BROWSE

Related Scientist

cnir's photo.

cnir
뇌과학이미징연구단
more info

ITEM VIEW & DOWNLOAD

dNP2 is a blood-brain barrier-permeable peptide enabling ctCTLA-4 protein delivery to ameliorate experimental autoimmune encephalomyelitis

DC Field Value Language
dc.contributor.authorLim, S.-
dc.contributor.authorKim, W.-J.-
dc.contributor.authorKim, Y.-H.-
dc.contributor.authorSohee Lee-
dc.contributor.authorKoo, J.-H.-
dc.contributor.authorLee, J.-A.-
dc.contributor.authorYoon, H.-
dc.contributor.authorKim, D.-H.-
dc.contributor.authorPark, H.-J.-
dc.contributor.authorKim, H.-M.-
dc.contributor.authorLee, H.-G.-
dc.contributor.authorYun Kim, J.-
dc.contributor.authorLee, J.-U.-
dc.contributor.authorHun Shin, J.-
dc.contributor.authorKyun Kim, L.-
dc.contributor.authorDoh, J.-
dc.contributor.authorHongtae Kim-
dc.contributor.authorLee, S.-K.-
dc.contributor.authorBothwell, A.L.M.-
dc.contributor.authorMinah Suh-
dc.contributor.authorJe-Min Choi-
dc.date.available2016-01-07T09:11:12Z-
dc.date.created2015-10-06ko
dc.date.issued2015-09-
dc.identifier.issn2041-1723-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/1901-
dc.description.abstractCentral nervous system (CNS)-infiltrating effector T cells play critical roles in the development and progression of multiple sclerosis (MS). However, current drugs for MS are very limited due to the difficulty of delivering drugs into the CNS. Here we identify a cell-permeable peptide, dNP2, which efficiently delivers proteins into mouse and human T cells, as well as various tissues. Moreover, it enters the brain tissue and resident cells through blood vessels by penetrating the tightly organized blood-brain barrier. The dNP2-conjugated cytoplasmic domain of cytotoxic T-lymphocyte antigen 4 (dNP2-ctCTLA-4) negatively regulates activated T cells and shows inhibitory effects on experimental autoimmune encephalomyelitis in both preventive and therapeutic mouse models, resulting in the reduction of demyelination and CNS-infiltrating T helper 1 and T helper 17 cells. Thus, this study demonstrates that dNP2 is a blood-brain barrier-permeable peptide and dNP2-ctCTLA-4 could be an effective agent for treating CNS inflammatory diseases such as MS. © 2015 Macmillan Publishers Limited. All rights reserved-
dc.description.uri1-
dc.language영어-
dc.publisherNATURE PUBLISHING GROUP-
dc.titledNP2 is a blood-brain barrier-permeable peptide enabling ctCTLA-4 protein delivery to ameliorate experimental autoimmune encephalomyelitis-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000363017500015-
dc.identifier.scopusid2-s2.0-84941758039-
dc.identifier.rimsid21290ko
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorSohee Lee-
dc.contributor.affiliatedAuthorHongtae Kim-
dc.contributor.affiliatedAuthorMinah Suh-
dc.contributor.affiliatedAuthorJe-Min Choi-
dc.identifier.doi10.1038/ncomms9244-
dc.identifier.bibliographicCitationNATURE COMMUNICATIONS, v.6, pp.8244-
dc.citation.titleNATURE COMMUNICATIONS-
dc.citation.volume6-
dc.citation.startPage8244-
dc.date.scptcdate2018-10-01-
dc.description.wostc17-
dc.description.scptc27-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlusDISEASE-MODIFYING THERAPIES-
dc.subject.keywordPlusCELL-PENETRATING PEPTIDES-
dc.subject.keywordPlusVECTOR-MEDIATED STRATEGY-
dc.subject.keywordPlusMULTIPLE-SCLEROSIS-
dc.subject.keywordPlusTRANSDUCTION DOMAIN-
dc.subject.keywordPlusT-CELLS-
dc.subject.keywordPlusCYTOPLASMIC DOMAIN-
dc.subject.keywordPlusHEPARAN-SULFATE-
dc.subject.keywordPlusFUSION PROTEINS-
dc.subject.keywordPlusINNATE IMMUNITY-
Appears in Collections:
Center for Neuroscience Imaging Research (뇌과학 이미징 연구단) > 1. Journal Papers (저널논문)
Files in This Item:
13.dNP2 is a blood-brain barrier-permeable peptide enabling ctCTLA-4 protein.pdfDownload

qrcode

  • facebook

    twitter

  • Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.
해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse