卡尔帕因小子单元介导的加列-3分泌调节引应力
Imjoo Jang1, Shalini Menon1, Indrajyoti Indra1
1Department of Biological Sciences, Wayne State University, Detroit, MI 48202, USA.
Biomedicines
|June 27, 2024
概括
卡尔帕因4 (Capn4) 通过通过分泌的加勒-3 (Gal3) 控制引力 (TF) 来调节细胞迁移. 这种机制独立于机械感知,突出了细胞运动中的新途径.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 分子生物学分子生物学
背景情况:
- 细胞迁移对发育和疾病至关重要,但其通过引力 (TF) 的调节尚未完全理解.
- 以前已经证明,calpain 4 (Capn4) 是calpain蛋白酶的非催化子单元,可以独立于calpain的蛋白解活性来调节TF.
- 此外,Capn4还促进了 galectin-3 (Gal3) 的分泌和氨酸酸化.
研究的目的:
- 研究细胞外加列-3 (Gal3) 在调节引力 (TF) 和焦点粘附中的作用.
- 阐明参与Capn4和Gal3介导的TF调节的信号通路.
- 为了确定Gal3是否影响细胞机械感知.
主要方法:
- 在capn4小鼠胚胎纤维细胞 (MEF) 中添加复合Gal3 (rGal3).
- 分析TF,焦点粘合分布,形态和粘合强度.
- 对c-Abl激酶活性和Gal3酸化在Y107.7的研究.
- 评估涉及β1整蛋白和焦粘附激酶 (FAK) 的信号通路.
主要成果:
- 细胞外Gal3增强了capn4MEF中的TF,并挽救了焦点粘附缺陷.
- 细胞外Gal3没有影响细胞机械感知.
- c-Abl激酶通过Y107对Gal3.3的酸化来调节Gal3分泌和TF产生.
- 3-介导的TF调节涉及β1整蛋白信号传递,而不是FAK Y397自酸化.
结论:
- Capn4和分泌的Gal3独立于机械感知来调节TF,为细胞迁移调节提供了新的见解.
- 这些发现揭示了在Gal3介导的TF控制中涉及β1整合素和c-Abl激酶的独特信号机制.
- 这项研究阐明了Capn4和Gal3通过TF调节在细胞运动中的作用.
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