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dc.contributor.authorJeremy, KP
dc.contributor.authorPlummer, ZE
dc.contributor.authorHead, DJ
dc.contributor.authorMadgett, TE
dc.contributor.authorSanders, KL
dc.contributor.authorWallington, A
dc.contributor.authorStorry, JR
dc.contributor.authorGilsanz, F
dc.contributor.authorDelaunay, J
dc.contributor.authorAvent, Neil
dc.date.accessioned2015-02-27T13:09:25Z
dc.date.available2015-02-27T13:09:25Z
dc.date.issued2009-10-01
dc.identifier.issn0390-6078
dc.identifier.issn1592-8721
dc.identifier.urihttp://hdl.handle.net/10026.1/3271
dc.description.abstract

BACKGROUND: Protein 4.1R is an important component of the red cell membrane skeleton. It imparts structural integrity and has transmembrane signaling roles by direct interactions with transmembrane proteins and other membrane skeletal components, notably p55 and calmodulin. DESIGN AND METHODS: Spontaneous and ligation-induced phosphatidylserine exposure on erythrocytes from two patients with 4.1R deficiency were studied, using CD47 glycoprotein and glycophorin C as ligands. We also looked for protein abnormalities in the 4.1R-based multiprotein complex. RESULTS: Phosphatidylserine exposure was significantly increased in 4.1R-deficient erythrocytes obtained from the two different individuals when ligands to CD47 glycoprotein were bound. Spontaneous phosphatidylserine exposure was normal. 4.1R, glycophorin C and p55 were missing or sharply reduced. Furthermore there was an alteration or deficiency of CD47 glycoprotein and a lack of CD44 glycoprotein. Based on a recent study in 4.1R-deficient mice, we found that there are clear functional differences between interactions of human red cell 4.1R and its murine counterpart. CONCLUSIONS: Glycophorin C is known to bind 4.1R, and we have defined previously that it also binds CD47. From our evidence, we suggest that 4.1R plays a role in the phosphatidylserine exposure signaling pathway that is of fundamental importance in red cell turnover. The linkage of CD44 to 4.1R may be relevant to this process.

dc.format.extent1354-1361
dc.format.mediumPrint
dc.languageen
dc.language.isoeng
dc.publisherFerrata Storti Foundation (Haematologica)
dc.subjectphosphatidylserine
dc.subject4.1R deficiency
dc.subjectCD44
dc.subjectCD47
dc.subjectglycophorin C
dc.title4.1R-deficient human red blood cells have altered phosphatidylserine exposure pathways and are deficient in CD44 and CD47 glycoproteins
dc.typejournal-article
dc.typeCase Reports
dc.typeComparative Study
dc.typeJournal Article
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000271092500006&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.issue10
plymouth.volume94
plymouth.publication-statusPublished
plymouth.journalHaematologica
dc.identifier.doi10.3324/haematol.2009.006585
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/School of Biomedical Sciences
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Research Groups/Plymouth Institute of Health and Care Research (PIHR)
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
dc.publisher.placeItaly
dc.identifier.eissn1592-8721
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.3324/haematol.2009.006585
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review


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