MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

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A proteomics approach to identifying key protein targets involved in VEGF inhibitor mediated attenuation of bleomycin-induced pulmonary fibrosis Transcriptional and posttranscriptional regulation of CXCL8/IL-8 gene expression induced by connective tissue growth factor.

P2860

Q28383207-D6CD0321-9873-4C77-B948-62F0DE036428 Q38864535-14EFAB10-611A-445B-B3E9-D6224472EDB7

P2860

MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

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http://www.wikidata.org/entity/Q40816517

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2011 nî lūn-bûn

@nan

2011年の論文

@ja

2011年論文

@yue

2011年論文

@zh-hant

2011年論文

@zh-hk

2011年論文

@zh-mo

2011年論文

@zh-tw

2011年论文

@wuu

2011年论文

@zh

2011年论文

@zh-cn

name

MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

@en

type

Item

label

MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

@en

prefLabel

MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

@en

P1476

MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

@en

P2093

Andrew Leask

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P2860

Selective expression of connective tissue growth factor in fibroblasts in vivo promotes systemic tissue fibrosis

Iloprost suppresses connective tissue growth factor production in fibroblasts and in the skin of scleroderma patients

A prostacyclin analogue, iloprost, protects from bleomycin-induced pulmonary fibrosis in mice

CCN2 is required for the TGF-β induced activation of Smad1-Erk1/2 signaling network

A soluble factor from Trypanosoma cruzi inhibits transforming growth factor-ß-induced MAP kinase activation and gene expression in dermal fibroblasts.

Thrombospondin 1 is a key mediator of transforming growth factor β-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism.

Matrix contraction by dermal fibroblasts requires transforming growth factor-beta/activin-linked kinase 5, heparan sulfate-containing proteoglycans, and MEK/ERK: insights into pathological scarring in chronic fibrotic disease.

MEK-ERK pathway modulation ameliorates pulmonary fibrosis associated with epidermal growth factor receptor activation

Potential therapeutic targets for cardiac fibrosis: TGFbeta, angiotensin, endothelin, CCN2, and PDGF, partners in fibroblast activation.

Autocrine transforming growth factor β signaling regulates extracellular signal-regulated kinase 1/2 phosphorylation via modulation of protein phosphatase 2A expression in scleroderma fibroblasts.

P2888

s12079-011-0156-9

P304

59-60

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scholarly article

P356

10.1007/S12079-011-0156-9

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P433

http://www.w3.org/2001/XMLSchema#string

P478

http://www.w3.org/2001/XMLSchema#string

P577

2011-12-01T00:00:00Z

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P5875

51843721

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P698

22131200

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P921

pulmonary fibrosis

P932

3271198

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MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

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P2860

P2860

MEK/ERK inhibitors: proof-of-concept studies in lung fibrosis.

description

name

type

label

prefLabel

P1433

P1476

P2093

P2860

P2888

P304

P31

P356

P433

P478

P577

P5875

P698

P921

P932

P356

P1433

P1476

P2093

P2860

P2888

P304

P31

P356

P433

P478

P577

P5875

P698

P921

P932