Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

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The Active Components of Fuzheng Huayu Formula and Their Potential Mechanism of Action in Inhibiting the Hepatic Stellate Cells Viability - A Network Pharmacology and Transcriptomics Approach.

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Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

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http://www.wikidata.org/entity/Q42784235

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2016 nî lūn-bûn

@nan

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

2016年论文

@zh

2016年论文

@zh-cn

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Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@en

Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@nl

type

Item

label

Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@en

Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@nl

prefLabel

Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@en

Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@nl

P1476

Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

@en

P2093

Lawrence A Scheving

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

William E Russell

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

Xiuqi Zhang

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

P2860

NIH Image to ImageJ: 25 years of image analysis

The Role of NADPH Oxidases (NOXs) in Liver Fibrosis and the Activation of Myofibroblasts

Diverse expression of ErbB receptor proteins during rat liver development and regeneration

Dexamethasone modulates ErbB tyrosine kinase expression and signaling through multiple and redundant mechanisms in cultured rat hepatocytes

Mouse model of carbon tetrachloride induced liver fibrosis: Histopathological changes and expression of CD133 and epidermal growth factor

Epidermal growth factor receptor inhibition attenuates liver fibrosis and development of hepatocellular carcinoma.

Biological clocks and the digestive system.

Pathobiology of liver fibrosis: a translational success story

Loss of hepatocyte EGFR has no effect alone but exacerbates carbon tetrachloride-induced liver injury and impairs regeneration in hepatocyte Met-deficient mice.

Hepatocyte Nicotinamide Adenine Dinucleotide Phosphate Reduced Oxidase 4 Regulates Stress Signaling, Fibrosis, and Insulin Sensitivity During Development of Steatohepatitis in Mice.

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G807-G816

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scholarly article

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10.1152/AJPGI.00423.2015

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311

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David W. Threadgill

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2016-09-01T00:00:00Z

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27586651

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5130544

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Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

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P2860

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Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.

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P1433

P1476

P2093

P2860

P304

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P356

P433

P478

P50

P577

P698

P932

P356

P1433

P1476

P2093

P2860

P304

P31

P356

P433

P478

P50

P577

P698

P932