Proteomics

Dataset Information

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Phosphodiesterase 9A Controls Nitric-oxide Independent cGMP and Hypertrophic Heart Disease

ABSTRACT: Rat neonatal cardiac myocytes were treated with PDE5 and PDE9 inhibitor in the presence and absence of L-NAME.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Cell Culture, Fetal Cardiomyocyte

SUBMITTER: Ronald Holewinski  

LAB HEAD: David A Kass

PROVIDER: PXD001585 | Pride | 2016-06-24

REPOSITORIES: Pride

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Dataset's files

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Action DRS
RH_141002_NRVM_Control-01_TiO2_run1.ms2 Other
RH_141002_NRVM_Control-01_TiO2_run1.pep.xml Pepxml
RH_141002_NRVM_Control-01_TiO2_run1.raw Raw
RH_141002_NRVM_Control-01_TiO2_run2.ms2 Other
RH_141002_NRVM_Control-01_TiO2_run2.pep.xml Pepxml
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Publications

Cyclic guanosine monophosphate (cGMP) is a second messenger molecule that transduces nitric-oxide- and natriuretic-peptide-coupled signalling, stimulating phosphorylation changes by protein kinase G. Enhancing cGMP synthesis or blocking its degradation by phosphodiesterase type 5A (PDE5A) protects against cardiovascular disease. However, cGMP stimulation alone is limited by counter-adaptions including PDE upregulation. Furthermore, although PDE5A regulates nitric-oxide-generated cGMP, nitric oxi  ...[more]

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