TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

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Proteomic profiling of TGFBI-null mouse corneas reveals only minor changes in matrix composition supportive of TGFBI knockdown as therapy against TGFBI-linked corneal dystrophies.Periostin function in communication with extracellular matrices.

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Q47424334-8AF88982-AC0C-4F1B-955D-2FB911B6FEBC Q47584948-1FB342FF-8812-4254-B49F-53F41B7EA317

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TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

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http://www.wikidata.org/entity/Q41153678

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TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

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TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

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TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

@en

P1476

TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

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P2093

Allen J York

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

Angela Lorts

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Demetria M Fischesser

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Jeffrey A Whitsett

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Kelly M Grimes

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Michelle A Sargent

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Simon J Conway

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P2860

Periostin shows increased evolutionary plasticity in its alternatively spliced region

cDNA cloning and sequence analysis of beta ig-h3, a novel gene induced in a human adenocarcinoma cell line after treatment with transforming growth factor-beta

Osteoblast-specific factor 2: cloning of a putative bone adhesion protein with homology with the insect protein fasciclin I

Corneal dystrophy-associated R124H mutation disrupts TGFBI interaction with Periostin and causes mislocalization to the lysosome

Periostin and TGF-β-induced protein: Two peas in a pod?

Identification and characterization of a novel protein, periostin, with restricted expression to periosteum and periodontal ligament and increased expression by transforming growth factor beta

Heart Disease and Stroke Statistics-2017 Update: A Report From the American Heart Association

Genetic lineage tracing defines myofibroblast origin and function in the injured heart.

Calcineurin/NFAT coupling participates in pathological, but not physiological, cardiac hypertrophy.

c-kit+ cells minimally contribute cardiomyocytes to the heart

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e0181945

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scholarly article

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10.1371/JOURNAL.PONE.0181945

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English

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

P478

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Jeffery D. Molkentin

Jennifer A Schwanekamp

Jason J Gokey

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2017-07-27T00:00:00Z

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28750100

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5531541

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TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

about

P2860

P2860

TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury

description

name

type

label

prefLabel

P1433

P1476

P2093

P2860

P304

P31

P356

P407

P433

P478

P50

P577

P698

P932

P356

P1433

P1476

P2093

P2860

P304

P31

P356

P407

P433

P478

P50

P577

P698

P932