Diverse mitochondrial abnormalities in a new cellular model of TAFFAZZIN deficiency are remediated by Cardiolipin-interacting small molecules

ABSTRACT: With the goal of identifying unappreciated pathways of mitochondrial dysregulation in Barth Syndrome, we utilized an unbiased proteomics strategy to identify pathways of metabolic dysregulation in an HEK293-based TAZ-deficiency model.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Hilary Vernon  

LAB HEAD: Hillary Vernon

PROVIDER: PXD026731 | Pride | 2022-02-17

REPOSITORIES: Pride