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

Eleven genes may be involved in Myalgic encephalomyelitis (ME) (1):

WASF3, NUP98, PRUNE1, KIRREL3, TNK2, EIF3C, HOXA1, PMS2P5, HDAC7, FFAR3, MAP3K2.

WASF3 and PRUNE1 are involved in mitochondrial dysfunction as previously described:

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

Is TNK2 also involved in regulation af mitochondrial function in ME?

In cancer cells TNK2 controls the ATP synthase (2), quote:
"The challenge of rapid macromolecular synthesis enforces the energy-hungry cancer cell mitochondria to switch their metabolic phenotypes, accomplished by activation of oncogenic tyrosine kinases. Precisely how kinase activity is directly exploited by cancer cell mitochondria to meet high-energy demand, remains to be deciphered. Here we show that a non-receptor tyrosine kinase, TNK2/ACK1 (tyrosine kinase non receptor 2), phosphorylated ATP5F1A (ATP synthase F1 subunit alpha) at Tyr243 and Tyr246 (Tyr200 and 203 in the mature protein, respectively) that not only increased the stability of complex V, but also increased mitochondrial energy output in cancer cells. Further, phospho-ATP5F1A (p-Y-ATP5F1A) prevented its binding to its physiological inhibitor, ATP5IF1 (ATP synthase inhibitory factor subunit 1), causing sustained mitochondrial activity to promote cancer cell growth. TNK2 inhibitor, (R)-9b reversed this process..."

If TNK2 is involved in ME and the control of ATP synthase, then TNK2 is not phosphorylating ATP5F1A. And hypothetically TNK2 may be downregulated.

In NK cells from ME patients, TNK2 is on top of the list of downregulated kinases (table 3 in ref 3). 

Is expression of TNK2 in ME involved in the function of ATP synthase?

Further reading: 

A Review of the Inhibition of the Mitochondrial ATP Synthase by IF1 in vivo: Reprogramming Energy Metabolism and Inducing Mitohormesis

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) Chouhan S, Sawant M, Weimholt C, Luo J, Sprung RW, Terrado M, Mueller DM, Earp HS, Mahajan NP. TNK2/ACK1-mediated phosphorylation of ATP5F1A (ATP synthase F1 subunit alpha) selectively augments survival of prostate cancer while engendering mitochondrial vulnerability. Autophagy. 2023 Mar;19(3):1000-1025. doi: 10.1080/15548627.2022.2103961. Epub 2022 Jul 27. PMID: 35895804; PMCID: PMC9980697.

https://pubmed.ncbi.nlm.nih.gov/35895804/

3) Chacko A, Staines DR, Johnston SC, Marshall-Gradisnik SM. Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients. Gene Regul Syst Bio. 2016 Aug 28;10:85-93. doi: 10.4137/GRSB.S40036. PMID: 27594784; PMCID: PMC5003121.

https://pubmed.ncbi.nlm.nih.gov/27594784/