TOR kinase complexes and cell migration
Open accessAbstract
Cell migration is a fundamental process in a wide array of biological and pathological responses. It is regulated by complex signal transduction pathways in response to external cues that couple to growth factor and chemokine receptors. In recent years, the target of rapamycin (TOR) kinase, as part of either TOR complex 1 (TORC1) or TOR complex 2 (TORC2), has been shown to be an important signaling component linking external signals to the cytoskeletal machinery in a variety of cell types and organisms. Thus, these complexes have emerged as key regulators of cell migration and chemotaxis.
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IGF-1 released from the bone matrix during bone resorption establishes an osteogenic microenvironment by activating mTOR signaling, which is critical for cellular energy metabolism and cell migration.
“Moreover, IGF-1 released from the bone matrix during bone resorption establishes an osteogenic microenvironment by activating mechanistic target of rapamycin (mTOR) signaling,217 which is critical for cellular energy metabolism and cell migration.218”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [218]
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- Authors
- Liu, L., & Parent, C. A.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Parent, Carole A.
- ORCID
- Parent, Carole A.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2011-09-19
- Volume
- 194
- Issue
- 6
- Pages
- 815-824
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC3226350
- OpenAlex
- W2149543951
- Cited by
- 87
- References
- 142
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 5 · 2018: 6 · 2017: 4 · 2016: 9 · 2015: 11 · 2014: 9 · 2013: 8 · 2012: 12
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- TOR kinase, cell migration, chemotaxis, signal transduction, cytoskeleton, growth factor receptors, chemokine receptors, rapamycin
- MeSH terms
- Animals, Cell Movement, Cytoskeleton, Humans, Signal Transduction, TOR Serine-Threonine Kinases
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