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dc.contributor.authorChen, Yang
dc.contributor.authorHuang, Lili
dc.contributor.authorQi, Xinzhou
dc.contributor.authorChen, Chen
dc.date.accessioned2019-11-11T07:10:17Z
dc.date.available2019-11-11T07:10:17Z
dc.date.issued2019
dc.identifier.issn1661-6596
dc.identifier.doi10.3390/ijms20205007
dc.identifier.urihttp://hdl.handle.net/10072/389046
dc.description.abstractInsulin receptor (INSR) has been extensively studied in the area of cell proliferation and energy metabolism. Impaired INSR activities lead to insulin resistance, the key factor in the pathology of metabolic disorders including type 2 diabetes mellitus (T2DM). The mainstream opinion is that insulin resistance begins at a post-receptor level. The role of INSR activities and trafficking in insulin resistance pathogenesis has been largely ignored. Ligand-activated INSR is internalized and trafficked to early endosome (EE), where INSR is dephosphorylated and sorted. INSR can be subsequently conducted to lysosome for degradation or recycled back to the plasma membrane. The metabolic fate of INSR in cellular events implies the profound influence of INSR on insulin signaling pathways. Disruption of INSR-coupled activities has been identified in a wide range of insulin resistance-related diseases such as T2DM. Accumulating evidence suggests that alterations in INSR trafficking may lead to severe insulin resistance. However, there is very little understanding of how altered INSR activities undermine complex signaling pathways to the development of insulin resistance and T2DM. Here, we focus this review on summarizing previous findings on the molecular pathways of INSR trafficking in normal and diseased states. Through this review, we provide insights into the mechanistic role of INSR intracellular processes and activities in the development of insulin resistance and diabetes.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherMDPI AG
dc.publisher.placeSwitzerland
dc.relation.ispartofpagefrom5007: 1
dc.relation.ispartofpageto5007: 16
dc.relation.ispartofissue20
dc.relation.ispartofjournalInternational Journal of Molecular Sciences
dc.relation.ispartofvolume20
dc.subject.fieldofresearchEndocrinology
dc.subject.fieldofresearchOther Chemical Sciences
dc.subject.fieldofresearchGenetics
dc.subject.fieldofresearchOther Biological Sciences
dc.subject.fieldofresearchcode110306
dc.subject.fieldofresearchcode0399
dc.subject.fieldofresearchcode0604
dc.subject.fieldofresearchcode0699
dc.subject.keywordsinsulin resistance
dc.subject.keywordsendocytosis
dc.subject.keywordsinsulin receptor
dc.titleInsulin Receptor Trafficking: Consequences for Insulin Sensitivity and Diabetes.
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationChen, Y; Huang, L; Qi, X; Chen, C, Insulin Receptor Trafficking: Consequences for Insulin Sensitivity and Diabetes., International Journal of Molecular Sciences, 2019, 20 (20), pp. 5007: 1-5007: 16
dcterms.dateAccepted2019-10-08
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/
dc.date.updated2019-11-08T00:40:54Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
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gro.griffith.authorChen, Chen


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