ArticleScience (New York, N.Y.)2011
Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes.
Article in Science (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Pooled it
- Wee Kinases, Big Impact: Wee and Myt Kinases as Critical Regulators of Meiotic Progression.Journal of developmental biology · 2026Review
- Genetic architecture and phenotypic diversity of oocyte and early embryo competence defects in female infertility.Nature medicine · 2026Article
- Novel homozygous variants in ASTL and WEE2 responsible for female infertility characterized by abnormal fertilization.Journal of assisted reproduction and genetics · 2025Article
- Protein-targeting reverse genetic approaches: the future of oocyte and preimplantation embryo research.Molecular human reproduction · 2025Review
- The C-terminal domain of Emi2 conjugated to cell-penetrating peptide activates mouse oocyte.Frontiers in cell and developmental biology · 2025Article
- No transcription, no problem: Protein phosphorylation changes and the transition from oocyte to embryo.Current topics in developmental biology · 2025Review
- Novel splicing mutations in PATL2 and WEE2 cause oocyte degradation and fertilization failure.Journal of assisted reproduction and genetics · 2024Article
- Single-cell profiling reveals transcriptome dynamics during bovine oocyte growth.BMC genomics · 2024Article
- The signal that stimulates mammalian embryo development.Frontiers in cell and developmental biology · 2024Review
- Calcium signaling in oocyte quality and functionality and its application.Frontiers in endocrinology · 2024Review
- Meiotic Cell Cycle Progression in Mouse Oocytes: Role of Cyclins.International journal of molecular sciences · 2023Review
- Cyclers' kinases in cell division: from molecules to cancer therapy.Cell death and differentiation · 2023Review
- Selective Translation of Maternal mRNA by eIF4E1B Controls Oocyte to Embryo Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- Targeting the DNA Damage Response for Cancer Therapy by Inhibiting the Kinase Wee1.Frontiers in oncology · 2022Review
- Comparative Transcriptomics Uncover the Uniqueness of Oocyte Development in the Donkey.Frontiers in genetics · 2022Article
- Novel WEE2 compound heterozygous mutations identified in patients with fertilization failure or poor fertilization.Journal of assisted reproduction and genetics · 2021Article
- Meiotic Instability Generates a Pathological Condition in Mammalian Ovum.Stem cell reviews and reports · 2021Review
- ERβ regulated ovarian kisspeptin plays an important role in oocyte maturation.Molecular and cellular endocrinology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Waves of cyclin synthesis and degradation regulate the activity of Cdc2 protein kinase during the cell cycle. Cdc2 inactivation by Wee1B-mediated phosphorylation is necessary for arrest of the oocyte at G2-prophase, but it is unclear whether this regulation functions later during the metaphase-to-anaphase transition. We show that reactivation of a Wee1B pathway triggers the decrease in Cdc2 activity during egg activation. When Wee1B is down-regulated, oocytes fail to form a pronucleus in response to Ca(2+) signals. Calcium-calmodulin-dependent kinase II (CaMKII) activates Wee1B, and CaMKII-driven exit from metaphase II is inhibited by Wee1B down-regulation, demonstrating that exit from metaphase requires not only a proteolytic degradation of cyclin B but also the inhibitory phosphorylation of Cdc2 by Wee1B.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.