ArticleThe Biochemical journal2005
Integrin-linked kinase is responsible for Ca2+-independent myosin diphosphorylation and contraction of vascular smooth muscle.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 112 citations in OpenAlex.
- Integrin-Linked Kinase Suppression Reduces SPARC's Effect on Intraocular Pressure and Extracellular Matrix.Investigative ophthalmology & visual science · 2026Article
- Advances in Understanding Calcium Sensitization in Gastrointestinal Smooth Muscles: Pathways, Interstitial Cells, and Disease.Journal of neurogastroenterology and motility · 2026Review
- ILK Deletion Protects Against Chronic Kidney Disease-Associated Vascular Damage.International journal of molecular sciences · 2025Article
- MLC2: Physiological Functions and Potential Roles in Tumorigenesis.Cell biochemistry and biophysics · 2025Review
- Effects of Rho inhibitors on membrane depolarization-induced contraction of male rat caudal arterial smooth muscle.Physiological reports · 2025Article
- Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Aging related decreases in NM myosin expression and contractility in a resistance vessel.Frontiers in physiology · 2024Article
- Myosin light chain phosphorylation exhibits a gradient across the wall of cerebellar arteries under sustained ex vivo vascular tone.Scientific reports · 2023Article
- p90RSK2, a new MLCK mediates contractility in myosin light chain kinase null smooth muscle.Frontiers in physiology · 2023Article
- Deletion of Notch3 Impairs Contractility of Renal Resistance Vessels Due to Deficient CaInternational journal of molecular sciences · 2022Article
- New Perspectives on the Role of Integrin-Linked Kinase (ILK) Signaling in Cancer Metastasis.Cancers · 2022Article
- Integrin-linked kinase (ILK): the known vs. the unknown and perspectives.Cellular and molecular life sciences : CMLS · 2022Review
- Thyroxine Induces Acute Relaxation of Rat Skeletal Muscle Arteries via Integrin αvβ3, ERK1/2 and Integrin-Linked Kinase.Frontiers in physiology · 2021Article
- Article
- RSK2 contributes to myogenic vasoconstriction of resistance arteries by activating smooth muscle myosin and the NaScience signaling · 2018Article
- The dominant protein phosphatase PP1c isoform in smooth muscle cells, PP1cβ, is essential for smooth muscle contraction.The Journal of biological chemistry · 2018Article
- Gene expression profiles and signaling mechanisms in αBMC systems biology · 2017Article
- A novel inhibitory effect of oxazol-5-one compounds on ROCKII signaling in human coronary artery vascular smooth muscle cells.Scientific reports · 2016Article
- Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles.Journal of neurogastroenterology and motility · 2016Review
- Myosin di-phosphorylation and peripheral actin bundle formation as initial events during endothelial barrier disruption.Scientific reports · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smooth muscle contraction is activated by phosphorylation at Ser-19 of LC20 (the 20 kDa light chains of myosin II) by Ca2+/calmodulin-dependent MLCK (myosin light-chain kinase). Diphosphorylation of LC20 at Ser-19 and Thr-18 is observed in smooth muscle tissues and cultured cells in response to various contractile stimuli, and in pathological circumstances associated with hypercontractility. MLCP (myosin light-chain phosphatase) inhibition can lead to LC20 diphosphorylation and Ca2+-independent contraction, which is not attributable to MLCK. Two kinases have emerged as candidates for Ca2+-independent LC20 diphosphorylation: ILK (integrin-linked kinase) and ZIPK (zipper-interacting protein kinase). Triton X-100-skinned rat caudal arterial smooth muscle was used to investigate the relative importance of ILK and ZIPK in Ca2+-independent, microcystin (phosphatase inhibitor)-induced LC20 diphosphorylation and contraction. Western blotting and in-gel kinase assays revealed that both kinases were retained in this preparation. Ca2+-independent contraction of calmodulin-depleted tissue in response to microcystin was resistant to MLCK inhibitors [AV25 (a 25-amino-acid peptide derived from the autoinhibitory domain of MLCK), ML-7, ML-9 and wortmannin], protein kinase C inhibitor (GF109203X) and Rho-associated kinase inhibitors (Y-27632 and H-1152), but blocked by the non-selective kinase inhibitor staurosporine. ZIPK was inhibited by AV25 (IC50 0.63+/-0.05 microM), whereas ILK was insensitive to AV25 (at concentrations as high as 100 microM). AV25 had no effect on Ca2+-independent, microcystin-induced LC20 mono- or di-phosphorylation, with a modest effect on force. We conclude that direct inhibition of MLCP in the absence of Ca2+ unmasks ILK activity, which phosphorylates LC20 at Ser-19 and Thr-18 to induce contraction. ILK is probably the kinase responsible for myosin diphosphorylation in vascular smooth muscle cells and tissues.
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