TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis - Wikidata - wikimedia - TriplyDB

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

http://www.wikidata.org/entity/Q28817018

about

BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through [Ca2+]i-TGF-β-Smad2/3 pathway.The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart.TRPC3-Nox2 complex mediates doxorubicin-induced myocardial atrophy.TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice TRPC3 Channels in Cardiac Fibrosis.Transient receptor potential vanilloid-3 (TRPV3) activation plays a central role in cardiac fibrosis induced by pressure overload in rats via TGF-β1 pathway.An optically controlled probe identifies lipid-gating fenestrations within the TRPC3 channel.TRPC5-eNOS Axis Negatively Regulates ATP-Induced Cardiomyocyte Hypertrophy.

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TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

http://www.wikidata.org/entity/Q28817018

description

2016 nî lūn-bûn

@nan

2016 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2016 թվականի դեկտեմբերին հրատարակված գիտական հոդված

@hy

2016年の論文

@ja

2016年論文

@yue

2016年論文

@zh-hant

2016年論文

@zh-hk

2016年論文

@zh-mo

2016年論文

@zh-tw

2016年论文

@wuu

name

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@ast

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@en

type

label

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@ast

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@en

prefLabel

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@ast

TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@en

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Scientific Reports

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TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis

@en

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Akiyuki Nishimura

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

Hideki Sumimoto

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

Kei Miyano

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

Koichiro Kuwahara

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

Lutz Birnbaumer

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

Naoyuki Kitajima

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

Takuro Numaga-Tomita

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

Takuya Kuroda

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

Tomomi Ide

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

Yasuo Mori

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

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Direct activation of human TRPC6 and TRPC3 channels by diacylglycerol

Muscle-specific signaling mechanism that links actin dynamics to serum response factor.

Modulation of adverse cardiac remodeling by STARS, a mediator of MEF2 signaling and SRF activity

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy

GEF means go: turning on RHO GTPases with guanine nucleotide-exchange factors

Generation of induced pluripotent stem cells without Myc from mouse and human fibroblasts

TRPC3 and TRPC6 are essential for angiotensin II-induced cardiac hypertrophy.

The Rho GEFs LARG and GEF-H1 regulate the mechanical response to force on integrins.

Oxidative stress contributes to lung injury and barrier dysfunction via microtubule destabilization

TGF-β regulates LARG and GEF-H1 during EMT to affect stiffening response to force and cell invasion.

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39383

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

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scholarly article

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10.1038/SREP39383

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6

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Motohiro Nishida

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2016-12-19T00:00:00Z

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1000783042

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27991560

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5171702

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