Phospholipid-dependent Ca2+-activated protein kinase (C-kinase) in the pituitary: Further characterization and endogenous redistribution

Hermon, Jacob; Azrad, Anat; Reiss, Nachum; Naor, Zvi

doi:10.1016/0303-7207(86)90113-9

Cited by 14 publications

(5 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study, we found 84% of C-kinase activity in the soluble form, whereas Hermon et al (3) found 70%. This discrepancy may be due to the different detergents used (Nonidet P-40 instead of Triton X-100) and/or to the different elutions of the enzyme from the DE-52 column (0.1 mol/1 NaCl in our study, a gradient from 0 to 0.4 mol/1 NaCl in theirs).…”

Section: Discussioncontrasting

confidence: 81%

“…C-kinase activity has already been characterized in rat pituitary glands (3), with a subcellular dis¬ tribution in particulate and soluble fractions. In our study, we found 84% of C-kinase activity in the soluble form, whereas Hermon et al (3) found 70%.…”

Section: Discussionmentioning

confidence: 99%

“…Residues were resuspended in icecold 20 mmol/1 TRIS-HC1, pH 7.5, and sonicated for 3 min at 4°C. Concentrations of diolein, PS and calcium were shown to be sufficient to activate C-kinase maxi¬ mally (3).…”

Section: Preparation Ofpituitary Extractsmentioning

confidence: 99%

“…C-kinase is activated by diacylglycerol generated during the phosphoinositide turnover from degradation of phospholipids by a specific phospholipase C (2). C-kinase activity has recently been characterized in rat pituitary tissue; it is mostly soluble (cytosolic) and partly paniculate (3). Whether this enzyme may be implicated in the pathogenesis of pituitary adenomas is unknown.…”

mentioning

confidence: 98%

See 3 more Smart Citations

The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502

Birman

Touraine²,

Bai-Grenier³

et al. 1989

Acta Endocrinologica

View full text Add to dashboard Cite

To investigate whether the modulation of lactotrope cell multiplication and prolactin secretion in rat pituitary glands implicated the phosphoinositide C-kinase system, female Wistar rats were treated or not with the dopamine agonist CV 205-502 or 8 days or with estradiol cervical implants for 8 for 15 days, alone or in combination with CV 205-502 for the last 8 days. CV 205-502 treatment induced a significant reduction in plasma PRL levels and in pituitary weights, whereas estradiol treatment induced a significant increase in both parameters.CV 205-502, in association with estradiol, counteracted estradiol stimulation of PRL levels and of pituitary weights. Total C-kinase activity in controls was 29.8 \ m=+-\ 9.9 pmol 32phosphorus/min (N = 7, mean \ m=+-\ sem), mainly found in the soluble fraction (84%). When administered alone, CV 205-502 induced a significant reduction (\p=n-\58%, p < 0.02) in C-kinase activity in the particulate fraction with no modification in the soluble fraction. Both 8 and 15 days estradiol treatment induced a significant stimulation of total C-kinase activity, 74% and 155% respectively. When combined with estradiol, CV 205-502 significantly (p < 0.02) counteracted the estradiol increase in total C-kinase activity, which was only 45% over control values. We conclude that treatment with a dopamine agonist and estradiol, which have antagonistic effects on the pituitary, exerts an opposite regulation of C-kinase activity.

show abstract

Section: Discussioncontrasting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Preparation Ofpituitary Extractsmentioning

confidence: 99%

mentioning

confidence: 98%

See 2 more Smart Citations

The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502

Birman

Touraine²,

Bai-Grenier³

et al. 1989

Acta Endocrinologica

View full text Add to dashboard Cite

show abstract

“…PKC is thought to be the main receptor for the tumor promoter phorbol esters, and therefore the en zyme is also implicated in transformation [39. 40], PKC is present in the pituitary [13, 14,60,61], where it is mostly soluble (70%) and partly particulate (30%). Stim ulation of the pituitary by GnRH results in translocation of PKC from the cytosol to the membrane [13,14], Such a redistribution exposes the inactive enzyme to phosphatidylserine (PS) and DG.…”

mentioning

confidence: 99%

The Gonadotropin-Releasing Hormone Receptor: Signals Involved in Gonadotropin Secretion and Biosynthesis

Dan-Cohen

Ben-Menahem²,

Naor³

1990

Horm Res

View full text Add to dashboard Cite

The neurohormone gonadotropin-releasing hormone (GnRH) is a decapeptide which is synthesized in the hypothalamus and released into the hypophysial portal system in a pulsatile manner. GnRH exerts its effect on the anterior pituitary gonadotrophs where it regulates the secretion and synthesis of gonadotropins (luteinizing hormone and follicle-stimulating hormone) through receptor-mediated actions. The GnRH receptor has been characterized and shown to be coupled to the formation of ‘second messengers’ which participate in signal transduction mechanisms. GnRH stimulation of luteinizing hormone release is a Ca²⁺-dependent process. G protein, phosphoinositide hydrolysis, protein kinase C as well as arachidonic acid and some of its metabolites were identified as possible mediators in the process.

show abstract

Phosphoinositide Turnover, Ca2+ Mobilization, and Protein Kinase C Activation in GnRH Action on Pituitary Gonadotropin Release

Naor

1987

Endocrinology and Physiology of Reproduction

View full text Add to dashboard Cite

Phospholipid-dependent Ca2+-activated protein kinase (C-kinase) in the pituitary: Further characterization and endogenous redistribution

Cited by 14 publications

References 31 publications

The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502

The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502

The Gonadotropin-Releasing Hormone Receptor: Signals Involved in Gonadotropin Secretion and Biosynthesis

Phosphoinositide Turnover, Ca2+ Mobilization, and Protein Kinase C Activation in GnRH Action on Pituitary Gonadotropin Release

Contact Info

Product

Resources

About