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Cardiovascular Research Advance Access first published online on April 8, 2008
This version [Corrected Proof] published online on April 24, 2008
Cardiovascular Research, 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{zeta}

Kristof Graf*

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{zeta} in the pulmonary artery adventitia’ by M. Das et al., doi:10.1093/cvr/cvn014.

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 ({alpha}, βI, βII, and {gamma}) are diacylglycerol (DAG) and calcium-dependent enzymes, whereas the novel PKCs ({delta}, {varepsilon}, {theta}, and {eta}) require DAG, but not calcium, for activation. The atypical PKCs . . . [Full Text of this Article]


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Hypoxia exposure induces the emergence of fibroblasts lacking replication repressor signals of PKC{zeta} in the pulmonary artery adventitia
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Hypoxia exposure induces the emergence of fibroblasts lacking replication repressor signals of PKC{zeta} in the pulmonary artery adventitia
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