Rho kinase in the regulation of cell death and survival
Open accessAbstract
Rho kinase (ROCK) belongs to a family of serine/threonine kinases that are activated via interaction with Rho GTPases. ROCK is involved in a wide range of fundamental cellular functions, such as contraction, adhesion, migration, and proliferation. Recent studies have shown that ROCK plays an important role in the regulation of apoptosis in various cell types and animal disease models. Two ROCK isoforms, ROCK1 and ROCK2, are assumed to be function redundant, this based largely on kinase construct overexpression and chemical inhibitors (Y27632 and fasudil) which inhibit both ROCK1 and ROCK2. Gene targeting and RNA interference approaches allow further dissection of distinct cellular, physiological, and patho-physiological functions of the two ROCK isoforms. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of ROCK signaling in the regulation of apoptosis and highlights new findings from recently generated ROCK-deficient mice.
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Cytoskeletal rearrangement induced by ROCK activation can be involved in apoptosis.
“The cytoskeletal rearrangement induced by ROCK activation can also be involved in apoptosis.”
From RhoA Signaling in Neurodegenerative Diseases (2022) · cites this paper as [130]
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- Authors
- Shi, J., & Wei, L.
- Affiliations
- Indiana University Indianapolis (US)
- Corresponding author
- Wei, Lei
- Venue
- Archivum Immunologiae et Therapiae Experimentalis
- Publisher
- Walter de Gruyter GmbH
- Published
- 2007-03-09
- Volume
- 55
- Issue
- 2
- Pages
- 61-75
- ISSN
- 0004-069X (ISSN-L)
- 1661-4917
- PMC
- PMC2612781
- OpenAlex
- W1980081948
- Cited by
- 254
- References
- 4
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 9 · 2023: 8 · 2022: 10 · 2021: 9 · 2020: 14 · 2019: 12 · 2018: 8 · 2017: 5 · 2016: 16 · 2015: 19 · 2014: 16 · 2013: 23 · 2012: 20
- FWCI
- 5.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Archivum Immunologiae et Therapiae Experimentalis (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-72897, P01HL085098, R01HL072897)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR059142)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Keywords
- Rho kinase, ROCK1, ROCK2, apoptosis, cell survival, Rho GTPases, ROCK signaling, fasudil, Y-27632, serine/threonine kinase
- MeSH terms
- Animals, Cell Survival, Models, Biological, Substrate Specificity, Signal Transduction, Gene Expression Regulation, Enzymologic, Cell Death, Apoptosis, Protein Serine-Threonine Kinases, Mice, Knockout, Protein Isoforms, Intracellular Signaling Peptides and Proteins, Mice, rho-Associated Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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