Linked Life Data

7700241

Source:http://linkedlifedata.com/resource/pubmed/id/7700241

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-4-28
pubmed:abstractText
Norepinephrine (NE) regulates melatonin production and many other aspects of pineal function through actions involving cAMP. In the present study the effects of NE on the phosphorylation of the cAMP response element-binding protein (CREB) were studied to determine whether CREB phosphorylation might be involved in cAMP signal transduction in this tissue. CREB was detected using gel mobility-shift analysis with the radiolabeled Ca2+/cAMP response element of the c-fos promoter. CREB phosphorylation was estimated in the gel mobility-shift assay using an antiserum specific for phosphorylated CREB. This antiserum generates a supershifted CREB signal with protein extracts obtained from glands treated with NE (EC50 approximately equal to 10 nM) in organ culture, demonstrating that NE stimulates CREB phosphorylation. CREB phosphorylation peaks 30-45 min after NE treatment is initiated and then gradually returns to base-line values. Pharmacological studies show that NE-stimulated CREB phosphorylation is mediated primarily through beta 1-adrenergic receptor-stimulated increases in cAMP. Activation of alpha 1-adrenergic receptors, which is known to elevate the intracellular free Ca2+ concentration, does not cause CREB phosphorylation. However, it is possible to produce CREB phosphorylation with certain pharmacological agents that elevate the intracellular free Ca2+ concentration. In vivo studies show that CREB phosphorylation can be induced by treatment with isoproterenol (1 mg/kg), demonstrating that phosphorylation of pineal CREB occurs in intact animals. These studies indicate that cAMP-dependent CREB phosphorylation could play a role in the adrenergic regulation of gene expression in pinealocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0026-895X
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
439-49
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:7700241-Animals, pubmed-meshheading:7700241-Base Sequence, pubmed-meshheading:7700241-Calcium, pubmed-meshheading:7700241-Cyclic AMP, pubmed-meshheading:7700241-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:7700241-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:7700241-Female, pubmed-meshheading:7700241-Isoproterenol, pubmed-meshheading:7700241-Kinetics, pubmed-meshheading:7700241-Light, pubmed-meshheading:7700241-Macromolecular Substances, pubmed-meshheading:7700241-Male, pubmed-meshheading:7700241-Molecular Sequence Data, pubmed-meshheading:7700241-Norepinephrine, pubmed-meshheading:7700241-Organ Culture Techniques, pubmed-meshheading:7700241-Phosphorylation, pubmed-meshheading:7700241-Pineal Gland, pubmed-meshheading:7700241-Rats, pubmed-meshheading:7700241-Rats, Sprague-Dawley, pubmed-meshheading:7700241-Receptors, Adrenergic, beta, pubmed-meshheading:7700241-Stimulation, Chemical
pubmed:year
1995
pubmed:articleTitle
Norepinephrine stimulation of pineal cyclic AMP response element-binding protein phosphorylation: primary role of a beta-adrenergic receptor/cyclic AMP mechanism.
pubmed:affiliation
Section of Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article