Protein kinase C-dependent phosphorylation of Borna disease virus P protein is required for efficient viral spread

2010 ◽  
Vol 155 (5) ◽  
pp. 789-793 ◽  
Author(s):  
Sonja Schmid ◽  
Philippe Metz ◽  
Christine M. A. Prat ◽  
Daniel Gonzalez-Dunia ◽  
Martin Schwemmle
1997 ◽  
Vol 272 (35) ◽  
pp. 21818-21823 ◽  
Author(s):  
Martin Schwemmle ◽  
Bishnu De ◽  
Licheng Shi ◽  
Amiya Banerjee ◽  
W. Ian Lipkin

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2133-P
Author(s):  
NIKKI L. FARNSWORTH ◽  
ROBERT A. PISCOPIO ◽  
RICHARD K. BENNINGER

2021 ◽  
Author(s):  
Ameya J. Limaye ◽  
George N. Bendzunas ◽  
Eileen Kennedy

Protein Kinase C (PKC) is a member of the AGC subfamily of kinases and regulates a wide array of signaling pathways and physiological processes. Protein-protein interactions involving PKC and its...


2001 ◽  
Vol 75 (21) ◽  
pp. 10460-10466 ◽  
Author(s):  
Jürgen Hausmann ◽  
Karin Schamel ◽  
Peter Staeheli

ABSTRACT Perforin-mediated lysis of target cells is the major antiviral effector mechanism of CD8+ T lymphocytes. We have analyzed the role of perforin in a mouse model for CD8+T-cell-mediated central nervous system (CNS) immunopathology induced by Borna disease virus. When a defective perforin gene was introduced into the genetic background of the Borna disease-susceptible mouse strain MRL, the resulting perforin-deficient mice developed strong neurological disease in response to infection indistinguishable from that of their perforin-expressing littermates. The onset of disease was slightly delayed. Brains of diseased perforin-deficient mice showed similar amounts and a similar distribution of CD8+ T cells as wild-type animals. Perforin deficiency had no impact on the kinetics of viral spread through the CNS. Unlike brain lymphocytes from diseased wild-type mice, lymphocytes from perforin-deficient MRL mice showed no in vitro cytolytic activity towards target cells expressing the nucleoprotein of Borna disease virus. Taken together, these results demonstrate that CD8+ T cells mediate Borna disease independent of perforin. They further suggest that the pathogenic potential of CNS-infiltrating CD8+ T cells does not primarily reside in their lytic activity but rather in other functions.


Author(s):  
Kohei Tsuji ◽  
Takahiro Ishii ◽  
T Kobayakawa ◽  
Nami Ohashi ◽  
Wataru Nomura ◽  
...  

Protein kinase C (PKC) is associated with a central cellular signal transduction pathway and disorders such as cancer and Alzheimer-type dementia and is therefore a target for treatment of these...


2014 ◽  
Vol 10 (11) ◽  
pp. 3002-3013 ◽  
Author(s):  
Narsimha Mamidi ◽  
Subhankar Panda ◽  
Rituparna Borah ◽  
Debasis Manna

Protein kinase C-C1 domain binding specificity of the anionic hybrid lipids.


2000 ◽  
Vol 74 (7) ◽  
pp. 3413-3417 ◽  
Author(s):  
Tahir H. Malik ◽  
Masahiko Kishi ◽  
Patrick K. Lai

ABSTRACT The Borna disease virus (BDV) is the prototype member of the Bornaviridae, and it replicates in the cell nucleus. The BDV p24P and p40N proteins carry nuclear localization signals (NLS) and are found in the nuclei of infected cells. The BDV p10 protein does not have an NLS, but it binds with P and/or N and is translocated to the nucleus. Hence, p10 may play a role in the replication of BDV in the cell nucleus. Here, we show that the P-binding domain is located in the N terminus of p10 and that S3 and L16 are important for the interaction.


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