ArticleThe Journal of biological chemistry2013
Calcium and calmodulin-dependent serine/threonine protein kinase type II (CaMKII)-mediated intramolecular opening of integrin cytoplasmic domain-associated protein-1 (ICAP-1α) negatively regulates β1 integrins.
Article in The Journal of biological chemistry, 2013. 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, 23 citations in OpenAlex.
- Article
- Force tuning through regulation of clathrin-dependent integrin endocytosis.The Journal of cell biology · 2023Article
- Review
- ICAP-1 loss impairs CD8European journal of immunology · 2022Article
- Serine phosphorylation of the small phosphoprotein ICAP1 inhibits its nuclear accumulation.The Journal of biological chemistry · 2020Article
- Mix and (mis-)match - The mechanosensing machinery in the changing environment of the developing, healthy adult and diseased heart.Biochimica et biophysica acta. Molecular cell research · 2020Review
- The Role of Calmodulin in Tumor Cell Migration, Invasiveness, and Metastasis.International journal of molecular sciences · 2020Review
- Cerebral Cavernous Malformation Proteins in Barrier Maintenance and Regulation.International journal of molecular sciences · 2020Review
- Activation of cell migration via morphological changes in focal adhesions depends on shear stress in MYCN-amplified neuroblastoma cells.Journal of the Royal Society, Interface · 2019Article
- Nuclear Localization of Integrin Cytoplasmic Domain-associated Protein-1 (ICAP1) Influences β1 Integrin Activation and Recruits Krev/Interaction Trapped-1 (KRIT1) to the Nucleus.The Journal of biological chemistry · 2017Article
- Dense fibrillar collagen is a potent inducer of invadopodia via a specific signaling network.The Journal of cell biology · 2015Article
- The aquaporin 1 C-terminal tail is required for migration and growth of pulmonary arterial myocytes.American journal of respiratory cell and molecular biology · 2014Article
- Signaling pathways and the cerebral cavernous malformations proteins: lessons from structural biology.Cellular and molecular life sciences : CMLS · 2014Review
- Integrin cytoplasmic tail interactions.Biochemistry · 2014Review
- Integrins protect cardiomyocytes from ischemia/reperfusion injury.The Journal of clinical investigation · 2013Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal adhesion turnover during cell migration is an integrated cyclic process requiring tight regulation of integrin function. Interaction of integrin with its ligand depends on its activation state, which is regulated by the direct recruitment of proteins onto the β integrin chain cytoplasmic domain. We previously reported that ICAP-1α, a specific cytoplasmic partner of β1A integrins, limits both talin and kindlin interaction with β1 integrin, thereby restraining focal adhesion assembly. Here we provide evidence that the calcium and calmodulin-dependent serine/threonine protein kinase type II (CaMKII) is an important regulator of ICAP-1α for controlling focal adhesion dynamics. CaMKII directly phosphorylates ICAP-1α and disrupts an intramolecular interaction between the N- and the C-terminal domains of ICAP-1α, unmasking the PTB domain, thereby permitting ICAP-1α binding onto the β1 integrin tail. ICAP-1α direct interaction with the β1 integrin tail and the modulation of β1 integrin affinity state are required for down-regulating focal adhesion assembly. Our results point to a molecular mechanism for the phosphorylation-dependent control of ICAP-1α function by CaMKII, allowing the dynamic control of β1 integrin activation and cell adhesion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.