PMID- 10085070
OWN - NLM
STAT- MEDLINE
DCOM- 19990429
LR  - 20210209
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 274
IP  - 13
DP  - 1999 Mar 26
TI  - Cyclic AMP- and cyclic GMP-dependent protein kinases differ in their regulation 
      of cyclic AMP response element-dependent gene transcription.
PG  - 8391-404
AB  - The ability of cGMP-dependent protein kinases (cGKs) to activate cAMP response 
      element (CRE)-dependent gene transcription was compared with that of 
      cAMP-dependent protein kinases (cAKs). Although both the type Ibeta 
      cGMP-dependent protein kinase (cGKIbeta) and the type II cAMP-dependent protein 
      kinase (cAKII) phosphorylated the cytoplasmic substrate VASP (vasodilator- and A 
      kinase-stimulated phosphoprotein) to a similar extent, cyclic nucleotide 
      regulation of CRE-dependent transcription was at least 10-fold higher in 
      cAKII-transfected cells than in cGKIbeta-transfected cells. Overexpression of 
      each kinase in mammalian cells resulted in a cytoplasmic localization of the 
      unactivated enzyme. As reported previously, the catalytic (C) subunit of cAKII 
      translocated to the nucleus following activation by 8-bromo-cyclic AMP. However, 
      cGKIbeta did not translocate to the nucleus upon activation by 8-bromo-cyclic 
      GMP. Replacement of an autophosphorylated serine (Ser79) of cGKIbeta with an 
      aspartic acid resulted in a mutant kinase with constitutive kinase activity in 
      vitro and in vivo. The cGKIbetaS79D mutant localized to the cytoplasm and was 
      only a weak activator of CRE-dependent gene transcription. However, an 
      amino-terminal deletion mutant of cGKIbeta was found in the nucleus as well as 
      the cytoplasm and was a strong activator of CRE-dependent gene transcription. 
      These data suggest that the inability of cGKs to translocate to the nucleus is 
      responsible for the differential ability of cAKs and cGKs to activate 
      CRE-dependent gene transcription and that nuclear redistribution of cGKs is not 
      required for NO/cGMP regulation of gene transcription.
FAU - Collins, S P
AU  - Collins SP
AD  - Department of Biological Chemistry and the Mental Health Research Institute, 
      University of Michigan, Ann Arbor, Michigan 48109, USA.
FAU - Uhler, M D
AU  - Uhler MD
LA  - eng
SI  - GENBANK/AF084547
SI  - GENBANK/AF084548
GR  - GM 38788/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Carrier Proteins)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Microfilament Proteins)
RN  - 0 (Phosphoproteins)
RN  - 0 (protein kinase modulator)
RN  - 0 (vasodilator-stimulated phosphoprotein)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinase Type II)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.12 (Cyclic GMP-Dependent Protein Kinases)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Brain/metabolism
MH  - Carrier Proteins/*genetics
MH  - Cell Adhesion Molecules/metabolism
MH  - Cell Line
MH  - Cloning, Molecular
MH  - Cyclic AMP/analogs & derivatives/pharmacology
MH  - Cyclic AMP-Dependent Protein Kinase Type II
MH  - Cyclic AMP-Dependent Protein Kinases/*genetics
MH  - Cyclic GMP/analogs & derivatives/pharmacology
MH  - Cyclic GMP-Dependent Protein Kinases/*genetics
MH  - Fluorescent Antibody Technique
MH  - Genes, Reporter/genetics
MH  - *Intracellular Signaling Peptides and Proteins
MH  - Mice
MH  - Microfilament Proteins
MH  - Molecular Sequence Data
MH  - Mutation/genetics
MH  - Phosphoproteins/metabolism
MH  - Phosphorylation
MH  - Transcriptional Activation/genetics
MH  - Transfection/genetics
EDAT- 1999/03/20 00:00
MHDA- 1999/03/20 00:01
CRDT- 1999/03/20 00:00
PHST- 1999/03/20 00:00 [pubmed]
PHST- 1999/03/20 00:01 [medline]
PHST- 1999/03/20 00:00 [entrez]
AID - S0021-9258(19)87347-7 [pii]
AID - 10.1074/jbc.274.13.8391 [doi]
PST - ppublish
SO  - J Biol Chem. 1999 Mar 26;274(13):8391-404. doi: 10.1074/jbc.274.13.8391.