Phosphorylated p38 and JNK MAPK proteins in hepatocellular carcinoma. (Q54479908)

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title

Phosphorylated p38 and JNK MAPK proteins in hepatocellular carcinoma. (English)

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Shen-Nien Wang

1

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King-Teh Lee

2

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Chia-Jung Tsai

3

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Yu-Jie Chen

4

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Yao-Tsung Yeh

5

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publication date

3 October 2012

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European Journal of Clinical Investigation

published in

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volume

42

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issue

12

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page(s)

1295-1301

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Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions

cites work

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Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain

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Signal transduction by the JNK group of MAP kinases

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Adiponectin modulates C-jun N-terminal kinase and mammalian target of rapamycin and inhibits hepatocellular carcinoma

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Comparison of recurrence of hepatocellular carcinoma after resection in patients with cirrhosis to its occurrence in a surveilled cirrhotic population

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Outcome after curative resection for a huge (>or=10 cm) hepatocellular carcinoma and prognostic significance of gross tumor classification.

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Liver resection improves the survival of patients with multiple hepatocellular carcinomas

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Factors predictive for long-term survival of male patients with hepatocellular carcinoma after curative resection

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Role of mitogen-activated protein kinase kinase kinases in signal integration

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Synergistic induction of tumor cell apoptosis by death receptor antibody and chemotherapy agent through JNK/p38 and mitochondrial death pathway

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Critical activities of Rac1 and Cdc42Hs in skeletal myogenesis: antagonistic effects of JNK and p38 pathways

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Antagonistic control of cell fates by JNK and p38-MAPK signaling.

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The functional contrariety of JNK

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p38α suppresses normal and cancer cell proliferation by antagonizing the JNK–c-Jun pathway

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Identifiers

DOI

10.1111/ECI.12003

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