Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response

Cell-to-substrate adhesion sites, also known as focal adhesion sites (FAs), are complexes of different proteins on the cell surface. FAs play important roles in communication between cells and the extracellular matrix (ECM), leading to signal transduction involving different proteins that ultimately...

Full description

Saved in:
Bibliographic Details
Main Author: Kazuo Katoh
Format: Article
Language:English
Published: IMR Press 2024-11-01
Series:Frontiers in Bioscience-Landmark
Subjects:
Online Access:https://www.imrpress.com/journal/FBL/29/11/10.31083/j.fbl2911392
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1846149055789400064
author Kazuo Katoh
author_facet Kazuo Katoh
author_sort Kazuo Katoh
collection DOAJ
description Cell-to-substrate adhesion sites, also known as focal adhesion sites (FAs), are complexes of different proteins on the cell surface. FAs play important roles in communication between cells and the extracellular matrix (ECM), leading to signal transduction involving different proteins that ultimately produce the cell response. This cell response involves cell adhesion, migration, motility, cell survival, and cell proliferation. The most important component of FAs are integrins. Integrins are transmembrane proteins that receive signals from the ECM and communicate them to the cytoplasm, thus activating several downstream proteins in a signaling cascade. Cellular Proto-oncogene tyrosine-protein kinase Src (c-Src) and focal adhesion kinase (FAK) are non-receptor tyrosine kinases that functionally interact to promote crucial roles in FAs. c-Src is a tyrosine kinase, activated by autophosphorylation and, in turn, activates another important protein, FAK. Activated FAK directly interacts with the cytoplasmic domain of integrin and activates other FA proteins by attaching to them. These proteins activated by FAK then activate other downstream pathways such as mitogen-activated protein kinase (MAPK) and Akt pathways involved in cell proliferation, migration, and cell survival. Src can induce detachment of FAK from the integrin to increase the focal adhesion turnover. As a result, the Src-FAK complex in FAs is critical for cell adhesion and survival mechanisms. Overexpression of FA proteins has been linked to a variety of pathological disorders, including cancers, growth retardation, and bone deformities. FAK and Src are overexpressed in various cancers. This review, which focuses on the roles of two important signaling proteins, c-Src and FAK, attempts to provide a thorough and up-to-date examination of the signal transduction mechanisms mediated by focal adhesions. The author also described that FAK and Src may serve as potential targets for future therapies against diseases associated with their overexpression, such as certain types of cancer.
format Article
id doaj-art-c78eafaa97ee440ab227d240612578ed
institution Kabale University
issn 2768-6701
language English
publishDate 2024-11-01
publisher IMR Press
record_format Article
series Frontiers in Bioscience-Landmark
spelling doaj-art-c78eafaa97ee440ab227d240612578ed2024-11-30T05:06:31ZengIMR PressFrontiers in Bioscience-Landmark2768-67012024-11-01291139210.31083/j.fbl2911392S2768-6701(24)01444-8Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell ResponseKazuo Katoh0Laboratory of Human Anatomy and Cell Biology, Faculty of Health Sciences, Tsukuba University of Technology, 305-8521 Tsukuba, JapanCell-to-substrate adhesion sites, also known as focal adhesion sites (FAs), are complexes of different proteins on the cell surface. FAs play important roles in communication between cells and the extracellular matrix (ECM), leading to signal transduction involving different proteins that ultimately produce the cell response. This cell response involves cell adhesion, migration, motility, cell survival, and cell proliferation. The most important component of FAs are integrins. Integrins are transmembrane proteins that receive signals from the ECM and communicate them to the cytoplasm, thus activating several downstream proteins in a signaling cascade. Cellular Proto-oncogene tyrosine-protein kinase Src (c-Src) and focal adhesion kinase (FAK) are non-receptor tyrosine kinases that functionally interact to promote crucial roles in FAs. c-Src is a tyrosine kinase, activated by autophosphorylation and, in turn, activates another important protein, FAK. Activated FAK directly interacts with the cytoplasmic domain of integrin and activates other FA proteins by attaching to them. These proteins activated by FAK then activate other downstream pathways such as mitogen-activated protein kinase (MAPK) and Akt pathways involved in cell proliferation, migration, and cell survival. Src can induce detachment of FAK from the integrin to increase the focal adhesion turnover. As a result, the Src-FAK complex in FAs is critical for cell adhesion and survival mechanisms. Overexpression of FA proteins has been linked to a variety of pathological disorders, including cancers, growth retardation, and bone deformities. FAK and Src are overexpressed in various cancers. This review, which focuses on the roles of two important signaling proteins, c-Src and FAK, attempts to provide a thorough and up-to-date examination of the signal transduction mechanisms mediated by focal adhesions. The author also described that FAK and Src may serve as potential targets for future therapies against diseases associated with their overexpression, such as certain types of cancer.https://www.imrpress.com/journal/FBL/29/11/10.31083/j.fbl2911392focal adhesion (fa)extracellular matrix (ecm)integrinfocal adhesion kinase (fak)c-src
spellingShingle Kazuo Katoh
Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response
Frontiers in Bioscience-Landmark
focal adhesion (fa)
extracellular matrix (ecm)
integrin
focal adhesion kinase (fak)
c-src
title Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response
title_full Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response
title_fullStr Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response
title_full_unstemmed Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response
title_short Signal Transduction Mechanisms of Focal Adhesions: Src and FAK-Mediated Cell Response
title_sort signal transduction mechanisms of focal adhesions src and fak mediated cell response
topic focal adhesion (fa)
extracellular matrix (ecm)
integrin
focal adhesion kinase (fak)
c-src
url https://www.imrpress.com/journal/FBL/29/11/10.31083/j.fbl2911392
work_keys_str_mv AT kazuokatoh signaltransductionmechanismsoffocaladhesionssrcandfakmediatedcellresponse