Protein Kinase C Deficiency Blocks Recovery from Agonist-induced Desensitization
Open Access
- 1 August 1996
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 271 (35) , 21478-21483
- https://doi.org/10.1074/jbc.271.35.21478
Abstract
No abstract availableKeywords
This publication has 25 references indexed in Scilit:
- The β-Adrenergic Receptor Is a Substrate for the Insulin Receptor Tyrosine KinaseJournal of Biological Chemistry, 1996
- Phosphorylation of Tyrosyl Residues 350/354 of the β-Adrenergic Receptor Is Obligatory for Counterregulatory Effects of InsulinJournal of Biological Chemistry, 1995
- Oligodeoxynucleotides antisense to mRNA encoding protein kinase A, protein kinase C, and beta-adrenergic receptor kinase reveal distinctive cell-type-specific roles in agonist-induced desensitization.Proceedings of the National Academy of Sciences, 1994
- Desensitization of the isolated .beta.2-adrenergic receptor by .beta.-adrenergic receptor kinase, cAMP-dependent protein kinase, and protein kinase C occurs via distinct molecular mechanismsBiochemistry, 1992
- cDNA cloning and chromosomal localization of the human α-adrenergic receptor kinaseFEBS Letters, 1991
- Turning off the signal: desensitization of β‐adrenergic receptor functionThe FASEB Journal, 1990
- Sequence of human protein kinase C αNucleic Acids Research, 1990
- Phosphorylation Sites on Two Domains of the β2-Adrenergic Receptor Are Involved in Distinct Pathways of Receptor DesensitizationJournal of Biological Chemistry, 1989
- Evidence for a second isoform of the catalytic subunit of cAMP-dependent protein kinase.Journal of Biological Chemistry, 1986
- Isolation of cDNA clones coding for the catalytic subunit of mouse cAMP-dependent protein kinase.Proceedings of the National Academy of Sciences, 1986