Proteomics

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Mouse Skin LC-MS/MS


ABSTRACT: Previously, we reported that a null mutation of the Zdhhc13 gene caused by ethylnitrosourea (ENU) mutagenesis in mice resulted in severe systematic phenotypes with amyloidosis, alopecia, dermatitis and osteoporosis. In this study we continued to delineate the pathological mechanism for the dermatitis phenotype and to explore potential palmitoylation substrates of ZDHHC13, which potentially explain the loss-of-function phenotype of ZDHHC13 in skin. Our data clearly suggested that protein S-palmitoylation of a constellation of skin barrier components by ZDHHC13 is crucial for their protein stability, functions, and overall barrier integrity.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skin

SUBMITTER: Yi-Ju Chen  

LAB HEAD: Yi-Ju Chen

PROVIDER: PXD002958 | Pride | 2022-02-25

REPOSITORIES: Pride

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Publications

Palmitoyl Acyltransferase Activity of ZDHHC13 Regulates Skin Barrier Development Partly by Controlling PADi3 and TGM1 Protein Stability.

Chen Li-Ying LY   Lin Kuo-Ray KR   Chen Yi-Ju YJ   Chiang Yun-Jung YJ   Ho Kun-Chin KC   Shen Li-Fen LF   Song I-Wen IW   Liu Kai-Ming KM   Yang-Yen Hsin-Fang HF   Chen Yu-Ju YJ   Chen Yuan-Tsong YT   Liu Fu-Tong FT   Yen Jeffrey J Y JJY  

The Journal of investigative dermatology 20191025 5


Deficiency of the palmitoyl-acyl transferase ZDHHC13 compromises skin barrier permeability and renders mice susceptible to environmental bacterial infection and inflammatory dermatitis. It had been unclear how the lack of ZDHHC13 proteins resulted in cutaneous abnormalities. In this study, we first demonstrate that enzymatic palmitoylation activity, rather than protein scaffolding, by ZDHHC13 is essential for skin barrier integrity, showing that knock-in mice bearing an enzymatically dead DQ-to-  ...[more]

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