ1.
- This interaction plays a significant role in KSHV-associated pathogenesis.
- Targeting the K1-AMPKγ1 interaction could be a therapeutic strategy for KSHV-related diseases.
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