TNK2/ACK1-mediated phosphorylation of ATP5F1A (ATP synthase F1 subunit alpha) selectively augments survival of prostate cancer while engendering mitochondrial vulnerability
Surbhi Chouhan, Mithila Sawant, Cody Weimholt, Jingqin Luo, Robert W. Sprung, Mailyn Terrado, David M. Mueller, H. Shelton Earp, Nupam P. Mahajan
Abstract
: ATP5F1A: ATP synthase F1 subunit alpha; ATP5IF1: ATP synthase inhibitory factor subunit 1; CRPC: castration-resistant prostate cancer; DNM1L: dynamin 1 like; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; Mdivi-1: mitochondrial division inhibitor 1; Mut-ATP5F1A: Y243,246A mutant of ATP5F1A; OXPHOS: oxidative phosphorylation; PC: prostate cancer; PINK1: PTEN induced kinase 1; p-Y-ATP5F1A: phosphorylated tyrosine 243 and 246 on ATP5F1A; TNK2/ACK1: tyrosine kinase non receptor 2; Ub: ubiquitin; WT: wild type.
Topics & Concepts
MitophagyBiologyMitochondrionCell biologyKinaseTyrosine kinaseCancer cellAutophagyCancer researchCancerBiochemistrySignal transductionApoptosisGeneticsATP Synthase and ATPases ResearchMitochondrial Function and PathologyRNA modifications and cancer