protein kinase c
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2022 ◽  
Author(s):  
Kimberly A Jones ◽  
Michael L Drummond ◽  
Ken Prehoda

Recruitment of the Par complex protein atypical Protein Kinase C (aPKC) to a specific membrane domain is a key step in the polarization of animal cells. While numerous proteins and phospholipids interact with aPKC, how these interactions cooperate to control its membrane recruitment has been unknown. Here we identify aPKC's C1 domain as a phospholipid interaction module that targets aPKC to the membrane of Drosophila neural stem cells (NSCs). The isolated C1 binds the NSC membrane in an unpolarized manner during interphase and mitosis and is uniquely sufficient among aPKC domains for targeting. Other domains, including the catalytic module and those that bind the upstream regulators Par-6 and Baz, restrict C1's membrane targeting activity spatially and temporally-to the apical NSC membrane during mitosis. Our results suggest that Par complex polarity results from cooperative activation of autoinhibited C1 membrane binding activity.


2022 ◽  
Vol 20 (4) ◽  
pp. 6-10
Author(s):  
A. V. Mukhomedzyanov ◽  
N. V. Naryzhnaya ◽  
L. N. Maslov

Background. Acute myocardial infarction (AMI) with ST segment elevation is associated with high incidence of complications. Mortality from AMI is about 5%, which has not decreased in recent years. Revascularization provides recovery of coronary blood flow, but also contributes to the occurrence of reperfusion injury to the heart. Remote ischemic postconditioning (RIPostC) is a promising, non-invasive method that can effectively and safely reduce the infarct size.The aim of the study was to investigate the role of protein kinase C and PI3-kinase in the development of the infarct-limiting effect of remote ischemic postconditioning.Materials and methods. The study was performed on Wistar rats. Coronary artery occlusion (45 min) and reperfusion (2 h) were performed. The infarct size (IS) and the size of area at risk (AAR) were assessed. RIPostC was modeled by applying tourniquets to the hind limbs in the hip joint immediately after the restoration of coronary blood flow. All inhibitors were administered intravenously 10 min before reperfusion.Results. In the control group, the IS / AAR ratio was 44%. RIPostC reduced the IS / AAR ratio by about 50%. Preliminary administration of the protein kinase C inhibitor chelerythrine and the PI3-kinase inhibitor wortmannin eliminated the cardioprotective effect of RIPostC.Conclusion. The mechanism of the infarct-limiting effect of RIPostC is implemented through activation of protein kinase C and PI3-kinase. 


2022 ◽  
Vol 47 (1) ◽  
pp. 19-30
Author(s):  
Hideaki Yokoyama ◽  
Taku Masuyama ◽  
Yuki Tanaka ◽  
Iori Tsubakihara ◽  
Kazuma Kondo ◽  
...  

2022 ◽  
pp. 110246
Author(s):  
Rubí Hernández-Rojas ◽  
Carolina Jiménez-Arellano ◽  
Marisol de la Fuente-Granada ◽  
David Ordaz-Rosado ◽  
Rocío García-Becerra ◽  
...  

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