Cardiovascular Research Advance Access originally published online on April 8, 2008
Cardiovascular Research 2008 78(3):409-410; doi:10.1093/cvr/cvn089
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
Pulmonary hyperplasia and the two sides of PKC
Department of Medicine/Cardiology, Deutsches Herzzentrum Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany
* Corresponding author. Tel: +49 30 4593 2413; fax: +49 30 4593 2415. E-mail address: graf@dhzb.de
The editorial refers to Hypoxia exposure induces the emergence of fibroblasts lacking replication repressor signals of PKC
in the pulmonary artery adventitia by M. Das et al.,8 pp. 440–448, this issue.
| The first 10% of the full text of this article appears below. |
Protein kinase C (PKC) was initially identified by Nishizuka and coworkers1 as a nucleotide-independent, Ca2+-dependent serine kinase. Molecular cloning identified at least 11 isozymes of PKC that were further divided into subfamilies based on sequence homology and mode of stimulation. The classical PKCs (
, βI, βII, and
) are diacylglycerol (DAG) and calcium-dependent enzymes, whereas the novel PKCs (
,
,
, and
) require DAG, but not calcium, for activation. The atypical
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Related articles in Cardiovasc Res:
- Hypoxia exposure induces the emergence of fibroblasts lacking replication repressor signals of PKC
in the pulmonary artery adventitia
- Mita Das, Nana Burns, Shelly J. Wilson, Wojciech M. Zawada, and Kurt R. Stenmark
Cardiovasc Res 2008 78: 440-448.[Abstract] [FREE Full Text]
Related Article
-
Hypoxia exposure induces the emergence of fibroblasts lacking replication repressor signals of PKC
in the pulmonary artery adventitia
- Mita Das, Nana Burns, Shelly J. Wilson, Wojciech M. Zawada, and Kurt R. Stenmark
Cardiovasc Res 2008 78: 440-448.[Abstract] [Full Text] [PDF]