ArticleThe Biochemical journal1992
Glucagon, vasopressin and angiotensin all elicit a rapid, transient increase in hepatocyte protein kinase C activity.
Article in The Biochemical journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 40 citations in OpenAlex.
- TACE/ADAM-17 phosphorylation by PKC-epsilon mediates premalignant changes in tobacco smoke-exposed lung cells.PloS one · 2011Article
- Cross-talk between angiotensin II and glucagon receptor signaling mediates phosphorylation of mitogen-activated protein kinases ERK 1/2 in rat glomerular mesangial cells.Biochemical pharmacology · 2006Article
- Long PDE4 cAMP specific phosphodiesterases are activated by protein kinase A-mediated phosphorylation of a single serine residue in Upstream Conserved Region 1 (UCR1).British journal of pharmacology · 2002Article
- The MAP kinase ERK2 inhibits the cyclic AMP-specific phosphodiesterase HSPDE4D3 by phosphorylating it at Ser579.The EMBO journal · 1999Article
- Protein kinase C in IL-2 signal transduction.Immunologic research · 1997Review
- Protein kinase C in cultured human placental trophoblasts: identification of isoforms and role in cAMP signalling.The Biochemical journal · 1996Article
- Streptozotocin-induced diabetes elicits the phosphorylation of hepatocyte Gi2 alpha at the protein kinase C site but not at the protein kinase A-controlled site.The Biochemical journal · 1996Article
- Insulin and vasopressin elicit inhibition of cholera-toxin-stimulated adenylate cyclase activity in both hepatocytes and the P9 immortalized hepatocyte cell line through an action involving protein kinase C.The Biochemical journal · 1995Article
- A role for protein kinase C-mediated phosphorylation in eliciting glucagon desensitization in rat hepatocytes.The Biochemical journal · 1995Article
- Inactive membrane protein kinase Cs: a possible target for receptor signalling.The Biochemical journal · 1994Article
- Multi-site phosphorylation of the inhibitory guanine nucleotide regulatory protein Gi-2 occurs in intact rat hepatocytes.The Biochemical journal · 1994Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Challenge of intact hepatocytes with one of the hormones vasopressin, angiotensin and glucagon or with the phorbol ester phorbol 12-myristate 13-acetate (PMA) led to a rapid increase in the activity of protein kinase C found in both cytosol and membrane fractions. Maximal activation by hormones occurred within 1-6 min of challenge of cells, after which activity declined. In membrane fractions protein kinase C activity return to basal levels some 15 min after exposure of cells to either angiotensin or glucagon. In cytosol fractions of cells challenged with hormones a second phase of activation ensued after about 10 min, with levels of protein kinase C activity remaining elevated above basal level 15 min afterwards. Activity changes elicited by PMA were rather different; it took about 15 min to achieve maximal activation of cytosolic protein kinase C activity. In membranes of cells challenged with PMA, an initial rapid and transient activation was followed by a sustained increase in activity occurring about 10 min after exposure of cells to this ligand. Only when hepatocytes were challenged with PMA was the translocation of protein kinase C from the cytosol to membrane fraction observed. The kinetics of PMA-induced translocation suggested that it accounted for the second phase of the increase in membrane protein kinase C activity which was unique to this ligand.
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