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首页> 外文期刊>Journal of Cellular Physiology >The Integrin-Mediated ILK-Parvin-alpha Pix Signaling Axis Controls Differentiation in Mammary Epithelial Cells
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The Integrin-Mediated ILK-Parvin-alpha Pix Signaling Axis Controls Differentiation in Mammary Epithelial Cells

机译：的Integrin-Mediated ILK-Parvin-alpha照片信号轴控制分化乳腺上皮细胞

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Epithelial cell adhesion to the surrounding extracellular matrix is necessary for their proper behavior and function. During pregnancy and lactation, mammary epithelial cells (MECs) receive signals from their interaction with laminin via beta 1-integrin (beta 1-itg) to establish apicobasal polarity and to differentiate in response to prolactin. Downstream of beta 1-itg, the scaffold protein Integrin Linked Kinase (ILK) has been identified as the key signal transducer that is required for both lactational differentiation and the establishment of apico-basal polarity. ILK is an adaptor protein that forms the IPP complex with PINCH and Parvins, which are central to its adaptor functions. However, it is not known how ILK and its interacting partners control tissue-specific gene expression. Expression of ILK mutants, which weaken the interaction between ILK and Parvin, revealed that Parvins have a role in mammary epithelial differentiation. This conclusion was supported by shRNA-mediated knockdown of the Parvins. In addition, shRNA knockdown of the Parvin-binding guanine nucleotide exchange factor alpha Pix prevented prolactin-induced differentiation. alpha Pix depletion did not disrupt focal adhesions, MEC proliferation, or polarity. This suggests that alpha Pix represents a differentiation-specific bifurcation point in beta 1-itg-ILK adhesive signaling. In summary, this study has identified a new role for Parvin and alpha Pix downstream of the integrin-ILK signaling axis for MEC differentiation. (C) 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc.
机译：上皮细胞粘附到周围细胞外基质对于他们是必要的适当的行为和功能。和哺乳期乳腺上皮细胞(mec)接收信号的交互层粘连蛋白通过β1-integrin(β一itg)建立apicobasal极性和区分在泌乳素。β一itg的下游,脚手架蛋白整合素连接激酶(同类)已被确定所需的关键信号传感器授乳的分化和建立apico-basal极性。适配器蛋白质形成了IPP复杂捏和帕文,这是它的中心适配器的功能。家族及其合作伙伴交互控制组织基因表达。相同的突变体,削弱之间的交互同类帕文,表明帕文有作用在乳腺上皮细胞分化。结论是由shRNA-mediated支持帕文击倒。Parvin-binding鸟嘌呤的击倒核苷酸交换因子α焦油预防prolactin-induced分化。消耗不破坏病灶粘连,MEC扩散,或极性。α影片代表一个differentiation-specific在β1-itg-ILK胶粘剂分歧点信号。一个新的角色帕文和αPix的下游MEC的integrin-ILK信号轴分化。细胞生理由威利出版期刊、公司。

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