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dc.contributor.authorChen, Kuang Qi-
dc.contributor.authorWei, Bang Hong-
dc.contributor.authorHao, Shuang Li-
dc.contributor.authorYang, Wan Xi-
dc.date.accessioned2023-02-23T11:42:20Z-
dc.date.available2023-02-23T11:42:20Z-
dc.date.issued2022-
dc.identifier.citationHistology and Histopathology Vol. 37, nº7 (2022)es
dc.identifier.issn0213-3911-
dc.identifier.issn1699-5848-
dc.identifier.urihttp://hdl.handle.net/10201/128692-
dc.description.abstractThe PI3K/AKT signaling pathway is one of the most crucial regulatory mechanisms in animal cells, which can mainly regulate proliferation, survival and anti-apoptosis in cell lines. In the seminiferous epithelium, most studies were concentrated on the role of PI3K/AKT signaling in immature Sertoli cells (SCs) and spermatogonia stem cells (SSCs). PI3K/AKT signaling can facilitate the proliferation and antiapoptosis of immature Sertoli cells and spermatogenic cells. Besides, in mature Sertoli cells, this pathway can disintegrate the structure of the blood-testis barrier (BTB) via regulatory protein synthesis and the cytoskeleton of Sertoli cells. All of these effects can directly and indirectly maintain and promote spermatogenesis in male testis.es
dc.formatapplication/pdfes
dc.format.extent16es
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectPI3K/AKT signalinges
dc.subjectSertoli celles
dc.subjectSpermatogonia stem celles
dc.subjectBlood testis barrieres
dc.subjectSpermatogenesises
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleThe PI3K/AKT signaling pathway: How does it regulate development of Sertoli cells and spermatogenic cells?es
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doihttps://doi.org/10.14670/HH-18-457-
Aparece en las colecciones:Vol.37, nº7 (2022)

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