Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/89568
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dc.contributorDepartment of Applied Biology and Chemical Technologyen_US
dc.creatorZhang, SJen_US
dc.creatorLi, XXen_US
dc.creatorYu, Yen_US
dc.creatorChiu, APen_US
dc.creatorLo, LHen_US
dc.creatorTo, JCen_US
dc.creatorRowlands, DKen_US
dc.creatorKeng, VWen_US
dc.date.accessioned2021-04-12T02:37:11Z-
dc.date.available2021-04-12T02:37:11Z-
dc.identifier.issn0006-291Xen_US
dc.identifier.urihttp://hdl.handle.net/10397/89568-
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.rights© 2019 Elsevier Inc. All rights reserved.en_US
dc.rights© 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/.en_US
dc.rightsThe following publication Zhang, S.-J., Li, X.-X., Yu, Y., Chiu, A. P., Lo, L. H., To, J. C., . . . Keng, V. W. (2019). Schwann cell-specific PTEN and EGFR dysfunctions affect neuromuscular junction development by impairing Agrin signaling and autophagy. Biochemical and Biophysical Research Communications, 515(1), 50-56 is available at https://dx.doi.org/10.1016/j.bbrc.2019.05.014en_US
dc.subjectNeuromuscular junctionen_US
dc.subjectSchwann cellsen_US
dc.subjectPtenen_US
dc.subjectEGFRen_US
dc.titleSchwann cell-specific PTEN and EGFR dysfunctions affect neuromuscular junction development by impairing Agrin signalingand autophagyen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage50en_US
dc.identifier.epage56en_US
dc.identifier.volume515en_US
dc.identifier.issue1en_US
dc.identifier.doi10.1016/j.bbrc.2019.05.014en_US
dcterms.abstractThe neuromuscular junction (NMJ) is formed by motor nerve terminals, post-junctional muscle membranes, and terminal Schwann cells (SCs). The formation of NMJ requires complex and dynamic molecular interactions. Nerve- and muscle-derived molecules have been well characterized but the mechanistic involvement of SC in NMJ development remains poorly understood. SC-specific phosphatase and tensin homolog (Pten) inactivation and epidermal growth factor receptor (EGFR) overexpression (Dhh-Cre; Cnp-EGFR; Ptenflox/flox or DET) mice were used and NMJ malformation was observed in these mice. Acetylcholine receptors (AChRs) were distorted and varicose presynaptic nerve terminals appeared in the tibialis anterior (TA) muscle of DET mice. Agrin signaling related to NMJ development, was downregulated in TA muscle. Both RAS/MEK/ERK and PI3K/AKT/mTOR signaling pathways were activated in the sciatic nerves of DET mice. In addition, autophagy was downregulated in these sciatic nerves. Interestingly, the use of Torin 2, an mTOR inhibitor, rescued the phenotype. The downregulated-autophagy might account for Agrin signaling abnormity, which induced NMJ malformation. Taken together, our results indicate that SCs-specific Pten and EGFR cooperation are essential for NMJ development.en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationBiochemical and biophysical research communications, 12 Jul 2019, v. 515, no. 1, p. 50-56en_US
dcterms.isPartOfBiochemical and biophysical research communicationsen_US
dcterms.issued2019-07-12-
dc.identifier.isiWOS:000471737500008-
dc.identifier.pmid31122699-
dc.identifier.eissn1090-2104en_US
dc.description.validate202104 bcrcen_US
dc.description.oaAccepted Manuscripten_US
dc.identifier.FolderNumbera0613-n03-
dc.identifier.SubFormID594-
dc.description.fundingSourceRGCen_US
dc.description.fundingTextC5012-15Een_US
dc.description.pubStatusPublisheden_US
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