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iRhom1 rescues cognitive dysfunction in multiple sclerosis via preventing myelin injury
Author(s) -
Sun Haolu,
Yang Hui,
Wu Yiwang,
Bian Hege,
Wang Menglin,
Huang Yan,
Jin Juan
Publication year - 2021
Publication title -
genes, brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.315
H-Index - 91
eISSN - 1601-183X
pISSN - 1601-1848
DOI - 10.1111/gbb.12771
Subject(s) - remyelination , disintegrin , metalloproteinase , multiple sclerosis , oligodendrocyte , myelin , demyelinating disorder , neuroscience , myelin sheath , microbiology and biotechnology , biology , medicine , matrix metalloproteinase , immunology , genetics , central nervous system
Multiple sclerosis (MS) is characterized by myelin sheath injury. A disintegrin and metalloprotease‐17 (ADAM17), a disintegrin and metalloproteinase, is essential in regulating oligodendrocyte (OL) regeneration and remyelination under demyelinating conditions. iRhom1, a highly conserved inactive protease that belongs to the rhomboid family, is one of key regulators for ADAM17 maturation. However, it is unknown whether iRhom1 also plays a role in central neuron system myelination under demyelinating conditions like MS. In this study, we investigated the function of iRhom1/ADAM17 in cognitive capability in MS by establishing the mice with iRhom1 overexpression in the hippocampus.

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