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Full-Text Articles in Biochemistry, Biophysics, and Structural Biology

The Role Of Jnk In The Development Of Hepatocellular Carcinoma, Madhumita Das, David S. Garlick, Dale Greiner, Roger J. Davis Mar 2011

The Role Of Jnk In The Development Of Hepatocellular Carcinoma, Madhumita Das, David S. Garlick, Dale Greiner, Roger J. Davis

Davis Lab Publications

The cJun NH(2)-terminal kinase (JNK) signal transduction pathway has been implicated in the growth of carcinogen-induced hepatocellular carcinoma. However, the mechanism that accounts for JNK-regulated tumor growth is unclear. Here we demonstrate that compound deficiency of the two ubiquitously expressed JNK isoforms (JNK1 and JNK2) in hepatocytes does not prevent hepatocellular carcinoma development. Indeed, JNK deficiency in hepatocytes increased the tumor burden. In contrast, compound JNK deficiency in hepatocytes and nonparenchymal cells reduced both hepatic inflammation and tumorigenesis. These data indicate that JNK plays a dual role in the development of hepatocellular carcinoma. JNK promotes an inflammatory hepatic ...


Jnk Regulates Foxo-Dependent Autophagy In Neurons, Ping Xu, Madhumita Das, Judith Reilly, Roger J. Davis Feb 2011

Jnk Regulates Foxo-Dependent Autophagy In Neurons, Ping Xu, Madhumita Das, Judith Reilly, Roger J. Davis

Davis Lab Publications

The cJun N-terminal kinase (JNK) signal transduction pathway is implicated in the regulation of neuronal function. JNK is encoded by three genes that play partially redundant roles. Here we report the creation of mice with targeted ablation of all three Jnk genes in neurons. Compound JNK-deficient neurons are dependent on autophagy for survival. This autophagic response is caused by FoxO-induced expression of Bnip3 that displaces the autophagic effector Beclin-1 from inactive Bcl-XL complexes. These data identify JNK as a potent negative regulator of FoxO-dependent autophagy in neurons.