scholarly journals Monitoring focal adhesion kinase phosphorylation dynamics in live cells

The Analyst ◽  
2017 ◽  
Vol 142 (15) ◽  
pp. 2713-2716 ◽  
Author(s):  
Nur P. Damayanti ◽  
Kevin Buno ◽  
Nagarajan Narayanan ◽  
Sherry L. Voytik Harbin ◽  
Meng Deng ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Focal Adhesion Kinase ◽  
Real Time ◽  
Focal Adhesion ◽  
Receptor Tyrosine Kinase ◽  
Live Cells ◽  
Real Time Monitoring ◽  
Cellular Functions ◽  
Focal Adhesion Kinase Phosphorylation ◽  
Kinase Phosphorylation

Focal adhesion kinase (FAK) is a cytoplasmic non-receptor tyrosine kinase essential for a diverse set of cellular functions. FAK FLIM-peptide biosensor enables real-time monitoring of FAK phopshorylation activity.

scholarly journals Evaluation of the Correlation between Focal Adhesion Kinase Phosphorylation and Cell Adhesion Force Using “DEP” Technology

Sensors ◽  
2012 ◽  
Vol 12 (5) ◽  
pp. 5951-5965 ◽  
Author(s):  
Chyung Ay ◽  
Chih-Chang Yeh ◽  
Min-Chih Hsu ◽  
Huaang-Youh Hurng ◽  
Philip Chi Lip Kwok ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Adhesion Force ◽  
Focal Adhesion Kinase Phosphorylation ◽  
Kinase Phosphorylation

scholarly journals Multiplexed High Content Screening Reveals That Cigarette Smoke Condensate-Altered Cell Signaling Pathways Are Accentuated Through FAK Inhibition in Human Bronchial Cells

2012 ◽  
Vol 31 (3) ◽  
pp. 257-266 ◽  
Author(s):  
Charleata A. Carter
Keyword(s):  
Focal Adhesion Kinase ◽  
Cigarette Smoke ◽  
Focal Adhesion ◽  
Cell Number ◽  
Cell Periphery ◽  
Cigarette Smoke Condensate ◽  
Mitogen Activated Protein ◽  
Focal Adhesion Kinase Phosphorylation ◽  
Altered Cell ◽  
Kinase Phosphorylation

The mechanisms by which cigarette smoke condensate (CSC) disrupts F-actin and decreases cell motility in human bronchial (BEAS-2B) cells were assessed. The hypothesis that CSC activated focal adhesion kinase (FAK), mitogen-activated protein kinases (MAPKs), and paxillin in BEAS-2B cells was tested. When BEAS-2B cells were treated with 20 to 100 μg/mL CSC for 1 hour, FAK increased. The CSC caused F-actin disruption, while FAK inhibition alone caused actin aggregates to collapse to the cell periphery, but FAK inhibition combined with CSC caused actin aggregates to distribute throughout the cells. The CSC treatment of BEAS-2B cells showed a dose-dependent increase in the activation of the MAPKs, c-Jun, JNK, ERK, p38, and heat shock protein 27 (Hsp27) and paxillin. Focal adhesion kinase phosphorylation inhibition combined with CSC treatment increased p38 and ERK at 1 hour and 24 hours along with decreased cell number and motility compared with CSC treatment alone. CSC exerts changes in BEAS-2B cells by altering morphology and activating MAPK pathways.

Sign in / Sign up

Export Citation Format

Share Document