Sanjoy Kumar Khan on Muck Rack

Sanjoy Kumar Khan

As seen in: Gut Journal, PNAS
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Articles

Hepatic gap junctions amplify alcohol liver injury by propagating cGAS-mediated IRF3 activation

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By Sanjoy Kumar Khan, Jay Luther, Manish K. Gala, Dmitry Kedrin
| PNAS Verified
Hepatic gap junctions amplify alcohol liver injury by propagating cGAS-mediated IRF3 activation Jay Luther, Sanjoy Khan, Manish K. Gala, Dmitry Kedrin, Gautham Sridharan, Russell P. Goodman, John J. Garber, Ricard Masia, Erik Diagacomo, Daniel Adams, Kevin R. King, Samuel Piaker, Hans-Christian Reinecker, Martin L. Yarmush, Josepmaria Argemi, Ramon Bataller, Jules L. Dienstag, Raymond T. Chung, Suraj J.
Open in Who Shared Issue with article?

Hepatic Hippo signaling inhibits protumoural microenvironment to suppress hepatocellular carcinoma

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By Wantae Kim, Sanjoy Kumar Khan, Yuchen Liu, Ruoshi Xu
| Gut Journal Verified
Objective Hippo signalling is a recently identified major oncosuppressive pathway that plays critical roles in inhibiting hepatocyte proliferation, survival and hepatocellular carcinoma (HCC) formation. Hippo kinase (Mst1 and Mst2) inhibits HCC proliferation by suppressing Yap/Taz transcription activities. As human HCC is mainly driven by chronic liver inflammation, it is not clear whether Hippo signalling inhibits HCC by shaping its inflammatory microenvironment.
Open in Who Shared Issue with article?

Hepatic Hippo signaling inhibits protumoural microenvironment to suppress hepatocellular carcinoma

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By Yuchen Liu, Wantae Kim, Sanjoy Kumar Khan, Ruoshi Xu
| Gut Journal Verified
Objective Hippo signalling is a recently identified major oncosuppressive pathway that plays critical roles in inhibiting hepatocyte proliferation, survival and hepatocellular carcinoma (HCC) formation. Hippo kinase (Mst1 and Mst2) inhibits HCC proliferation by suppressing Yap/Taz transcription activities. As human HCC is mainly driven by chronic liver inflammation, it is not clear whether Hippo signalling inhibits HCC by shaping its inflammatory microenvironment.
Open in Who Shared Issue with article?
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