scholarly journals Anti-Angiogenic and Anti-Cancer Effects by Targeting the Protein Kinase G Type-Iα (PKG-Iα) Signaling Pathway and its Downstream Effects on Expression of Inhibitor of Apoptosis Proteins, C-IAP1, Livin and Survivin

10.5772/60774 ◽  
2016 ◽  
Author(s):  
Janica C. Wong ◽  
Priyatham Gorjala ◽  
Benjamin Costantino ◽  
Ronald R. Fiscus
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Protein Kinase G ◽  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Proteins ◽  
Downstream Effects ◽  
Anti Cancer ◽  
Apoptosis Proteins

Inhibitor of apoptosis proteins (IAP) in adrenocortical tumors

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
B Altieri ◽  
S Sbiera ◽  
S Della Casa ◽  
S Steinhauer ◽  
V Wild ◽  
...  
Keyword(s):  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Proteins ◽  
Adrenocortical Tumors ◽  
Apoptosis Proteins

scholarly journals Cellular inhibitor of apoptosis proteins prevent clearance of hepatitis B virus

2015 ◽  
Vol 112 (18) ◽  
pp. 5797-5802 ◽  
Author(s):  
Gregor Ebert ◽  
Simon Preston ◽  
Cody Allison ◽  
James Cooney ◽  
Jesse G. Toe ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hbv Infection ◽  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Proteins ◽  
Immunocompetent Mouse ◽  
Immune Mediated ◽  
B Virus ◽  
Chronic Hbv ◽  
Apoptosis Proteins

Hepatitis B virus (HBV) infection can result in a spectrum of outcomes from immune-mediated control to disease progression, cirrhosis, and liver cancer. The host molecular pathways that influence and contribute to these outcomes need to be defined. Using an immunocompetent mouse model of chronic HBV infection, we identified some of the host cellular and molecular factors that impact on infection outcomes. Here, we show that cellular inhibitor of apoptosis proteins (cIAPs) attenuate TNF signaling during hepatitis B infection, and they restrict the death of infected hepatocytes, thus allowing viral persistence. Animals with a liver-specific cIAP1 and total cIAP2 deficiency efficiently control HBV infection compared with WT mice. This phenotype was partly recapitulated in mice that were deficient in cIAP2 alone. These results indicate that antagonizing the function of cIAPs may promote the clearance of HBV infection.

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