Inactivation of  TMEM106A  promotes lipopolysaccharide‐induced inflammation via the MAPK and NF‐κB signaling pathways in macrophages | Zendy

Zhang X. | Zendy; Feng T. | Zendy; Zhou X. | Zendy; Sullivan P. M. | Zendy; Hu F. | Zendy; Lou Y. | Zendy; Yu J. | Zendy; Feng J. | Zendy; Liu H. | Zendy; Chen Y. | Zendy

Open Access

Inactivation of TMEM106A promotes lipopolysaccharide‐induced inflammation via the MAPK and NF‐κB signaling pathways in macrophages

Author(s) -

Zhang X.,

Feng T.,

Zhou X.,

Sullivan P. M.,

Hu F.,

Lou Y.,

Yu J.,

Feng J.,

Liu H.,

Chen Y.

Publication year - 2021

Publication title -

clinical & experimental immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.329

H-Index - 135

eISSN - 1365-2249

pISSN - 0009-9104

DOI - 10.1111/cei.13528

Subject(s) - lipopolysaccharide , tumor necrosis factor alpha , inflammation , biology , immunology , microbiology and biotechnology , signal transduction , macrophage polarization , cd80 , mapk/erk pathway , macrophage , cd40 , cytotoxic t cell , biochemistry , in vitro

TMEM106A levels were increased in mouse and human monocytes/macrophages. Tmem106a deletion promotes the activation of macrophages and polarization towards M1 phenotype. Tmem106a inactivation promotes the activation of the MAPK and NF‐κB signaling pathways in macrophages during LPS stimulation.

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