Table 2.

The interactome of VDAC in various states along with the associated diseases. The gating of VDAC includes: open, closed, multimeric, and blockage of pore by specific proteins and metabolites. When these interactions are disrupted, they lead to disease states, listed in the “Disease States” row.

Gating of VDAC	Molecules that Bind to Each State of VDAC	Disease States
Open	ADP/ATP [35] Cl- [35] NADH/NAD+ [7,10]	NADH increases during anoxia and leads to VDAC closure to ATP [67]
Closed	Calcium [17] ○ Mitochondria-Associated Membranes (MAMS) [64] ○ IP3R [63], ○ Grp75 [63] Mcl-1 [66]	Increase in calcium into the mitochondria leads to apoptosis [62] Friedreich’s ataxia (FA) with dysregulation of MAMs [64] Lung cancer cell migration due to decreased calcium uptake with binding to Mcl-1 [66]
Multimeric	Mitochondrial DNA [68] Cytochrome C [69] Bcl-XL [70] BAX [71] BAK [71]	Parkinson’s disease due to oligomerization [68] Systemic lupus erythematosus (SLE) due to mtDNA release into cytosol [68] Apoptosis due to cytochrome C release into cytosol [15] Association to Bcl-XL as well as other proteins leads to disease states such as ischemia reperfusion injury [70,72]
Blockage of Pore	Free Tubulin [73,74] Alpha-synuclein [63] Hexokinase II [75]	Antagonism of Tubulin’s association with VDAC leads to Cancerogenesis and cell proliferation [73,74] Alpha-synuclein, the Parkinson’s disease associated protein can cause dysregulation in calcium homeostasis. [72] Growth of tumor cells due to hexokinase binding to hVDAC1 [76] Bacterial infections such as Chlamydia trachomatis due to hexokinase association with hVDAC1 [76]