Signaling pathways in insulin- and IGF-I mediated oocyte maturation in lower vertebrates.

IF 1.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Indian journal of biochemistry & biophysics Pub Date : 2014-12-01
Dilip Mukherjee, Suravi Majumder, Sujata Roy Moulick, Puja Pal, Buddhadeb Mallick, Arindam Chakraborty, Shreyasi Gupta
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Abstract

The endocrine control of oocyte maturation in fish and amphibians has proved to be a valuable model for investigating the rapid and non-genomic steroid actions at the cell surface. Considerable progress has made over the last decade in elucidating signaling pathways in steroid-induced oocyte maturation. In addition to steroids, various growth factors have also been reported to be involved in this process and progress being made to elucidate their mechanism of actions. Exposure of fully-grown oocytes to steroids or growth factors (insulin/IGFs) initiates various signaling cascade, leading to formation and activation of maturation-promoting factor (MPF), a key enzyme that catalyzes entry into M-phase of meiosis I and II. Whereas the function of MPF in promoting oocyte maturation is ubiquitous, there are differences in signaling pathways between steroids- and growth factors-induced oocyte maturation in amphibian and fish. Here, we have reviewed the recent advances on the signaling pathways in insulin- and IGF-I-induced oocyte maturation in these two groups of non-mammalian vertebrates. New findings demonstrating the involvement of PI3 kinase and MAP kinase in induction of oocyte maturation by insulin and IGF-I are presented.

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胰岛素和igf - 1介导的低等脊椎动物卵母细胞成熟的信号通路。
鱼类和两栖动物卵母细胞成熟的内分泌控制已被证明是研究细胞表面快速和非基因组类固醇作用的有价值的模型。在过去的十年中,在阐明激素诱导卵母细胞成熟的信号通路方面取得了相当大的进展。除类固醇外,各种生长因子也被报道参与了这一过程,并在阐明其作用机制方面取得了进展。完全发育的卵母细胞暴露于类固醇或生长因子(胰岛素/IGFs)会启动各种信号级联,导致成熟促进因子(MPF)的形成和激活,MPF是催化减数分裂I和II进入m期的关键酶。虽然MPF在促进卵母细胞成熟中的作用是普遍存在的,但在两栖动物和鱼类中,类固醇和生长因子诱导的卵母细胞成熟的信号通路存在差异。本文综述了胰岛素和igf -i诱导两组非哺乳动物卵母细胞成熟信号通路的最新进展。新发现表明PI3激酶和MAP激酶参与胰岛素和IGF-I诱导卵母细胞成熟。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Indian journal of biochemistry & biophysics
Indian journal of biochemistry & biophysics 生物-生化与分子生物学
CiteScore
2.90
自引率
50.00%
发文量
88
审稿时长
3 months
期刊介绍: Started in 1964, this journal publishes original research articles in the following areas: structure-function relationships of biomolecules; biomolecular recognition, protein-protein and protein-DNA interactions; gene-cloning, genetic engineering, genome analysis, gene targeting, gene expression, vectors, gene therapy; drug targeting, drug design; molecular basis of genetic diseases; conformational studies, computer simulation, novel DNA structures and their biological implications, protein folding; enzymes structure, catalytic mechanisms, regulation; membrane biochemistry, transport, ion channels, signal transduction, cell-cell communication, glycobiology; receptors, antigen-antibody binding, neurochemistry, ageing, apoptosis, cell cycle control; hormones, growth factors; oncogenes, host-virus interactions, viral assembly and structure; intermediary metabolism, molecular basis of disease processes, vitamins, coenzymes, carrier proteins, toxicology; plant and microbial biochemistry; surface forces, micelles and microemulsions, colloids, electrical phenomena, etc. in biological systems. Solicited peer reviewed articles on contemporary Themes and Methods in Biochemistry and Biophysics form an important feature of IJBB. Review articles on a current topic in the above fields are also considered. They must dwell more on research work done during the last couple of years in the field and authors should integrate their own work with that of others with acumen and authenticity, mere compilation of references by a third party is discouraged. While IJBB strongly promotes innovative novel research works for publication as full length papers, it also considers research data emanating from limited objectives, and extension of ongoing experimental works as ‘Notes’. IJBB follows “Double Blind Review process” where author names, affiliations and other correspondence details are removed to ensure fare evaluation. At the same time, reviewer names are not disclosed to authors.
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