Archipelago architecture of the focal adhesion: Membrane molecules freely enter and exit from the focal adhesion zone

Cytoskeleton ◽  
2012 ◽  
Vol 69 (6) ◽  
pp. 380-392 ◽  
Author(s):  
Akihiro C. E. Shibata ◽  
Takahiro K. Fujiwara ◽  
Limin Chen ◽  
Kenichi G. N. Suzuki ◽  
Yoshiro Ishikawa ◽  
...  
Keyword(s):  
Focal Adhesion ◽  
Adhesion Zone

Kinetics of Membrane Spreading on Compliant Bio-Adhesive Substrates

2010 ◽  
Author(s):  
Alireza Sarvestani
Keyword(s):  
Focal Adhesion ◽  
Early Stage ◽  
Thermodynamic Force ◽  
Mechanical Stiffness ◽  
Compliant Substrates ◽  
Wide Range ◽  
Adhesion Zone ◽  
Spread Area ◽  
Substrate Elasticity ◽  
Kinetics Of

The contact formation between cell membrane and a bio-adhesive substrate is driven by binding between transmembrane mobile receptors (e.g., integrin) and complementary ligand molecules on the substrate (fibronectin, collagen, etc.) This short range specific adhesion is alleviated by a phalanx of interfacial non-specific forces. In addition to cell-substrate interfacial interactions, cell adhesion can be mediated by a wide range of substrate physiochemical properties. In particular, mechanical stiffness of the substrate has been recognized as one of the major regulators for bio-adhesion. Cells in general, exhibit an apparent adhesion preference for stiffer substrates and switch from a round to spread morphology as the substrate stiffness increases. Understanding the mechano-chemical pathways mediating the interplay between the substrate properties and cell behavior could be critical for effective performance of synthetic biomaterials in tissue engineering applications. In this study, we consider the effect of substrate elasticity on the dynamics of membrane spreading and growth of focal adhesion zone. The formation and growth of the focal adhesion points during the early stage of adhesion process is a result of spontaneous spreading of membrane on the substrate. This can be considered as a non-equilibrium kinetic process which is controlled by the diffusibility of receptor molecules. In order to study the effect of substrate elasticity on the kinetics of membrane-substrate association, receptors are assumed as ideal solute particles laterally diffusing within the plane of the membrane until they are stabilized through association with their complementary ligands which are immobilized on the surface of a compliant substrate. Considering different mechanical stiffness for the substrates, the displacement and speed of spreading at the edge of adhesion zone are predicted as a function of time. Results show that decreasing the stiffness of bio-adhesive substrates reduces the rate of membrane spreading, due to a weaker thermodynamic force which drives the membrane-substrate association. This mechanism restrains the growth of focal adhesion zones on compliant substrates and can be considered as a reason for smaller spread area of the cells after stabilization of adhesion.

Early signalling events of autophagy

2013 ◽  
Vol 55 ◽  
pp. 1-15 ◽  
Author(s):  
Laura E. Gallagher ◽  
Edmond Y.W. Chan
Keyword(s):  
Protein Kinase ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Mammalian Cells ◽  
Mammalian Target Of Rapamycin ◽  
Interacting Protein ◽  
The Core ◽  
Autophagy Gene ◽  
Autophagy Induction ◽  
Cellular Pathways

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.

111-OR: Pancreatic Elastase Regulates Human Beta-Cell Proliferation via the Focal Adhesion and PAR2 Signaling Pathways

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 111-OR
Author(s):  
GIORGIO BASILE ◽  
AMEDEO VETERE ◽  
KA-CHEUK LIU ◽  
JIANG HU ◽  
OLOV ANDERSSON ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Beta Cell ◽  
Signaling Pathways ◽  
Focal Adhesion ◽  
Beta Cell Proliferation ◽  
Pancreatic Elastase ◽  
Human Beta Cell
Sign in / Sign up

Export Citation Format

Share Document