ArticleDevelopment (Cambridge, England)2006
Phosphorylation of IP3R1 and the regulation of [Ca2+]i responses at fertilization: a role for the MAP kinase pathway.
Article in Development (Cambridge, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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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Who cites it
46 citing papers in PubMed, 102 citations in OpenAlex.
- The therapeutic potential of Zuogui Wan in oligoasthenozoospermia: insights from network pharmacology, molecular docking, molecular dynamics simulation, and experimental validation.Scientific reports · 2025Article
- Molecular Mechanism of Oocyte Activation in Mammals: Past, Present, and Future Directions.Biomolecules · 2024Review
- Calcium signaling in oocyte quality and functionality and its application.Frontiers in endocrinology · 2024Review
- ZneLife · 2023Article
- ZnbioRxiv : the preprint server for biology · 2023Article
- Bcl-xL acts as an inhibitor of IPCell death and differentiation · 2022Article
- Review
- Age-related alterations in fertilization-induced Ca2+ oscillations depend on the genetic background of mouse oocytes†.Biology of reproduction · 2020Article
- Modulators of calcium signalling at fertilization.Open biology · 2020Review
- CaCold Spring Harbor perspectives in biology · 2019Review
- Postovulatory ageing modifies sperm-induced CaScientific reports · 2019Article
- Role of Type 1 Inositol 1,4,5-triphosphate Receptors in Mammalian Oocytes.Development & reproduction · 2019Review
- Ion Channel Function During Oocyte Maturation and Fertilization.Frontiers in cell and developmental biology · 2018Review
- Maintained MPF Level after Oocyte Vitrification Improves Embryonic Development after IVF, but not after Somatic Cell Nuclear Transfer.Molecules and cells · 2017Article
- Calcium influx and sperm-evoked calcium responses during oocyte maturation and egg activation.Oncotarget · 2017Review
- Biochemical alterations in the oocyte in support of early embryonic development.Cellular and molecular life sciences : CMLS · 2017Review
- Mutations in TUBB8 cause a multiplicity of phenotypes in human oocytes and early embryos.Journal of medical genetics · 2016Article
- Effect of M-phase kinase phosphorylations on type 1 inositol 1,4,5-trisphosphate receptor-mediated Ca2+ responses in mouse eggs.Cell calcium · 2015Article
- Excess cholesterol induces mouse egg activation and may cause female infertility.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Role of caspase-3 cleaved IP3 R1 on Ca(2+) homeostasis and developmental competence of mouse oocytes and eggs.Journal of cellular physiology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
A sperm-induced intracellular Ca2+ signal ([Ca2+]i) underlies the initiation of embryo development in most species studied to date. The inositol 1,4,5 trisphosphate receptor type 1 (IP3R1) in mammals, or its homologue in other species, is thought to mediate the majority of this Ca2+ release. IP3R1-mediated Ca2+ release is regulated during oocyte maturation such that it reaches maximal effectiveness at the time of fertilization, which, in mammalian eggs, occurs at the metaphase stage of the second meiosis (MII). Consistent with this, the [Ca2+]i oscillations associated with fertilization in these species occur most prominently during the MII stage. In this study, we have examined the molecular underpinnings of IP3R1 function in eggs. Using mouse and Xenopus eggs, we show that IP3R1 is phosphorylated during both maturation and the first cell cycle at a MPM2-detectable epitope(s), which is known to be a target of kinases controlling the cell cycle. In vitro phosphorylation studies reveal that MAPK/ERK2, one of the M-phase kinases, phosphorylates IP3R1 at at least one highly conserved site, and that its mutation abrogates IP3R1 phosphorylation in this domain. Our studies also found that activation of the MAPK/ERK pathway is required for the IP3R1 MPM2 reactivity observed in mouse eggs, and that eggs deprived of the MAPK/ERK pathway during maturation fail to mount normal [Ca2+]i oscillations in response to agonists and show compromised IP3R1 function. These findings identify IP3R1 phosphorylation by M-phase kinases as a regulatory mechanism of IP3R1 function in eggs that serves to optimize [Ca2+]i release at fertilization.
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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.