Title : Loss of tafazzin results in decreased myoblast differentiation in C2C12 cells: A myoblast model of Barth syndrome and cardiolipin deficiency.

Pub. Date : 2018 Aug

PMID : 29694924






3 Functional Relationships(s)
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Protein Name
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1 TAZ-KO cells exhibit mitochondrial deficits consistent with other models of BTHS, including accumulation of monolyso-CL (MLCL), decreased mitochondrial respiration, and increased mitochondrial ROS production. monolysocardiolipin tafazzin, phospholipid-lysophospholipid transacylase Mus musculus
2 TAZ-KO cells exhibit mitochondrial deficits consistent with other models of BTHS, including accumulation of monolyso-CL (MLCL), decreased mitochondrial respiration, and increased mitochondrial ROS production. monolysocardiolipin tafazzin, phospholipid-lysophospholipid transacylase Mus musculus
3 TAZ-KO cells exhibit mitochondrial deficits consistent with other models of BTHS, including accumulation of monolyso-CL (MLCL), decreased mitochondrial respiration, and increased mitochondrial ROS production. ros tafazzin, phospholipid-lysophospholipid transacylase Mus musculus