Literature summary for 3.4.22.B26 extracted from

Miyazaki, T.; Tonami, K.; Hata, S.; Aiuchi, T.; Ohnishi, K.; Lei, X.F.; Kim-Kaneyama, J.R.; Takeya, M.; Itabe, H.; Sorimachi, H.; Kurihara, H.; Miyazaki, A.
Calpain-6 confers atherogenicity to macrophages by dysregulating pre-mRNA splicing (2016), J. Clin. Invest., 126, 3417-3432 .

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	O35646	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
macrophage	-	Mus musculus	-

General Information

General Information	Comment	Organism
physiological function	inflammatory cytokines induce nonproteolytic calpain-6 (CAPN6), which associates with the essential exon junction complex-loading factor CWC22 in the cytoplasm. This association disturbs the nuclear localization of CWC22, thereby suppressing the splicing of target genes, including those related to Rac1 signaling. CAPN6 deficiency in low density lipoprotein receptor-deficient mice restores CWC22/EJC/Rac1 signaling, reduces pinocytotic deposition of native low density lipoprotein in macrophages, and attenuates macrophage recruitment into the lesions, generating an atheroprotective phenotype in the aorta. In macrophages, the induction of CAPN6 in the atheroma interior limits macrophage movements, resulting in a decline in cell clearance from the lesions. Myeloid CAPN6 contributes to atherogenesis in a murine model of bone marrow transplantation	Mus musculus

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Release 2023.1 (January 2023)