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Ablation of cyclase-associated protein 2 (CAP2) leads to cardiomyopathy
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Ablation of cyclase-associated protein 2 (CAP2) leads to cardiomyopathy
Bibliographic description
| title: | Ablation of cyclase-associated protein 2 (CAP2) leads to cardiomyopathy |
| author: | Peche Vivek S., Holak Tadeusz  , Burgute Bhagyashri D., Kosmas Kosmas, Kale Sushant P., Wunderlich Thomas F., Elhamine Fatiha, Stehle Robert, Pfizer Gabriele, Nohroudi Klaus, Addicks Klaus, Stöckigt Florian, Schrickel Jan W., Gallinger Julia, Schleicher Michael, Noegel Angelika A. |
| journal title: | Cellular and Molecular Life Sciences |
| volume: | 70 |
| issue: | 3 |
| date of publication : | 2013 |
| pages: | 527-543 |
| ISSN: |
1420-682X |
| eISSN: |
1420-9071 |
| DOI: | |
| notes: | Na publikacji autor podpisany: Tad A. Holak |
| language: | English |
| journal language: | English |
| abstract in English: | Cyclase-associated proteins are highly con- served proteins that have a role in the regulation of actin dynamics. Higher eukaryotes have two isoforms, CAP1 and CAP2. To study the in vivo function of CAP2, we generated mice in which the CAP2 gene was inactivated by a gene-trap approach. Mutant mice showed a decrease in body weight and had a decreased survival rate. Further, they developed a severe cardiac defect marked by dilated cardiomyopathy (DCM) associated with drastic reduction in basal heart rate and prolongations in atrial and ventricular conduction times. Moreover, CAP2-deficient myofibrils exhibited reduced cooperativity of calcium- regulated force development. At the microscopic level, we observed disarrayed sarcomeres with development of fibrosis. We analyzed CAP2’s role in actin assembly and found that it sequesters G-actin and efficiently fragments filaments. This activity resides completely in its WASP homology domain. Thus CAP2 is an essential component of the myocardial sarcomere and is essential for physio- logical functioning of the cardiac system, and a deficiency leads to DCM and various cardiac defects. |
| affiliation: | Wydział Chemii : Zakład Chemii Organicznej |
| type: | journal article |
| subtype: | academic paper |
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Projekt „Repozytorium otwartego dostępu do dorobku naukowego i dydaktycznego UJ” współfinansowany w ramach poddziałania 2.3.1 „Cyfrowe udostępnianie zasobów nauki” Programu Operacyjnego Polska Cyfrowa z Europejskiego Funduszu Rozwoju Regionalnego i budżetu państwa na podstawie umowy o dofinansowanie nr POPC.02.03.01-00-0030/17-00
