Dataset Information

Protein quality control by MARCH6/TRC8

ABSTRACT: Forward genetic screens in human cells we find that the proteasome-mediated degradation of the soluble misfolded reporter, mCherry-CL1, involves two ER-resident E3 ligases, MARCH6 and TRC8. To identify a more physiological correlate we used quantitative mass spectrometry and found that TRC8 and MARCH6 depletion altered the turnover of the tail-anchored protein Heme-Oxygenase-1 (HO-1).

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: James Williamson

LAB HEAD: James Nathan

PROVIDER: PXD008955 | Pride | 2018-04-18

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	JN-SSB_Knockouts_TMT10_20pc_F1.raw	Raw
	JN-SSB_Knockouts_TMT10_20pc_F10.raw	Raw
	JN-SSB_Knockouts_TMT10_20pc_F11.raw	Raw
	JN-SSB_Knockouts_TMT10_20pc_F12.raw	Raw
	JN-SSB_Knockouts_TMT10_20pc_F13.raw	Raw

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Publications

MARCH6 and TRC8 facilitate the quality control of cytosolic and tail-anchored proteins.

Stefanovic-Barrett Sandra S Dickson Anna S AS Burr Stephen P SP Williamson James C JC Lobb Ian T IT van den Boomen Dick Jh DJ Lehner Paul J PJ Nathan James A JA

EMBO reports 20180308 5

Misfolded or damaged proteins are typically targeted for destruction by proteasome-mediated degradation, but the mammalian ubiquitin machinery involved is incompletely understood. Here, using forward genetic screens in human cells, we find that the proteasome-mediated degradation of the soluble misfolded reporter, mCherry-CL1, involves two ER-resident E3 ligases, MARCH6 and TRC8. mCherry-CL1 degradation is routed via the ER membrane and dependent on the hydrophobicity of the substrate, with comp ...[more]

PMID: 29519897

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