PRUNE1 is involved in Myalgic encephalomyelitis and in exercise biology

Eleven genes may be involved in Myalgic encephalomyelitis (ME) (1):
WASF3, NUP98, PRUNE1, KIRREL3, TNK2, EIF3C, HOXA1, PMS2P5, HDAC7, FFAR3, MAP3K2.

ME patients have Post Exertional Malaise (PEM). PEM is the worsening of symptoms following even minor physical or mental exertion that would have been tolerated previously. Symptoms typically worsen 12 to 48 hours after activity. PEM can last for days or even weeks (2). Cardiopulmonary and metabolic responses during a 2-day CPET in myalgic encephalomyelitis showed the problems (3).

In a preprint page 12 and 13 (4):
Molecular Landscape of Modality-Specific Exercise Adaptation in Human Skeletal Muscle through Large-Scale Multi-OMICs Integration

you can read this, quote:

"Exercise modality-specific analyses revealed 13 intersected genes (CLIC1, SMTNL1, MRPL23, ITGA7, IFITM3, IGFBP7, SLC41A3, CHTOP, CTBP1, PRUNE1, THY1, RPRD1B, and PODXL) associated with aerobic exercise across all OMIC layers, excluding mRNA followed by inactivity."

"However, five genes (CLIC1, IFITM3, PRUNE1, RPRD1B and PODXL) appear to be newly associated with aerobic exercise training."

"PRUNE1 is implicated in various cellular processes, including cell proliferation, mitigation and survival. Its expression has been shown to be positively correlated with tumour metastasis (Ferrucci et al., 2024). Although there is no direct evidence linking PRUNE1 to exercise, its involvement in cellular processes such as cell proliferation, differentiation, and tissue repair can be indirectly associated with exercise. Exercise-induced muscle adaptation and repair processes could potentially be influenced by the mechanisms in which PRUNE1 is involved, highlighting its relevance in the context of exercise biology."

Further reading: 

Regulation of PRUNE and the ATP synthase is involved in Myalgic encephalomyelitis

Is TNK2 involved in the function of ATP synthase in Myalgic encephalomyelitis?

References

1) Pihur V, Datta S, Datta S. Meta analysis of Chronic Fatigue Syndrome through integration of clinical, gene expression, SNP and proteomic data. Bioinformation. 2011 Apr 22;6(3):120-4. doi: 10.6026/97320630006120. PMID: 21584188; PMCID: PMC3089886.

https://pubmed.ncbi.nlm.nih.gov/21584188/ 

2) https://www.cdc.gov/me-cfs/hcp/clinical-care/treating-the-most-disruptive-symptoms-first-and-preventing-worsening-of-symptoms.html

3) Keller B, Receno CN, Franconi CJ, Harenberg S, Stevens J, Mao X, Stevens SR, Moore G, Levine S, Chia J, Shungu D, Hanson MR. Cardiopulmonary and metabolic responses during a 2-day CPET in myalgic encephalomyelitis/chronic fatigue syndrome: translating reduced oxygen consumption to impairment status to treatment considerations. J Transl Med. 2024 Jul 5;22(1):627. doi: 10.1186/s12967-024-05410-5. PMID: 38965566; PMCID: PMC11229500.

https://pubmed.ncbi.nlm.nih.gov/38965566/

4) PREPRINT
Molecular Landscape of Modality-Specific Exercise Adaptation in Human Skeletal Muscle through Large-Scale Multi-OMICs Integration
Macsue Jacques, Shanie Landen, Adam P Sharples, Andrew Garnham, Ralf Schittenhelm, Joel Stele, Aino Heikkinen, Elina Sillanpää, Miina Ollikainen, James Broatch, Navabeh Zarekookandeh, Ola Hanson, Ola Ekström, Olof Asplund, Séverine Lamon, Sarah E. Alexander, Cassandra Smith, Carlie Bauer, Mary N. Woessner, Itamar Levinger, Andrew E Teschendorff, Linn Gillberg, Ida Blom, Jørn Wulff Helge, Nicholas R Harvey, Larisa M Haupt, Lyn R Griffiths, Atul S. Deshmukh, Kirsi H Pietiläinen, Päivi Piirilä, Robert AE Seaborne, Bernadette Jones-Freeman, Nir Eynon
bioRxiv 2024.07.14.603458; doi: https://doi.org/10.1101/2024.07.14.603458

https://www.biorxiv.org/content/10.1101/2024.07.14.603458v1.supplementary-material