Impaired flow-induced dilation in mesenteric resistance arteries from mice lacking vimentin. - Wikidata - awgldk - TriplyDB

Impaired flow-induced dilation in mesenteric resistance arteries from mice lacking vimentin.

Impaired flow-induced dilation in mesenteric resistance arteries from mice lacking vimentin.

http://www.wikidata.org/entity/Q36894216

about

MICAL, a novel CasL interacting molecule, associates with vimentin Impaired flow-induced dilation in mesenteric resistance arteries from receptor protein tyrosine phosphatase-mu-deficient mice Nesprin-3 regulates endothelial cell morphology, perinuclear cytoskeletal architecture, and flow-induced polarization Introducing intermediate filaments: from discovery to disease Critical role of actin-associated proteins in smooth muscle contraction, cell proliferation, airway hyperresponsiveness and airway remodeling Intermediate Filaments Play a Pivotal Role in Regulating Cell Architecture and Function Flow (shear stress)-induced endothelium-dependent dilation is altered in mice lacking the gene encoding for dystrophin Key role of alpha(1)beta(1)-integrin in the activation of PI3-kinase-Akt by flow (shear stress) in resistance arteries Cardiovascular abnormalities with normal blood pressure in tissue kallikrein-deficient mice Plectin reinforces vascular integrity by mediating crosstalk between the vimentin and the actin networks.Lack of vimentin impairs endothelial differentiation of embryonic stem cells.Fluid shear stress on endothelial cells modulates mechanical tension across VE-cadherin and PECAM-1.Vimentin contributes to changes in chondrocyte stiffness in osteoarthritis Shear stress-induced mechanotransduction protein deregulation and vasculopathy in a mouse model of progeria.Soluble CD44 interacts with intermediate filament protein vimentin on endothelial cell surface.Role of the cytoskeleton in formation and maintenance of angiogenic sprouts Isometric contraction induces the Ca2+-independent activation of the endothelial nitric oxide synthase.Role of shear stress in nitric oxide-dependent modulation of renal angiotensin II vasoconstriction Dissociation of Crk-associated substrate from the vimentin network is regulated by p21-activated kinase on ACh activation of airway smooth muscle.Altered acetylcholine, bradykinin and cutaneous pressure-induced vasodilation in mice lacking the TREK1 potassium channel: the endothelial link Long Lasting Microvascular Tone Alteration in Rat Offspring Exposed In Utero to Maternal Hyperglycaemia.Toward functional genomics of flow-induced outward remodeling of resistance arteries.Intermediate filaments in smooth muscle.Notch transcriptional control of vascular smooth muscle regulatory gene expression and function.Role of the cytoskeleton in flow (shear stress)-induced dilation and remodeling in resistance arteries.A new trick for an old dogma: ENaC proteins as mechanotransducers in vascular smooth muscle.Cdc42GAP, reactive oxygen species, and the vimentin network Role of advanced glycation end products with oxidative stress in resistance artery dysfunction in type 2 diabetic mice.Role of p47(phox) in regulating Cdc42GAP, vimentin, and contraction in smooth muscle cells Plectin isoforms as organizers of intermediate filament cytoarchitecture.The role of apical cell-cell junctions and associated cytoskeleton in mechanotransduction.Transforming growth factor β suppresses osteoblast differentiation via the vimentin activating transcription factor 4 (ATF4) axis.Mechanotransduction of shear stress occurs through changes in VE-cadherin and PECAM-1 tension: implications for cell migration.Impaired vascular mechanotransduction in a transgenic mouse model of CADASIL arteriopathy.Absence of dystrophin in mice reduces NO-dependent vascular function and vascular density: total recovery after a treatment with the aminoglycoside gentamicin.Vimentin inhibits ATF4-mediated osteocalcin transcription and osteoblast differentiation The endothelial αENaC contributes to vascular endothelial function in vivo.Hemoglobin mediated contraction of the isolated rat thoracic aorta: why is precontraction necessary?Endothelial microtubule disruption blocks flow-dependent dilation of arterioles.Arterial vimentin is a transglutaminase substrate: a link between vasomotor activity and remodeling?

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P2860

Impaired flow-induced dilation in mesenteric resistance arteries from mice lacking vimentin.

http://www.wikidata.org/entity/Q36894216

description

1997 nî lūn-bûn

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1997年の論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年论文

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1997年论文

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1997年论文

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Impaired flow-induced dilation ...... es from mice lacking vimentin.

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Impaired flow-induced dilation ...... es from mice lacking vimentin.

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Impaired flow-induced dilation ...... es from mice lacking vimentin.

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P2093

Babinet C

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Boulanger CM

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Briand P

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Colucci-Guyon E

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Duriez M

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Friedlander G

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Henrion D

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Lévy BI

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Matrougui K

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Poitevin P

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P2860

Mice lacking vimentin develop and reproduce without an obvious phenotype.

Flow modulates myogenic responses in isolated microperfused rabbit afferent arterioles via endothelium-derived nitric oxide.

Flow-mediated endothelial mechanotransduction.

Alteration of flow-induced dilatation in mesenteric resistance arteries of L-NAME treated rats and its partial association with induction of cyclo-oxygenase-2.

Viscoelastic properties of vimentin compared with other filamentous biopolymer networks.

Mechanical behavior of pressurized in vitro prearteriolar vessels determined with a video system.

Pressure and flow-dependent vascular tone.

Chronic blockade of AT2-subtype receptors prevents the effect of angiotensin II on the rat vascular structure.

Disruption of cytoskeletal structures mediates shear stress-induced endothelin-1 gene expression in cultured porcine aortic endothelial cells.

Mechanotransduction by vascular smooth muscle.

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2909-2914

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10.1172/JCI119840

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11

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100

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508498

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