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果蝇中的躯干通路:研究受体酪氨酸激酶信号转导的模型系统。

The torso pathway in Drosophila: a model system to study receptor tyrosine kinase signal transduction.

作者信息

Lu X, Perkins L A, Perrimon N

机构信息

Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, MA 02115.

出版信息

Dev Suppl. 1993:47-56.

PMID:8049487
Abstract

In the Drosophila embryo, specification of terminal cell fates that result in the formation of both the head (acron) and tail (telson) regions is under the control of the torso (tor) receptor tyrosine kinase. The current knowledge suggests that activation of tor at the egg pole initiates a signal transduction pathway that is mediated sequentially by the guanine nucleotide releasing factor son of sevenless (Sos), the p21Ras1 GTPase, the serine/threonine kinase D-raf and the tyrosine/threonine kinase MAPKK (Dsor1). Subsequently, it is postulated that activation, possibly by phosphorylation, of a transcription factor at the egg poles activates the transcription of the terminal gap genes tailless and huckebein. These gap genes, which encode putative transcription factors, then control the expression of more downstream factors that ultimately result in head and tail differentiation. Also involved in tor signaling is the non-receptor protein tyrosine phosphatase corkscrew (csw). Here, we review the current model and discuss future research directions in this field.

摘要

在果蝇胚胎中,导致头部(顶节)和尾部(尾节)区域形成的末端细胞命运的特化受躯干(tor)受体酪氨酸激酶的控制。目前的知识表明,卵极处tor的激活启动了一条信号转导途径,该途径依次由鸟嘌呤核苷酸释放因子七less之子(Sos)、p21Ras1 GTP酶、丝氨酸/苏氨酸激酶D-raf和酪氨酸/苏氨酸激酶MAPKK(Dsor1)介导。随后,据推测,卵极处一种转录因子的激活(可能通过磷酸化)激活了末端间隙基因无尾和驼背的转录。这些间隙基因编码假定的转录因子,然后控制更多下游因子的表达,最终导致头部和尾部的分化。非受体蛋白酪氨酸磷酸酶螺旋(csw)也参与tor信号传导。在这里,我们综述了当前的模型并讨论了该领域未来的研究方向。

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