| Interactor | Main localization | Notes(s) | Reference |
| BAD | Cytosol mitochondria | By antagonizing BAD, BCL-XL modulates the metabolic functions of a mitochondrial multiprotein complex involving glucokinase, PKA, and PP1 | [64] | Beclin 1 | Cytosol Golgi network | BCL-XL binds to Beclin 1, thus inhibiting stress-induced, but not baseline, autophagy | [94, 97, 100] | DRP1 | Mitochondria | BCL-XL interacts with DRP1, altering the mitochondrial function of neurons to stimulate the formation of synapses | [117] | F1FO ATP synthase | Mitochondria | BCL-XL increases the enzymatic activity of the F1FO ATP synthase, hence, stabilizing the and maximizing mitochondrial ATP synthesis | [67, 68] | IP3R | ER | BCL-XL reduces Ca2+ concentration in the ER | [25–27] | Krebs’s cycle | Mitochondria | BCL-XL overexpression reduces the levels of virtually all TCA (but not glycolytic) intermediates, modulating both N--acetylation and autophagy | [74, 79–82] | MAPK9 PLK1 | Cytosol nucleus | BCL-XL is phosphorylated at S49 by PLK1 and MAPK9 in a cell cycle-dependent fashion | [104] | NLRP1 inflammasome | Cytosol | BCL-XL inhibits the NLRP1 inflammasome, interfering with the secretion of IL-1 and IL-18 | [118, 120] | p53 | Cytosol mitochondria | BCL-XL binds to p53, hence, inhibiting both its pro-apoptotic and metabolic functions | [54, 60, 66] | PKM2 | Cytosol mitochondria | PKM2 stimulates the expression of BCL-XL at the transcriptional level | [78] | PLK3 | Cytosol nucleus | PLK3 phosphorylates BCL-XL at S62 in response to DNA-damaging agents, favoring a cell cycle arrest at the G2 checkpoint | [105] | RAC2 | Cytosol plasma membrane | In some settings, antiapoptotic BCL-2 family members exert prooxidant functions, perhaps linked to their interaction with RAC2 | [70–72] | VDAC1 | Mitochondria | BCL-XL promotes the exchange of metabolites between the cytosol and the mitochondrial matrix | [24, 44] |
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