Publication:
Transmembrane tumor necrosis factor is a potent inducer of colitis even in the absence of its secreted form

cris.virtual.author-orcid0000-0002-3921-8678
cris.virtualsource.author-orcidf56acaf0-7c60-4d5b-a449-577102f3ee3a
cris.virtualsource.author-orcidd81010df-1b8d-4998-805a-b8f9a8c4ff7e
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dc.contributor.authorCorazza, Nadia
dc.contributor.authorBrunner, Thomas
dc.contributor.authorBuri, Caroline
dc.contributor.authorRihs, Silvia
dc.contributor.authorImboden, Martin A
dc.contributor.authorSeibold, Inge
dc.contributor.authorMüller, Christoph
dc.date.accessioned2024-10-14T10:16:37Z
dc.date.available2024-10-14T10:16:37Z
dc.date.issued2004
dc.description.abstractTumor necrosis factor (TNF) is cleaved proteolytically from a 26-kilodalton transmembrane precursor protein into secreted 17-kilodalton monomers. Transmembrane (tm) and secreted trimeric TNF are biologically active and may mediate distinct activities. We assessed the consequences of a complete inhibition of TNF processing on the course of colitis in recombination activating gene (RAG)2 -/- mice on transfer of CD4 CD45RB hi T cells.
dc.description.numberOfPages10
dc.description.sponsorshipUniversitätspoliklinik für Endokrinologie, Diabetologie und Klinische Ernährung
dc.description.sponsorshipInstitut für Pathologie
dc.identifier.isi000223834500018
dc.identifier.pmid15362037
dc.identifier.publisherDOI10.1053/j.gastro.2004.06.036
dc.identifier.urihttps://boris-portal.unibe.ch/handle/20.500.12422/110437
dc.language.isoen
dc.publisherElsevier
dc.publisher.placePhiladelphia, Pa.
dc.relation.ispartofGastroenterology
dc.relation.issn0016-5085
dc.relation.organizationDCD5A442BF89E17DE0405C82790C4DE2
dc.relation.organizationDCD5A442C012E17DE0405C82790C4DE2
dc.subject.ddc500 - Science::570 - Life sciences; biology
dc.subject.ddc600 - Technology::610 - Medicine & health
dc.titleTransmembrane tumor necrosis factor is a potent inducer of colitis even in the absence of its secreted form
dc.typearticle
dspace.entity.typePublication
oaire.citation.endPage25
oaire.citation.issue3
oaire.citation.startPage816
oaire.citation.volume127
oairecerif.author.affiliationUniversitätspoliklinik für Endokrinologie, Diabetologie und Klinische Ernährung
oairecerif.author.affiliationInstitut für Pathologie
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unibe.description.ispublishedpub
unibe.eprints.legacyId37213
unibe.journal.abbrevTitleGASTROENTEROLOGY
unibe.refereedtrue
unibe.subtype.articlejournal

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