Effects of protein kinase C activators on germinal vesicle breakdown and polar body emission of mouse oocytes

1986 ◽  
Vol 165 (2) ◽  
pp. 507-517 ◽  
Author(s):  
Elayne A. Bornslaeger ◽  
William T. Poueymirou ◽  
Peter Mattei ◽  
Richard M. Schultz
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Polar Body ◽  
Germinal Vesicle ◽  
Germinal Vesicle Breakdown ◽  
Mouse Oocytes ◽  
Kinase C ◽  
Protein Kinase C Activators

Pleiotropic effect of okadaic acid on maturing mouse oocytes

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 971-980 ◽  
Author(s):  
H. Alexandre ◽  
A. Van Cauwenberge ◽  
Y. Tsukitani ◽  
J. Mulnard
Keyword(s):  
Protein Kinase ◽  
Okadaic Acid ◽  
Protein Phosphatases ◽  
Chromatin Condensation ◽  
Polar Body ◽  
Germinal Vesicle ◽  
Inhibitory Effect ◽  
Negative Control ◽  
Germinal Vesicle Breakdown ◽  
Mouse Oocytes

Okadaic acid (OA), a potent inhibitor of types 1 and 2A protein phosphatases, was shown recently to induce chromatin condensation and germinal vesicle breakdown (GVBD) in mouse oocytes arrested at the dictyate stage by dibutyryl cAMP (dbcAMP), isobutyl methylxanthine (IBMX) and 12,13-phorbol dibutyrate (PDBu). We confirm these results using IBMX and another phorbol diester, 12-O-tetradecanoylphorbol-13-acetate (TPA) and show that OA also bypasses the inhibitory effect of 6-dimethylaminopurine (6-DMAP). It has been concluded that protein phosphatases 1 and/or 2A (PP1, 2A), involved in the negative control of MPF activation, are thus operating downstream from both the protein kinase A and protein kinase C catalysed phosphorylation steps that prevent the breakdown of GV. Similar enzymatic activities are also able to counteract the general inhibition of protein phosphorylation. However, PP1 and/or PP2A are positively involved in the activation of pericentriolar material (PCM) into microtubule organizing centres (MTOCs). This explains the inhibitory effect of OA on spindle assembly. Finally, OA interferes with the integrity and/or function of actomyosin filaments. This results in a dramatic ruffling of the plasma membrane leading to the internalization of large vacuoles, the inhibition of chromosome centrifugal displacement and, consequently, the prevention of polar body extrusion.

Phosphorylation of MAP kinase and p90rsk and its regulation during in vitro maturation of cumulus-enclosed rabbit oocytes

Zygote ◽  
2002 ◽  
Vol 10 (4) ◽  
pp. 311-316 ◽  
Author(s):  
Hai-Quan Yu ◽  
Shorgan Bou ◽  
Da-Yuen Chen ◽  
Qing-Yuan Sun
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Map Kinase ◽  
Active Form ◽  
Germinal Vesicle ◽  
Germinal Vesicle Breakdown ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Mitogen Activated Protein

Numerous studies have demonstrated that activation of the mitogen-activated protein (MAP) kinase is involved in the maturation of oocytes. In this study, the expression and phosphorylation of MAP kinase and p90rsk, one of the substrates of MAP kinase, during rabbit oocyte maturation were studied. The results showed that MAP kinase phosphorylation began to occur after germinal vesicle breakdown (GVBD) and the active form was maintained until metaphase II. p90rsk was also activated after GVBD following MAP kinase activation. Immunofluorescent analysis showed that p90rsk was enriched in the nuclear area after GVBD and was gradually localised to the spindle. When GVBD was inhibited by increased cAMP or decreased protein kinase C activity, the phosphorylation of both MAP kinase and p90rsk was blocked. Our data suggest that (1) MAP kinase/p90rsk activation is not necessary for GVBD, but plays an important role in the post-GVBD events including spindle assembly in rabbit oocytes; and (2) MAP kinase/p90rsk activation is down-regulated by cAMP and up-regulated by protein kinase C in cumulus-enclosed rabbit oocytes.

Protein Kinase C Activators as Synaptogenic and Memory Therapeutics

2009 ◽  
Vol 342 (12) ◽  
pp. 689-698 ◽  
Author(s):  
Miao-Kun Sun ◽  
Daniel L. Alkon
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase C ◽  
Protein Kinase C Activators

scholarly journals Induction of heparin-binding epidermal growth factor-like growth factor mRNA by protein kinase C activators

1994 ◽  
Vol 46 (3) ◽  
pp. 690-695 ◽  
Author(s):  
Mian-Shin Tan ◽  
Jer-Chia Tsai ◽  
Yau-Jiunn Lee ◽  
Hung-Chun Chen ◽  
Shyi-Jang Shin ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Epidermal Growth Factor ◽  
Heparin Binding ◽  
Kinase C ◽  
Protein Kinase C Activators ◽  
Epidermal Growth

scholarly journals Identification of Combinations of Protein Kinase C Activators and Histone Deacetylase Inhibitors that Potently Reactivate Latent HIV

Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 609
Author(s):  
Francesca Curreli ◽  
Shahad Ahmed ◽  
Sofia M. Benedict Victor ◽  
Asim K. Debnath
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Synergistic Effect ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Latent Virus ◽  
Hiv Latency ◽  
Kinase C ◽  
Protein Kinase C Activators ◽  
Latent Hiv

Combination antiretroviral therapy (cART) is successful in maintaining undetectable levels of HIV in the blood; however, the persistence of latent HIV reservoirs has become the major barrier for a HIV cure. Substantial efforts are underway in finding the best latency-reversing agents (LRAs) to purge the latent viruses from the reservoirs. We hypothesize that identifying the right combination of LRAs will be the key to accomplishing that goal. In this study, we evaluated the effect of combinations of three protein kinase C activators (prostratin, (-)-indolactam V, and TPPB) with four histone deacetylase inhibitors (AR-42, PCI-24781, givinostat, and belinostat) on reversing HIV latency in different cell lines including in a primary CD4+ T-cell model. Combinations including indolactam and TPPB with AR-42 and PCI produced a strong synergistic effect in reactivating latent virus as indicated by higher p24 production and envelope gp120 expression. Furthermore, treatment with TPPB and indolactam greatly downregulated the cellular receptor CD4. Indolactam/AR-42 combination emerged from this study as the best combination that showed a strong synergistic effect in reactivating latent virus. Although AR-42 alone did not downregulate CD4 expression, indolactam/AR-42 showed the most efficient downregulation. Our results suggest that indolactam/AR-42 is the most effective combination, showing a strong synergistic effect in reversing HIV latency combined with the most efficient CD4 downregulation.

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