ArticleBiochemical and biophysical research communications2014
Regulation of cell-matrix adhesion by OLA1, the Obg-like ATPase 1.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- A Mechanistic Model of Cry2Ab12 Toxicity AgainstToxins · 2026Article
- Bi-allelic variants in OLA1 cause a neurodevelopmental disorder with joint hypermobility.American journal of human genetics · 2026Article
- Conserved GTPase OLA1 promotes efficient translation on D/E-rich mRNA.Nature communications · 2025Article
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- Discovery of dysregulated circular RNAs in whole blood transcriptomes from cystic fibrosis patients - implication of a role for cellular senescence in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023Article
- Association of Common Variants inInternational journal of molecular sciences · 2022Article
- The Role of the Universally Conserved ATPase YchF/Ola1 in Translation Regulation during Cellular Stress.Microorganisms · 2021Review
- OLA1 is a potential prognostic molecular biomarker for endometrial cancer and promotes tumor progression.Oncology letters · 2021Article
- Obg-like ATPase 1 inhibited oral carcinoma cell metastasis through TGFβ/SMAD2 axis in vitro.BMC molecular and cell biology · 2020Article
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- Article
- OLA1, a Translational Regulator of p21, Maintains Optimal Cell Proliferation Necessary for Developmental Progression.Molecular and cellular biology · 2016Article
- OLA1 contributes to epithelial-mesenchymal transition in lung cancer by modulating the GSK3β/snail/E-cadherin signaling.Oncotarget · 2016Article
- Redox Activation of the Universally Conserved ATPase YchF by Thioredoxin 1.Antioxidants & redox signaling · 2016Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Attachment of cells to the extracellular matrix induces clustering of membrane receptor integrins which in turn triggers the formation of focal adhesions (FAs). The adaptor/scaffold proteins in FAs provide linkage to actin cytoskeleton, whereas focal adhesion kinase (FAK) and other FA-associated kinases and phosphatases transduce integrin-mediated signaling cascades, promoting actin polymerization and progression of cell spreading. In this study, we explored the role of OLA1, a newly identified member of Obg-like ATPases, in regulating cell adhesion processes. We showed that in multiple human cell lines RNAi-mediated downregulation of OLA1 significantly accelerated cell adhesion and spreading, and conversely overexpression of OLA1 by gene transfection resulted in delayed cell adhesion and spreading. We further found that OLA1-deficient cells had elevated levels of FAK protein and decreased Ser3 phosphorylation of cofilin, an actin-binding protein and key regulator of actin filament dynamics, while OLA1-overexpressing cells exhibited the opposite molecular alterations in FAK and cofilin. These findings suggest that OLA1 plays an important negative role in cell adhesion and spreading, in part through the regulation of FAK expression and cofilin phosphorylation, and manipulation of OLA1 may lead to significant changes in cell adhesion and the associated phenotypes.
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Registered trials
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