scholarly journals Increased Resistance to Apoptosis in Cells Overexpressing Thymosin Beta Four: A Role for Focal Adhesion Kinase pp125FAK

2000 ◽  
Vol 7 (4) ◽  
pp. 311-320 ◽  
Author(s):  
M. Niu ◽  
V. T. Nachmias
2021 ◽  
Author(s):  
Jean A. Castillo-Badillo ◽  
N. Gautam

Cell shape regulation is important but the mechanisms that govern shape are not fully understood, in part due to limited experimental models where cell shape changes and underlying molecular processes can be rapidly and non-invasively monitored in real time. Here, we use an optogenetic tool to activate RhoA in the middle of mononucleated macrophages to induce contraction, resulting in a side with the nucleus that retains its shape and a non-nucleated side which was unable to maintain its shape and collapsed. In cells overexpressing focal adhesion kinase (FAK), the non-nucleated side exhibited a wide flat morphology and was similar in adhesion area to the nucleated side. In cells overexpressing fascin, an actin bundling protein, the non-nucleated side assumed a spherical shape and was similar in height to the nucleated side. This effect of fascin was also observed in fibroblasts even without inducing furrow formation. Based on these results, we conclude that FAK and fascin work together to maintain cell shape by regulating adhesion area and height, respectively, in different cell types.


2003 ◽  
Vol 21 (2) ◽  
pp. 83-93 ◽  
Author(s):  
Andrea Contestabile ◽  
Dario Bonanomi ◽  
Ferran Burgaya ◽  
Jean‐Antoine Girault ◽  
Flavia Valtorta

2014 ◽  
Vol 290 (1) ◽  
pp. 478-491 ◽  
Author(s):  
Gress Kadaré ◽  
Nicolas Gervasi ◽  
Karen Brami-Cherrier ◽  
Heike Blockus ◽  
Said El Messari ◽  
...  

FEBS Letters ◽  
1998 ◽  
Vol 432 (3) ◽  
pp. 197-201 ◽  
Author(s):  
Kazue Ueki ◽  
Toshihide Mimura ◽  
Tetsuya Nakamoto ◽  
Terukatsu Sasaki ◽  
Shinichi Aizawa ◽  
...  

2013 ◽  
Vol 55 ◽  
pp. 1-15 ◽  
Author(s):  
Laura E. Gallagher ◽  
Edmond Y.W. Chan

Autophagy is a conserved cellular degradative process important for cellular homoeostasis and survival. An early committal step during the initiation of autophagy requires the actions of a protein kinase called ATG1 (autophagy gene 1). In mammalian cells, ATG1 is represented by ULK1 (uncoordinated-51-like kinase 1), which relies on its essential regulatory cofactors mATG13, FIP200 (focal adhesion kinase family-interacting protein 200 kDa) and ATG101. Much evidence indicates that mTORC1 [mechanistic (also known as mammalian) target of rapamycin complex 1] signals downstream to the ULK1 complex to negatively regulate autophagy. In this chapter, we discuss our understanding on how the mTORC1–ULK1 signalling axis drives the initial steps of autophagy induction. We conclude with a summary of our growing appreciation of the additional cellular pathways that interconnect with the core mTORC1–ULK1 signalling module.


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