| First Author | Chen L | Year | 2020 |
| Journal | FEBS Lett | Volume | 594 |
| Issue | 17 | Pages | 2881-2893 |
| PubMed ID | 32531799 | Mgi Jnum | J:306879 |
| Mgi Id | MGI:6718020 | Doi | 10.1002/1873-3468.13859 |
| Citation | Chen L, et al. (2020) Islet-cell autoantigen 69 accelerates liver regeneration by downregulating Tgfbr1 and attenuating Tgfbeta signaling in mice. FEBS Lett 594(17):2881-2893 |
| abstractText | Regeneration is a unique defense mechanism of liver tissue in response to functional cell loss induced by toxic chemicals or surgical resection. In this study, we found that Islet-cell autoantigen 69 (Ica69) accelerates liver regeneration in mice. Following 70% partial hepatectomy, both Ica69 mRNA and protein are significantly upregulated in mouse hepatocytes at the early stage of liver regeneration. Compared with the wild-type mice, Ica69-deficient mice have more severe liver injury, delayed liver regeneration, and high surgical accidental mortality following hepatectomy. Mechanistically, Ica69 interacts with Pick1 protein to regulate Tgfbr1 protein expression and Tgfbeta-induced Smad2 phosphorylation. Our findings suggest that Ica69 in liver tissue is a new potential target for promoting liver regeneration. |
