Proteomics

Dataset Information

0

LC-MS/M of GABARAPL1 and GABARAPL1Y49A/L50A immunoprecipitates


ABSTRACT: To identify substrates or adaptors of selective autophagy, we performed a differential interactome screen using wild-type GABARAPL1 and the LIR-docking site mutant GABARAPL1Y49A/N50A,

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Early Embryonic Cell

DISEASE(S): Disease Free

SUBMITTER: Yasuhiro Yamamoto  

LAB HEAD: Noboru Mizushima

PROVIDER: PXD024290 | Pride | 2021-04-09

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
LC-MSMS_of_GABARAPL1__raw.xlsx Xlsx
Table_S1.xlsx Xlsx
checksum.txt Txt
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Publications

NEK9 regulates primary cilia formation by acting as a selective autophagy adaptor for MYH9/myosin IIA.

Yamamoto Yasuhiro Y   Chino Haruka H   Tsukamoto Satoshi S   Ode Koji L KL   Ueda Hiroki R HR   Mizushima Noboru N  

Nature communications 20210602 1


Autophagy regulates primary cilia formation, but the underlying mechanism is not fully understood. In this study, we identify NIMA-related kinase 9 (NEK9) as a GABARAPs-interacting protein and find that NEK9 and its LC3-interacting region (LIR) are required for primary cilia formation. Mutation in the LIR of NEK9 in mice also impairs in vivo cilia formation in the kidneys. Mechanistically, NEK9 interacts with MYH9 (also known as myosin IIA), which has been implicated in inhibiting ciliogenesis t  ...[more]

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