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Author Notes:

Alysia D. Vrailas‐Mortimer, School of Biological Sciences, Illinois State University, Science Laboratory Building, Normal, IL 61790, USA. Email: admorti@ilstu.edu

S. Ryan, M. Almassey, A. Burch, G. Ngo, J. Martin, D. Myers, D. Compton, S. Archie, M. Cross, L. Naeger, A. Salzman, A. Virola‐Iarussi, N. Mortimer, and A. Vrailas‐Mortimer performed experiments. S. Ryan, N. Mortimer, S. Barbee, S. Sanyal, and A. Vrailas‐Mortimer made intellectual contributions to experimental design and data interpretation. All authors were involved in reading and editing the manuscript.

We would also like to acknowledge the Bloomington Drosophila Stock Center (NIH P40OD018537), the Vienna Drosophila Resource Center, and Kyoto Stock Center for providing fly stocks used in this study. A. Vrailas‐Mortimer was funded by start‐up funds from the University of Denver, a Knoebel Center for the Study of Aging pilot grant, start‐up funds from Illinois State University and was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number R15AR070505. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. S. Sanyal was funded by start‐up funds from Emory University. S. Ryan was supported by a Knoebel Center for the Study of Aging pilot grant to A. Vrailas‐Mortimer and S. Barbee, N. Mortimer was funded by start‐up funds from Illinois State University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

The authors have no conflicts of interest.

Subject:

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • Geriatrics & Gerontology
  • aging
  • BAG-3
  • starvin
  • Lamin
  • p38 MAPK
  • protein aggregation
  • TARGETING MISFOLDED PROTEINS
  • OXIDATIVE STRESS
  • IN-VIVO
  • NUCLEAR LAMIN
  • SELECTIVE AUTOPHAGY
  • MOTOR FUNCTION
  • CAAX MOTIF
  • CELLS
  • BAG3
  • PROTEOSTASIS

Drosophila p38 MAPK interacts with BAG-3/starvin to regulate age-dependent protein homeostasis

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Journal Title:

AGING CELL

Volume:

Volume 20, Number 11

Publisher:

, Pages e13481-e13481

Type of Work:

Article | Final Publisher PDF

Abstract:

As organisms age, they often accumulate protein aggregates that are thought to be toxic, potentially leading to age-related diseases. This accumulation of protein aggregates is partially attributed to a failure to maintain protein homeostasis. A variety of genetic factors have been linked to longevity, but how these factors also contribute to protein homeostasis is not completely understood. In order to understand the relationship between aging and protein aggregation, we tested how a gene that regulates lifespan and age-dependent locomotor behaviors, p38 MAPK (p38Kb), influences protein homeostasis as an organism ages. We find that p38Kb regulates age-dependent protein aggregation through an interaction with starvin, a regulator of muscle protein homeostasis. Furthermore, we have identified Lamin as an age-dependent target of p38Kb and starvin.

Copyright information:

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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