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The phenotypes were not rescued by expression of a palmitoylation-deficient CKAP4 mutant. These results suggest that CKAP4 plays a role in maintaining mitochondrial functions through the binding to VDAC2 at ER-mitochondria contact sites and that palmitoylation is required for this novel function of CKAP4.This article has an associated First Person interview with the first author of the paper.Vaccinia-related kinase 3 (VRK3) has been reported to be a negative regulator of ERK (ERK1 and ERK2; also known as MAPK3 and MAPK1, respectively) th
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