ArticleCell proliferation2011
Influence of proline-rich inositol polyphosphate 5-phosphatase, on early development of fertilized mouse eggs, via inhibition of phosphorylation of Akt.
Article in Cell proliferation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Hormesis of low-dose inhibition of pAkt1 (Ser473) followed by a great increase of proline-rich inositol polyphosphate 5-phosphatase (PIPP) level in oocytes.In vitro cellular & developmental biology. Animal · 2021Article
- Involvement of CaMKII in regulating the release of diplotene-arrested mouse oocytes by pAkt1 (Ser473).Cell cycle (Georgetown, Tex.) · 2019Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesProline-rich inositol polyphosphate 5-phosphatase (PIPP) is one of the signal-modifying enzymes that play pivotal regulatory roles in PI3K signalling pathway. The aim of this study was to determine the role of PIPP in early development of fertilized mouse eggs, via inhibition of Akt activity and subsequent downstream signalling events. MATERIALS AND
methodsThe mRNA transcript levels of endogenous PIPP and Akt1, Akt2, Akt3 were detected in G(1) , S, G(2) and M phases of fertilized mouse eggs by RT-PCR. Levels of exogenous PIPP, phosphorylated Akt at Ser473, dephosphorylated cdc2 at Tyr15 and levels of CCNB1, were detected respectively by immunoblotting. Changes in Akt localization were observed by fluoroimmunoassay; meanwhile, changes in activity of Akt and its downstream MPF were detected. Percentages of cells undergoing division were determined by counting, using a dissecting microscope.
resultsPIPP and Akt1 transcripts were detectable in G(1), S, G(2) and M phases of fertilized mouse eggs, but Akt2 and Akt3 were not. We also observed that overexpression of PIPP in fertilized eggs decreased expression of phosphorylated Akt at Ser473 and altered membrane localization of phosphorylated Akt at Ser473 specifically. Furthermore, overexpression of PIPP resulted in decreases in mitosis-phase promoting factor activity, level of dephosphorylated cdc2 at Tyr15 and cleavage rate of fertilized mouse eggs.
conclusionsOur data suggest, for the first time, that PIPP may affect development of fertilized mouse eggs by inhibition of level of phosphorylated Akt at Ser473 and subsequent inhibition of downstream signal cascades.
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