ArticleBMC developmental biology2007
The oxidative stress adaptor p66Shc is required for permanent embryo arrest in vitro.
Article in BMC developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 62 citations in OpenAlex.
- Extracellular matrix dysregulation in aging, calcification, and cancer diseases: insights into cellular senescence, inflammation, and novel therapeutic strategies.International journal of biological sciences · 2025Review
- A nutrigeroscience approach: Dietary macronutrients and cellular senescence.Cell metabolism · 2024Review
- The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.American journal of physiology. Cell physiology · 2023Review
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- p66Shc in Cardiovascular Pathology.Cells · 2022Review
- Senescence and Apoptosis DuringFrontiers in cell and developmental biology · 2020Review
- Shc and the mechanotransduction of cellular anchorage and metastasis.Small GTPases · 2019Review
- Knockdown of p66Shc Alters Lineage-Associated Transcription Factor Expression in Mouse Blastocysts.Stem cells and development · 2018Article
- p66Molecular and cellular biology · 2016Article
- P66Shc, a key regulator of metabolism and mitochondrial ROS production, is dysregulated by mouse embryo culture.Molecular human reproduction · 2016Article
- Endoplasmic reticulum stress signaling in mammalian oocytes and embryos: life in balance.International review of cell and molecular biology · 2015Review
- The p66Shc adapter protein regulates the morphogenesis and epithelial maturation of fetal mouse lungs.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- The p66(Shc) adaptor protein controls oxidative stress response in early bovine embryos.PloS one · 2014Article
- TEAD4 establishes the energy homeostasis essential for blastocoel formation.Development (Cambridge, England) · 2013Article
- The Effects of ISM1 Medium on Embryo Quality and Outcomes of IVF/ICSI Cycles.International journal of fertility & sterility · 2013Article
- Pro-apoptotic Effect of Pifithrin-α on Preimplantation Porcine In vitro Fertilized Embryo Development.Asian-Australasian journal of animal sciences · 2012Article
- Developmental expression of the cellular prion protein (PrP(C) ) in bovine embryos.Molecular reproduction and development · 2012Article
- NLRP5 mediates mitochondrial function in mouse oocytes and embryos.Biology of reproduction · 2012Article
- Automated microinjection of recombinant BCL-X into mouse zygotes enhances embryo development.PloS one · 2011Article
- p66shc inhibits insulin-like growth factor-I signaling via direct binding to Src through its polyproline and Src homology 2 domains, resulting in impairment of Src kinase activation.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExcessive developmental failure occurs during the first week of in vitro embryo development due to elevated levels of cell death and arrest. We hypothesize that permanently arrested embryos enter a stress-induced "senescence-like" state that is dependent on the oxidative stress-adaptor and lifespan determinant protein p66Shc. The aim of this study was to selectively diminish p66Shc gene expression in bovine oocytes and embryos using post-transcriptional gene silencing by RNA-mediated interference to study the effects of p66Shc knockdown on in vitro fertilized bovine embryos.
resultsApproximately 12,000-24,000 short hairpin (sh)RNAi molecules specific for p66Shc were microinjected into bovine germinal vesicle stage oocytes or zygotes. Experiments were comprised of a control group undergoing IVF alone and two groups microinjected with and without p66Shc shRNAi molecules prior to IVF. The amount of p66Shc mRNA quantified by Real Time PCR was significantly (P < 0.001) lowered upon p66Shc shRNAi microinjection. This reduction was selective for p66Shc mRNA, as both histone H2a and p53 mRNA levels were not altered. The relative signal strength of p66Shc immuno-fluorescence revealed a significant reduction in the number of pixels for p66Shc shRNAi microinjected groups compared to controls (P < 0.05). A significant decrease (P < 0.001) in the incidence of arrested embryos upon p66Shc shRNAi microinjection was detected compared to IVF and microinjected controls along with significant reductions (P < 0.001) in both cleavage divisions and blastocyst development. No significant differences in p66Shc mRNA levels (P = 0.314) were observed among the three groups at the blastocyst stage.
conclusionThese results show that p66Shc is involved in the regulation of embryo development specifically in mediating early cleavage arrest and facilitating development to the blastocyst stage for in vitro produced bovine embryos.
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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.