Smad3 signaling is required for epithelial-mesenchymal transition of lens epithelium after injury.
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BMP-7 does not protect against bleomycin-induced lung or skin fibrosisInhibition of transforming growth factor-beta1-induced signaling and epithelial-to-mesenchymal transition by the Smad-binding peptide aptamer Trx-SARAOsteopontin-A Master Regulator of Epithelial-Mesenchymal TransitionReciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosismiR-204 targeting of Ankrd13A controls both mesenchymal neural crest and lens cell migration.Progress in corneal wound healingOxidative stress and glutathione in TGF-beta-mediated fibrogenesisDact2 is expressed in the developing ureteric bud/collecting duct system of the kidney and controls morphogenetic behavior of collecting duct cellsAGEs in human lens capsule promote the TGFβ2-mediated EMT of lens epithelial cells: implications for age-associated fibrosisDual function of TGFβ in lens epithelial cell fate: implications for secondary cataract.Smad4 dependency defines two classes of transforming growth factor {beta} (TGF-{beta}) target genes and distinguishes TGF-{beta}-induced epithelial-mesenchymal transition from its antiproliferative and migratory responses.Dermal transforming growth factor-beta responsiveness mediates wound contraction and epithelial closure.Lens-specific expression of TGF-beta induces anterior subcapsular cataract formation in the absence of Smad3Fate-determining mechanisms in epithelial-myofibroblast transition: major inhibitory role for Smad3Long noncoding RNA expression profile in HLE B-3 cells during TGF-β2-induced epithelial-mesenchymal transition.Mechanisms of the epithelial-mesenchymal transition by TGF-betaRegulation of lens gap junctions by Transforming Growth Factor beta.Suppression of injury-induced epithelial-mesenchymal transition in a mouse lens epithelium lacking tenascin-CEpithelial origin of myofibroblasts during fibrosis in the lung.Tetrandrine suppresses activation of human subconjunctival fibroblasts in vitro.Molecular mechanisms and treatment of radiation-induced lung fibrosisRadiation therapy causes loss of dermal lymphatic vessels and interferes with lymphatic function by TGF-beta1-mediated tissue fibrosis.Downregulation of transforming growth factor-β type II receptor prohibit epithelial-to-mesenchymal transition in lens epithelium.Cell signaling pathways in vertebrate lens regeneration.Subepithelial corneal fibrosis partially due to epithelial-mesenchymal transition of ocular surface epitheliumRole of Smad2/3 and p38 MAP kinase in TGF-β1-induced epithelial-mesenchymal transition of pulmonary epithelial cellsTransforming growth factor-β and the hallmarks of cancer.Lysyl oxidase contributes to mechanotransduction-mediated regulation of transforming growth factor-β signaling in breast cancer cells.E-cadherin antagonizes transforming growth factor β1 gene induction in hepatic stellate cells by inhibiting RhoA-dependent Smad3 phosphorylation.A novel approach for the generation of genetically modified mammary epithelial cell cultures yields new insights into TGFβ signaling in the mammary glandExpression of Smad7 in mouse eyes accelerates healing of corneal tissue after exposure to alkaliTransition of mesothelial cell to fibroblast in peritoneal dialysis: EMT, stem cell or bystander?Expression of lumican in the articular disc of the human temporomandibular joint.Smad phosphoisoform signaling specificity: the right place at the right timeQuantitative analysis of injury-induced anterior subcapsular cataract in the mouse: a model of lens epithelial cells proliferation and epithelial-mesenchymal transitionHistone acetyltransferase inhibitor C646 reverses epithelial to mesenchymal transition of human peritoneal mesothelial cells via blocking TGF-β1/Smad3 signaling pathway in vitroMarkers of fibrosis and epithelial to mesenchymal transition demonstrate field cancerization in histologically normal tissue adjacent to breast tumors.Smad phosphoisoform signals in acute and chronic liver injury: similarities and differences between epithelial and mesenchymal cells.Smad3 as a mediator of the fibrotic response.Transforming Growth Factor-β and Interleukin-1β Signaling Pathways Converge on the Chemokine CCL20 Promoter.
P2860
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P2860
Smad3 signaling is required for epithelial-mesenchymal transition of lens epithelium after injury.
description
2004 nî lūn-bûn
@nan
2004 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2004 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
name
Smad3 signaling is required fo ...... lens epithelium after injury.
@ast
Smad3 signaling is required fo ...... lens epithelium after injury.
@en
type
label
Smad3 signaling is required fo ...... lens epithelium after injury.
@ast
Smad3 signaling is required fo ...... lens epithelium after injury.
@en
prefLabel
Smad3 signaling is required fo ...... lens epithelium after injury.
@ast
Smad3 signaling is required fo ...... lens epithelium after injury.
@en
P2093
P2860
P1476
Smad3 signaling is required fo ...... lens epithelium after injury.
@en
P2093
Akira Ooshima
Chia-Yang Liu
Kathleen C Flanders
Mario Anzano
Misako Sato
Satoko Kono-Saika
Shizuya Saika
Winston W-Y Kao
Yasuteru Muragaki
P2860
P304
P356
10.1016/S0002-9440(10)63153-7
P407
P577
2004-02-01T00:00:00Z