rho-Associated Kinases

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  Subject Areas on Research

  • A novel mouse model of cerebral cavernous malformations based on the two-hit mutation hypothesis recapitulates the human disease. 
  • A phase I/IIa clinical trial of a recombinant Rho protein antagonist in acute spinal cord injury. 
  • Abundant expression of ponsin, a focal adhesion protein, in lens and downregulation of its expression by impaired cytoskeletal signaling. 
  • Beneficial effects of the Rho kinase inhibitor Y27632 in murine puromycin aminonucleoside nephrosis. 
  • Characterization of cytoskeleton-enriched protein fraction of the trabecular meshwork and ciliary muscle cells. 
  • Corneal Endothelial Cell Migration and Proliferation Enhanced by Rho Kinase (ROCK) Inhibitors in In Vitro and In Vivo Models. 
  • Current and Emerging Treatment for Diabetic Macular Edema. 
  • Cyclic mechanical stress and trabecular meshwork cell contractility. 
  • Discovery of substituted 4-(pyrazol-4-yl)-phenylbenzodioxane-2-carboxamides as potent and highly selective Rho kinase (ROCK-II) inhibitors. 
  • Effects of Y27632 on keratinocyte procurement and wound healing. 
  • Elevated levels of RhoA in the optic nerve head of human eyes with glaucoma. 
  • Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutations. 
  • Expression levels of mRNA for Rho A/Rho kinase and its role in isoprostane-induced vasoconstriction of human placental and maternal vessels. 
  • Expression of dominant negative Rho-binding domain of Rho-kinase in organ cultured human eye anterior segments increases aqueous humor outflow. 
  • Ezrin Orchestrates Signal Transduction in Airway Cells. 
  • Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease. 
  • G12 signaling through c-Jun NH2-terminal kinase promotes breast cancer cell invasion. 
  • Human neural progenitors express functional lysophospholipid receptors that regulate cell growth and morphology. 
  • Inhibition of Rho-kinase induces alphaB-crystallin expression in lens epithelial cells. 
  • Lesions from patients with sporadic cerebral cavernous malformations harbor somatic mutations in the CCM genes: evidence for a common biochemical pathway for CCM pathogenesis. 
  • Long-term Safety and Ocular Hypotensive Efficacy Evaluation of Netarsudil Ophthalmic Solution: Rho Kinase Elevated IOP Treatment Trial (ROCKET-2). 
  • Lysophosphatidic acid stimulates cell growth by different mechanisms in SKOV-3 and Caov-3 ovarian cancer cells: distinct roles for Gi- and Rho-dependent pathways. 
  • Micro-computed tomography in murine models of cerebral cavernous malformations as a paradigm for brain disease. 
  • Modulation of aqueous humor outflow facility by the Rho kinase-specific inhibitor Y-27632. 
  • Netarsudil Increases Outflow Facility in Human Eyes Through Multiple Mechanisms. 
  • Netarsudil/Latanoprost Fixed-Dose Combination for Elevated Intraocular Pressure: Three-Month Data from a Randomized Phase 3 Trial. 
  • PTEN as an effector in the signaling of antimigratory G protein-coupled receptor. 
  • Phenotypic characterization of murine models of cerebral cavernous malformations. 
  • Phosphorylation of adducin by Rho-kinase plays a crucial role in cell motility. 
  • ROCK1 phosphorylates and activates zipper-interacting protein kinase. 
  • Reactivation of p53 by a Cytoskeletal Sensor to Control the Balance Between DNA Damage and Tumor Dissemination. 
  • Regulation of cofilin phosphorylation in glomerular podocytes by testis specific kinase 1 (TESK1). 
  • Regulation of myosin light chain phosphorylation in the trabecular meshwork: role in aqueous humour outflow facility. 
  • Regulation of the association of adducin with actin filaments by Rho-associated kinase (Rho-kinase) and myosin phosphatase. 
  • Release of nonmuscle myosin II from the cytosolic domain of tumor necrosis factor receptor 2 is required for target gene expression. 
  • Rho A/Rho kinase: human umbilical artery mRNA expression in normal and pre eclamptic pregnancies and functional role in isoprostane-induced vasoconstriction. 
  • Rho GTPase/Rho kinase inhibition as a novel target for the treatment of glaucoma. 
  • Rho Kinase Inhibition Blunts Lesion Development and Hemorrhage in Murine Models of Aggressive Pdcd10/Ccm3 Disease. 
  • Rho Kinase Inhibitors as a Novel Treatment for Glaucoma and Ocular Hypertension. 
  • Rho kinase differentially regulates phosphorylation of nonmuscle myosin II isoforms A and B during cell rounding and migration. 
  • Rho kinase inhibitors for glaucoma treatment - Review. 
  • Rho kinase promotes alloimmune responses by regulating the proliferation and structure of T cells. 
  • Rho-kinase inhibitors offer a new approach in the treatment of glaucoma. 
  • RhoA Kinase Inhibition With Fasudil Versus Simvastatin in Murine Models of Cerebral Cavernous Malformations. 
  • RhoA activity and post-ischemic inflammation in an experimental model of adult rodent anterior ischemic optic neuropathy. 
  • Role of the Rho GTPase/Rho kinase signaling pathway in pathogenesis and treatment of glaucoma: Bench to bedside research. 
  • Stanniocalcin-1 Is an Ocular Hypotensive Agent and a Downstream Effector Molecule That Is Necessary for the Intraocular Pressure-Lowering Effects of Latanoprost. 
  • The GNA13-RhoA signaling axis suppresses expression of tumor protective Kallikreins. 
  • The effect of Rho-associated kinase inhibition on the ocular penetration of timolol maleate. 
  • The integrin-linked kinase regulates cell morphology and motility in a rho-associated kinase-dependent manner. 
  • The rho-guanine nucleotide exchange factor domain of obscurin activates rhoA signaling in skeletal muscle. 
  • The rho-guanine nucleotide exchange factor domain of obscurin regulates assembly of titin at the Z-disk through interactions with Ran binding protein 9. 
  • Vinculin Force-Sensitive Dynamics at Focal Adhesions Enable Effective Directed Cell Migration. 
  • Wound contraction is attenuated by fasudil inhibition of Rho-associated kinase. 
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  Keywords of People

  • Bennett, Vann, George Barth Geller Distinguished Professor of Molecular Biology, Duke Cancer Institute