Shoc2-tranduced ERK1/2 motility signals – novel insights from functional genomics
Autor: | Emilia Galperin, Xiaohong Li, Jinpeng Liu, Chi Wang, Eric C. Rouchka, Eun Ryoung Jang, Myoungkun Jeoung |
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Jazyk: | angličtina |
Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Scaffold protein MAP Kinase Signaling System medicine.medical_treatment Motility Article Extracellular matrix 03 medical and health sciences Cell Movement Chlorocebus aethiops medicine Animals Cell adhesion Transcription factor Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 biology Growth factor Intracellular Signaling Peptides and Proteins Cell Biology Transforming growth factor beta Genomics Molecular biology Cell biology Crosstalk (biology) 030104 developmental biology COS Cells biology.protein Transcriptome |
Popis: | The extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway plays a central role in defining various cellular fates. Scaffold proteins modulating ERK1/2 activity control growth factor signals transduced by the pathway. Here, we analyzed signals transduced by Shoc2, a critical positive modulator of ERK1/2 activity. We found that loss of Shoc2 results in impaired cell motility and delays cell attachment. As ERKs control cellular fates by stimulating transcriptional response, we hypothesized that the mechanisms underlying changes in cell adhesion could be revealed by assessing the changes in transcription of Shoc2-depleted cells. Using quantitative RNA-seq analysis, we identified 853 differentially expressed transcripts. Characterization of the differentially expressed genes showed that Shoc2 regulates the pathway at several levels, including expression of genes controlling cell motility, adhesion, crosstalk with the transforming growth factor beta (TGFβ) pathway, and expression of transcription factors. To understand the mechanisms underlying delayed attachment of cells depleted of Shoc2, changes in expression of the protein of extracellular matrix (lectin galactoside-binding soluble 3-binding protein; LGALS3BP) were functionally analyzed. We demonstrated that delayed adhesion of the Shoc2-depleted cells is a result of attenuated expression and secretion of LGALS3BP. Together our results suggest that Shoc2 regulates cell motility by modulating ERK1/2 signals to cell adhesion. |
Databáze: | OpenAIRE |
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