Proteomics

Dataset Information

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Proteomic Analysis of Livers from Fat-fed Mice Deficient in Either PKCδ or PKCɛ


ABSTRACT: To investigate the mechanisms of lipid-activated protein kinase C (PKC) family, PKCδ or PKCɛ, involved in insulin resistance and fatty acid metabolism, we employed an in vivo adaptation of SILAC to examine the effects of a fat diet together with deletion of PKCδ or PKCɛ on the expression of liver proteins.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Bing Qing Liao  

LAB HEAD: Carsten Schmitz-Peiffer

PROVIDER: PXD000971 | Pride | 2014-11-04

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
KR_240111_KOC_F1.raw Raw
KR_240111_KOC_F10.raw Raw
KR_240111_KOC_F11.raw Raw
KR_240111_KOC_F12.raw Raw
KR_240111_KOC_F13.raw Raw
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Publications

Proteomic analysis of livers from fat-fed mice deficient in either PKCδ or PKCε identifies Htatip2 as a regulator of lipid metabolism.

Liao Bing M BM   Raddatz Katy K   Zhong Ling L   Parker Benjamin L BL   Raftery Mark J MJ   Schmitz-Peiffer Carsten C  

Proteomics 20141014 21-22


Insulin resistance contributes to the development of Type 2 diabetes, and is associated with lipid oversupply. Deletion of isoforms of the lipid-activated protein kinase C (PKC) family, PKCδ or PKCε, improves insulin action in fat-fed mice, but differentially affects hepatic lipid metabolism. To investigate the mechanisms involved, we employed an in vivo adaptation of SILAC to examine the effects of a fat diet together with deletion of PKCδ or PKCε on the expression of liver proteins. We identif  ...[more]

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