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AuthorMannes, Marcodc.contributor.author
AuthorDopler, Arthurdc.contributor.author
AuthorHuber-Lang, Markusdc.contributor.author
AuthorSchmidt, Christoph Q.dc.contributor.author
Date of accession2021-05-06T07:20:14Zdc.date.accessioned
Available in OPARU since2021-05-06T07:20:14Zdc.date.available
Date of first publication2020-10-15dc.date.issued
AbstractThe alternative pathway regulator Factor H-like protein 1 (FHL-1) is composed of the first 7 N-terminal complement control protein domains of Factor H (FH) and protects host surfaces from uncontrolled complement attack. Although FHL-1 shares the N-terminal regulatory domains with FH, it was thought to be a weaker regulator. Recently, the regulatory activity of FHL-1 was shown to be comparable to FH. Nonetheless, the question remained whether FHL-1 is an indispensable, unique regulator. The discovery that FHL-1 is the predominant regulator on Bruch’s membrane, a critical site for the onset and progression of age-related-macular degeneration (AMD), showed that FHL-1 is essential for complement regulation. A common single nucleotide polymorphism in FH/FHL-1 that predisposes for AMD underlines the important role of FHL-1 in this context. Reports that some cancer tissues specifically upregulate FHL-1 expression, thereby evading immune surveillance, suggests a pronounced regulatory activity of the splice variant. Several microorganisms specifically recruit FHL-1 to evade complement attack. From a phylogenetic point of view, FHL-1 appears much later than other complement regulators, which could imply a specific role that is possibly not systemic but rather tissue specific. This review focuses on the current knowledge of FHL-1 and its physiological and pathophysiological roles.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseCC BY 4.0 Internationaldc.rights
Link to license texthttps://creativecommons.org/licenses/by/4.0/dc.rights.uri
KeywordFactor H-like protein 1dc.subject
Keywordcell protectiondc.subject
Keywordcomplement systemdc.subject
Keywordregulatory selectivitydc.subject
KeywordREGULATORS FACTOR-Hdc.subject
KeywordBRUCHS MEMBRANE IMPLICATIONSdc.subject
KeywordNONSELF DISCRIMINATIONdc.subject
KeywordTREPONEMA-DENTICOLAdc.subject
KeywordHEPARAN-SULFATEdc.subject
KeywordBINDINGdc.subject
KeywordDISEASEdc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
MeSHC-reactive proteindc.subject.mesh
MeSHCytoprotectiondc.subject.mesh
MeSHComplement factor Hdc.subject.mesh
MeSHBruch membranedc.subject.mesh
MeSHMacular degenerationdc.subject.mesh
MeSHHeparitin sulfatedc.subject.mesh
TitleTuning the Functionality by Splicing: Factor H and Its Alternative Splice Variant FHL-1 Share a Gene but Not All Functionsdc.title
Resource typeWissenschaftlicher Artikeldc.type
SWORD Date2020-12-09T19:34:19Zdc.date.updated
VersionpublishedVersiondc.description.version
DOIhttp://dx.doi.org/10.18725/OPARU-37049dc.identifier.doi
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-oparu-37111-0dc.identifier.urn
GNDFaktor Hdc.subject.gnd
GNDCytoprotektiondc.subject.gnd
GNDHeparansulfatdc.subject.gnd
InstitutionUKU. Institut für Naturheilkunde und Klinische Pharmakologieuulm.affiliationSpecific
InstitutionUKU. Institut für Klinische und Experimentelle Trauma-Immunologieuulm.affiliationSpecific
Peer reviewjauulm.peerReview
DCMI TypeCollectionuulm.typeDCMI
CategoryPublikationenuulm.category
DOI of original publication10.3389/fimmu.2020.596415dc.relation1.doi
Source - Title of sourceFrontiers in Immunologysource.title
Source - Place of publicationFrontiers Mediasource.publisher
Source - Volume11source.volume
Source - Year2020source.year
Source - Article number596415source.articleNumber
Source - ISSN1664-3224source.identifier.issn
Source - eISSN1664-3224source.identifier.eissn
FundingDFG [SCHM3018/2-2]uulm.funding
CommunityUniversitätsklinikum Ulmuulm.community
Bibliographyuulmuulm.bibliographie


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