ArticleProceedings of the National Academy of Sciences of the United States of America2013
Inositol kinase and its product accelerate wound healing by modulating calcium levels, Rho GTPases, and F-actin assembly.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Mechanochemical mechanism underlying intercellular CaNature communications · 2025Article
- Duox is the primary NADPH oxidase responsible for ROS production during adult caudal fin regeneration in zebrafish.iScience · 2023Article
- Bring the pain: wounding reveals a transition from cortical excitability to epithelial excitability inFrontiers in cell and developmental biology · 2023Review
- Leading-edge elongation by follower cell interruption in advancing epithelial cell sheets.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mechanosensitive calcium flashes promote sustained RhoA activation during tight junction remodeling.The Journal of cell biology · 2022Article
- Drp1-mediated mitochondrial fission regulates calcium and F-actin dynamics during wound healing.Biology open · 2020Article
- Wounding triggers MIRO-1 dependent mitochondrial fragmentation that accelerates epidermal wound closure through oxidative signaling.Nature communications · 2020Article
- The role of nitric oxide during embryonic wound healing.BMC genomics · 2019Article
- Calcium-Sensing Receptor Regulates Epidermal Intracellular CaThe Journal of investigative dermatology · 2019Article
- Septin-dependent remodeling of cortical microtubule drives cell reshaping during epithelial wound healing.Journal of cell science · 2018Article
- Intracellular calcium signal at the leading edge regulates mesodermal sheet migration during Xenopus gastrulation.Scientific reports · 2018Article
- CaCell reports · 2018Article
- Adult human dermal fibroblasts exposed to nanosecond electrical pulses exhibit genetic biomarkers of mechanical stress.Biochemistry and biophysics reports · 2017Article
- Inositol, neural tube closure and the prevention of neural tube defects.Birth defects research · 2017Review
- Mechanics of epithelial tissues during gap closure.Current opinion in cell biology · 2016Review
- The cellular and molecular mechanisms of tissue repair and regeneration as revealed by studies inRegeneration (Oxford, England) · 2016Article
- The Xenopus ORFeome: A resource that enables functional genomics.Developmental biology · 2015Article
- Calcium-dependent neuroepithelial contractions expel damaged cells from the developing brain.Developmental cell · 2014Article
- Spontaneous calcium transients manifest in the regenerating muscle and are necessary for skeletal muscle replenishment.Cell calcium · 2014Article
- A global profile of gene promoter methylation in treatment-naïve urothelial cancer.Epigenetics · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Wound healing is essential for survival. We took advantage of the Xenopus embryo, which exhibits remarkable capacities to repair wounds quickly and efficiently, to investigate the mechanisms responsible for wound healing. Previous work has shown that injury triggers a rapid calcium response, followed by the activation of Ras homolog (Rho) family guanosine triphosphatases (GTPases), which regulate the formation and contraction of an F-actin purse string around the wound margin. How these processes are coordinated following wounding remained unclear. Here we show that inositol-trisphosphate 3-kinase B (Itpkb) via its enzymatic product inositol 1,3,4,5-tetrakisphosphate (InsP4) plays an essential role during wound healing by modulating the activity of Rho family GTPases and F-actin ring assembly. Furthermore, we show that Itpkb and InsP4 modulate the speed of the calcium wave, which propagates from the site of injury into neighboring uninjured cells. Strikingly, both overexpression of itpkb and exogenous application of InsP4 accelerate the speed of wound closure, a finding that has potential implications in our quest to find treatments that improve wound healing in patients with acute or chronic wounds.
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Registered trials
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.