Autophagy related gene 13
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Autophagy Related 13 or ATG13 is a gene that is involved in controlling autophagy.[1]
Function[edit | edit source]
ME/CFS[edit | edit source]
In May 2022, Simmaron Research announced that they were inserting several human genes including ATG13 into mice in order to research post-exertional malaise and fatigue.[2] ATG13 activates the myokines interleukin 6 (IL-6) and Regulated upon activation, normally T-expressed, and presumably secreted (RANTES).[2]
Notable studies[edit | edit source]
- 2021, Molecular evidence of autophagy impairment as serum level of ATG13 is elevated in patients with myalgic encephalomyelitis and chronic fatigue syndrome: two independent case-control studies[3] - (Pre-print, Full text)
- 2022, Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE)[4] - (Abstract)
See also[edit | edit source]
Learn more[edit | edit source]
- ATG13 Gene - Gene cards
- May 2022, Seeing ME/CFS: Creating the First Mouse Models for the Disease - Simmaron Research
- Sep 2022, Cleaning Crisis? Is Defective Mitochondrial Cleanup Impairing Energy Production in ME/CFS? - Simmaron Research
References[edit | edit source]
- ↑ "ATG13 Gene card". Gene cards. Retrieved November 5, 2022.
- ↑ 2.0 2.1 "Seeing ME/CFS: Creating the First Mouse Models for the Disease". Simmaron Research. May 10, 2022. Retrieved November 5, 2022.
- ↑ Avik, R; Gottschalk, Carl G; Peterson, Daniel; Knox, K; Maynard, M; Whelan, RJ (September 29, 2021). "Molecular evidence of autophagy impairment as serum level of ATG13 is elevated in patients with myalgic encephalomyelitis and chronic fatigue syndrome: two independent case-control studies". Researchsquare. doi:10.21203/rs.3.rs-925403/v1. Retrieved November 5, 2022.
- ↑ Gottschalk, Carl G; Peterson, Daniel; Knox, Konstance; Maynard, Marco; Whelan, Ryan J.; Roy, Avik (May 1, 2022). "Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE)". Molecular and Cellular Neuroscience. 120: 103731. doi:10.1016/j.mcn.2022.103731. ISSN 1044-7431.
