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DPY19L3 参与 C2C12 成肌细胞的肌发生分化。

Involvement of DPY19L3 in Myogenic Differentiation of C2C12 Myoblasts.

机构信息

Department of Applied Chemistry, Faculty of Science and Technology, Keio University, 3-14-1 Hiyoshi, Kohoku-ku, Yokohama 223-8522, Japan.

出版信息

Molecules. 2021 Sep 19;26(18):5685. doi: 10.3390/molecules26185685.

Abstract

DPY19L3 has been identified as a -mannosyltransferase for thrombospondin type-1 repeat domain-containing proteins. In this study, we focused on the role of DPY19L3 in the myogenic differentiation of C2C12 mouse myoblast cells. We carried out DPY19L3 gene depletion using the CRISPR/Cas9 system. The result showed that these DPY19L3-knockout cells could not be induced for differentiation. Moreover, the phosphorylation levels of MEK/ERK and p70S6K were suppressed in the DPY19L3-knockout cells compared with that of parent cells, suggesting that the protein(s) that is(are) DPY19L3-mediated -mannosylated and regulate(s) MEK/ERK or p70S6K signaling is(are) required for the differentiation.

摘要

DPY19L3 被鉴定为一种血栓反应素型-1 重复结构域蛋白的 -甘露糖基转移酶。在本研究中,我们专注于 DPY19L3 在 C2C12 小鼠成肌细胞的成肌分化中的作用。我们使用 CRISPR/Cas9 系统进行 DPY19L3 基因缺失。结果表明,这些 DPY19L3 敲除细胞不能被诱导分化。此外,与亲本细胞相比,DPY19L3 敲除细胞中 MEK/ERK 和 p70S6K 的磷酸化水平受到抑制,这表明 DPY19L3 介导的 -甘露糖化并调节 MEK/ERK 或 p70S6K 信号的蛋白对于分化是必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9dee/8467457/7401fd325a36/molecules-26-05685-g001.jpg

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