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Identification of nutrient dependend PIK3C2B regulators

ABSTRACT: To identify factors responsible for the differential localization and activity of PIK3C2Bin the presence or absence of serum mitogens we took a quantitative functional proteomics approach based on stable isotope labeling of amino acids in cell culture (SILAC). Genome-engineered HEK293T cells endogenously expressing eGFP-PI3KC15were cultured in serum-containing or serum-deprived media containing heavy or light amino acids, and subjected to affinity capture using a GFP trap matrix and LC-MS/MS

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Alexander Wallroth

LAB HEAD: Volker Haucke

PROVIDER: PXD014533 | Pride | 2019-10-02

REPOSITORIES: Pride

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			Action	DRS
	MS810_HS670_AspN.raw	Raw
	MS810_HS670_T.raw	Raw
	PeptideSummaryReport_AspN.htm	Other
	PeptideSummaryReport_Trypsin.htm	Other

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Publications

Protein kinase N controls a lysosomal lipid switch to facilitate nutrient signalling via mTORC1.

Wallroth Alexander A Koch Philipp A PA Marat Andrea L AL Krause Eberhard E Haucke Volker V

Nature cell biology 20190826 9

Mechanistic target of rapamycin (mTOR) kinase functions in two multiprotein complexes: lysosomal mTOR complex 1 (mTORC1) and mTORC2 at the plasma membrane. mTORC1 modulates the cell response to growth factors and nutrients by increasing protein synthesis and cell growth, and repressing the autophagy-lysosomal pathway1-4; however, dysfunction in mTORC1 is implicated in various diseases3,5,6. mTORC1 activity is regulated by phosphoinositide lipids7-10. Class I phos ...[more]

PMID: 31451768

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