Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/197915
Type: Artigo de periódico
Title: Arhgap21 Associates With Fak And Pkczeta And Is Redistributed After Cardiac Pressure Overload.
Author: Borges, Luciene
Bigarella, Carolina Louzão
Baratti, Mariana Ozello
Crosara-Alberto, Daniella P
Joazeiro, Paulo P
Franchini, Kleber G
Costa, Fernando F
Saad, Sara Teresinha Olalla
Abstract: ARHGAP21 is highly expressed in the heart, which demonstrates activity over Cdc42 and interacts with proteins of the cytoskeleton and adherent junctions. The main cause of cardiac hypertrophy is mechanical stimulus; therefore we analyzed ARHGAP21 expression after acute mechanical stress in the myocardium and its association with FAK and PKCzeta. We demonstrated that ARHGAP21 is relocated to Z-lines and costameres after pressure overload, and interacts with PKCzeta and FAK in control rats (sham), rats submitted to aortic clamping and spontaneously hypertensive rats (SHR). Co-transfection using ARHGAP21 and PKCzeta constructions demonstrated that ARHGAP21 associates with PKCzeta-GST and endogenous FAK. Pulldown assay showed that ARHGAP21 binds to the C-terminal region of FAK. Moreover, ARHGAP21 binds to PKCzeta phosphorylated on Thr410 in sham and SHR. However, ARHGAP21 only binds to FAK phosphorylated on Tyr925 of SHR. Additionally, PKCzeta is phosphorylated by mechanical stimuli. These results suggest that ARHGAP21 may act as a signaling or scaffold protein of FAK and PKCzeta signaling pathways, developing an important function during cardiac stress.
Subject: Active Transport, Cell Nucleus
Adaptor Proteins, Signal Transducing
Animals
Cell Line
Cell Nucleus
Disease Models, Animal
Focal Adhesion Kinase 1
Hypertrophy, Left Ventricular
Male
Mice
Molecular Chaperones
Myocytes, Cardiac
Phosphorylation
Pressure
Rats
Rats, Inbred Shr
Rats, Wistar
Rights: fechado
Identifier DOI: 10.1016/j.bbrc.2008.07.085
Address: http://www.ncbi.nlm.nih.gov/pubmed/18662671
Date Issue: 2008
Appears in Collections:Unicamp - Artigos e Outros Documentos

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