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β-Actin specifically controls cell growth, migration, and the G-actin pool.

Molecular biology of the cell (2011-09-09)
Tina M Bunnell, Brandon J Burbach, Yoji Shimizu, James M Ervasti
ABSTRACT

Ubiquitously expressed β-actin and γ-actin isoforms play critical roles in most cellular processes; however, their unique contributions are not well understood. We generated whole-body β-actin-knockout (Actb(-/-)) mice and demonstrated that β-actin is required for early embryonic development. Lethality of Actb(-/-) embryos correlated with severe growth impairment and migration defects in β-actin-knockout primary mouse embryonic fibroblasts (MEFs) that were not observed in γ-actin-null MEFs. Migration defects were associated with reduced membrane protrusion dynamics and increased focal adhesions. We also identified migration defects upon conditional ablation of β-actin in highly motile T cells. Of great interest, ablation of β-actin altered the ratio of globular actin (G-actin) to filamentous actin in MEFs, with corresponding changes in expression of genes that regulate the cell cycle and motility. These data support an essential role for β-actin in regulating cell migration and gene expression through control of the cellular G-actin pool.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Monoclonal Anti-β-Actin antibody produced in mouse, clone AC-74, ascites fluid
Sigma-Aldrich
Monoclonal Anti-β-Actin−Peroxidase antibody produced in mouse, clone AC-15, purified from hybridoma cell culture
Sigma-Aldrich
MONOCLONAL ANTI-BETA-ACTIN antibody produced in mouse, clone 8H10D10, crude ascites, buffered aqueous solution
Sigma-Aldrich
Anti-β-Actin–FITC antibody, Mouse monoclonal, clone AC-15, purified from hybridoma cell culture
Sigma-Aldrich
Anti-beta-Actin antibody, Rabbit monoclonal, clone SP124, recombinant, expressed in proprietary host, affinity isolated antibody