scholarly journals Rudhira/BCAS3 couples microtubules and intermediate filaments to promote cell migration for angiogenic remodeling

2018 ◽  
Author(s):  
Divyesh Joshi ◽  
Maneesha S. Inamdar
Keyword(s):  
Cell Migration ◽  
Intermediate Filaments ◽  
Control Cell ◽  
The Novel ◽  
Mouse Development ◽  
Cytoskeleton Organization ◽  
Sprouting Angiogenesis ◽  
Microtubule Stability ◽  
Promote Cell Migration ◽  
Necessary And Sufficient

AbstractBlood 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 implicated in metastatic disease. Here, we report that Rudhira mediates cytoskeleton organization and dynamics during EC migration. Rudhira binds to both microtubules and Vimentin intermediate filaments (IFs) and stabilizes microtubules. Rudhira depletion impairs cytoskeletal crosstalk, microtubule stability and hence focal adhesion disassembly. The BCAS3 domain of Rudhira is necessary and sufficient for microtubule-IF crosslinking and cell migration. Pharmacologically restoring microtubule stability rescues gross cytoskeleton organization and angiogenic sprouting in Rudhira depleted cells. Our study identifies the novel and essential role of Rudhira in cytoskeletal crosstalk 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.

scholarly journals Rudhira/BCAS3 couples microtubules and intermediate filaments to promote cell migration for angiogenic remodeling

2019 ◽  
Vol 30 (12) ◽  
pp. 1437-1450 ◽  
Author(s):  
Divyesh Joshi ◽  
Maneesha S. Inamdar
Keyword(s):  
Cell Migration ◽  
Intermediate Filaments ◽  
Cross Talk ◽  
Control Cell ◽  
The Novel ◽  
Mouse Development ◽  
Cytoskeleton Organization ◽  
Sprouting Angiogenesis ◽  
Promote Cell Migration ◽  
Necessary And Sufficient

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.

scholarly journals The Novel Secreted Factor MIG-18 Acts with MIG-17/ADAMTS to Control Cell Migration in Caenorhabditis elegans

Genetics ◽  
2013 ◽  
Vol 196 (2) ◽  
pp. 471-479 ◽  
Author(s):  
Hon-Song Kim ◽  
Yuko Kitano ◽  
Masataka Mori ◽  
Tomomi Takano ◽  
Thomas Edward Harbaugh ◽  
...  
Keyword(s):  
Cell Migration ◽  
Caenorhabditis Elegans ◽  
Control Cell ◽  
The Novel

scholarly journals Fascin in Cell Migration: More Than an Actin Bundling Protein

Biology ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 403
Author(s):  
Maureen C. Lamb ◽  
Tina L. Tootle
Keyword(s):  
Cell Migration ◽  
Protein Interactions ◽  
Cancer Metastasis ◽  
Control Cell ◽  
Actin Binding ◽  
Linc Complex ◽  
Protein Protein Interactions ◽  
Post Translational Modifications ◽  
Promote Cell Migration ◽  
The Many

Fascin, an actin-binding protein, regulates many developmental migrations and contributes to cancer metastasis. Specifically, Fascin promotes cell motility, invasion, and adhesion by forming filopodia and invadopodia through its canonical actin bundling function. In addition to bundling actin, Fascin has non-canonical roles in the cell that are thought to promote cell migration. These non-canonical functions include regulating the activity of other actin-binding proteins, binding to and regulating microtubules, mediating mechanotransduction to the nucleus via interaction with the Linker of the Nucleoskeleton and Cytoskeleton (LINC) Complex, and localizing to the nucleus to regulate nuclear actin, the nucleolus, and chromatin modifications. The many functions of Fascin must be coordinately regulated to control cell migration. While much remains to be learned about such mechanisms, Fascin is regulated by post-translational modifications, prostaglandin signaling, protein–protein interactions, and transcriptional means. Here, we review the structure of Fascin, the various functions of Fascin and how they contribute to cell migration, the mechanisms regulating Fascin, and how Fascin contributes to diseases, specifically cancer metastasis.

scholarly journals The apoptotic members CD95, BclxL, and Bcl-2 cooperate to promote cell migration by inducing Ca2+ flux from the endoplasmic reticulum to mitochondria

2016 ◽  
Vol 23 (10) ◽  
pp. 1702-1716 ◽  
Author(s):  
A Fouqué ◽  
E Lepvrier ◽  
L Debure ◽  
Y Gouriou ◽  
M Malleter ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Migration ◽  
Promote Cell Migration

scholarly journals Clathrin light chains are required for the gyrating-clathrin recycling pathway and thereby promote cell migration

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Sophia R. Majeed ◽  
Lavanya Vasudevan ◽  
Chih-Ying Chen ◽  
Yi Luo ◽  
Jorge A. Torres ◽  
...  
Keyword(s):  
Cell Migration ◽  
Light Chains ◽  
Promote Cell Migration ◽  
Recycling Pathway
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