scholarly journals Phosphorylation of ACAP1 by Akt Regulates the Stimulation-Dependent Recycling of Integrin β1 to Control Cell Migration

2005 ◽  
Vol 9 (5) ◽  
pp. 663-673 ◽  
Author(s):  
Jian Li ◽  
Bryan A. Ballif ◽  
Aimee M. Powelka ◽  
Jun Dai ◽  
Steven P. Gygi ◽  
...  
2019 ◽  
Vol 30 (12) ◽  
pp. 1437-1450 ◽  
Author(s):  
Divyesh Joshi ◽  
Maneesha S. Inamdar

Blood vessel formation requires endothelial cell (EC) migration that depends on dynamic remodeling of the cytoskeleton. Rudhira/Breast Carcinoma Amplified Sequence 3 (BCAS3) is a cytoskeletal protein essential for EC migration and sprouting angiogenesis during mouse development and is implicated in metastatic disease. Here, we report that Rudhira mediates cytoskeleton organization and dynamics during EC migration. Rudhira binds to both microtubules (MTs) and vimentin intermediate filaments (IFs) and stabilizes MTs. Rudhira depletion impairs cytoskeletal cross-talk, MT stability, and hence focal adhesion disassembly. The BCAS3 domain of Rudhira is necessary and sufficient for MT-IF cross-linking and cell migration. Pharmacologically restoring MT stability rescues gross cytoskeleton organization and angiogenic sprouting in Rudhira-depleted cells. Our study identifies the novel and essential role of Rudhira in cytoskeletal cross-talk and assigns function to the conserved BCAS3 domain. Targeting Rudhira could allow tissue-restricted cytoskeleton modulation to control cell migration and angiogenesis in development and disease.


Genetics ◽  
2013 ◽  
Vol 196 (2) ◽  
pp. 471-479 ◽  
Author(s):  
Hon-Song Kim ◽  
Yuko Kitano ◽  
Masataka Mori ◽  
Tomomi Takano ◽  
Thomas Edward Harbaugh ◽  
...  

2019 ◽  
Vol 4 (1-2) ◽  
pp. 43-49 ◽  
Author(s):  
Steffen Berger ◽  
Jan Kiebist ◽  
Elisabeth Pötschke ◽  
Katrin Salchert

2018 ◽  
Author(s):  
Andrea A. Villanueva ◽  
Ernesto Muñoz-Palma ◽  
Carlos Cubo ◽  
Vicente A. Torres ◽  
Pilar Sanchez-Gomez ◽  
...  

2012 ◽  
Vol 65 (3) ◽  
pp. 455-462 ◽  
Author(s):  
Chengyu Zou ◽  
Qing Luo ◽  
Jian Qin ◽  
Yisong Shi ◽  
Li Yang ◽  
...  

2021 ◽  
Vol 15 (1) ◽  
pp. 58-73
Author(s):  
Andrea A. Villanueva ◽  
Pilar Sanchez-Gomez ◽  
Ernesto Muñoz-Palma ◽  
Sofía Puvogel ◽  
Bárbara S. Casas ◽  
...  

Small GTPases ◽  
2017 ◽  
Vol 10 (5) ◽  
pp. 323-330 ◽  
Author(s):  
Giulia Zago ◽  
Marco Biondini ◽  
Jacques Camonis ◽  
Maria Carla Parrini

2021 ◽  
Author(s):  
Ling-Yea Yu ◽  
Ting-Jen Tseng ◽  
Hsuan-Chao Lin ◽  
Ting-Xuan Lu ◽  
Chia-Jung Tsai ◽  
...  

AbstractIntegrating signals is essential for cell survival, leading to the concept of synthetic lethality. However, how signaling is integrated to control cell migration remains unclear. By conducting a “two-hit” screen, we revealed the synergistic reduction of cell migration when serine-threonine kinase 40 (STK40) and mitogen-activated protein kinase (MAPK) were simultaneously suppressed. Single-cell analyses showed that STK40 knockdown reduced cell motility and coordination by strengthening focal adhesion (FA) complexes. Furthermore, STK40 knockdown reduced translocation of yes-associated protein (YAP) into the nucleus, while MAPK inhibition further weakened YAP activities in the nucleus to disturb FA remodeling. Altogether, we unveiled an integrated STK40-YAP-MAPK system regulating cell migration, and introduced “synthetic dysmobility” as a novel strategy to collaboratively control cell migration.One Sentence SummaryBlocking collaborative pathways within the integrated signaling network synergistically disrupts the migration of cells.


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