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Bim--Bcl-2 Homology 2 Mimetic Therapy in Effective at Suppressing Inflammatory Arthritis Through the Activation of Myeloid Cell Apoptosis

dc.contributor.authorScatizzi, John C.
dc.contributor.authorHutcheson, Jack
dc.contributor.authorPope, Richard M.
dc.contributor.authorFirestein, Gary S.
dc.contributor.authorKoch, Alisa E.
dc.contributor.authorMavers, Melissa
dc.contributor.authorSmason, Avraham
dc.contributor.authorAgrawal, Hemant
dc.contributor.authorHaines, G. Kenneth III
dc.contributor.authorChandel, Navdeep S.
dc.contributor.authorHotchkiss, Richard S.
dc.contributor.authorPerlman, Harris
dc.date.accessioned2010-02-19T14:28:10Z
dc.date.available2010-02-19T14:28:10Z
dc.date.issued2010-02
dc.identifier.citationScatizzi, John C.; Hutcheson, Jack; Pope, Richard M.; Firestein, Gary S.; Koch, Alisa E.; Mavers, Melissa; Smason, Avraham; Agrawal, Hemant; Haines, G. Kenneth; Chandel, Navdeep S.; Hotchkiss, Richard S.; Perlman, Harris (2010). "Bim–Bcl-2 homology 3 mimetic therapy is effective at suppressing inflammatory arthritis through the activation of myeloid cell apoptosis." Arthritis & Rheumatism 62(2): 441-451. <http://hdl.handle.net/2027.42/65034>en_US
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=20112357&dopt=citationen_US
dc.description.abstractObjective: Rheumatoid arthritis (RA) is a destructive autoimmune disease characterized by an increased inflammation in the joint. Therapies that activate the apoptotic cascade may have potential for use in RA; however, few therapeutic agents fit this category. The purpose of this study was to examine the potential of Bim, an agent that mimics the action of Bcl-2 homology 3 (BH3) domain-only proteins that have shown success in preclinical studies of cancer in the treatment of autoimmune disease...en_US
dc.format.extent610615 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen_US
dc.publisherAmerican College of Rheumatologyen_US
dc.titleBim--Bcl-2 Homology 2 Mimetic Therapy in Effective at Suppressing Inflammatory Arthritis Through the Activation of Myeloid Cell Apoptosisen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialties
dc.subject.hlbtoplevelHealth Sciences
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan Medical School, Ann Arbor, Michiganen_US
dc.contributor.affiliationumVA Medical Service, Deparment of Veterans Affairsen_US
dc.contributor.affiliationotherSt. Louis University School of Medicine, St. Louis, Missourien_US
dc.contributor.affiliationotherNorthwestern University, Feinbergy School of Medicine, Chicago, Illinoisen_US
dc.contributor.affiliationotherUniversity of California, San Diego School of Medicine, La Jolla, Californiaen_US
dc.contributor.affiliationotherYale University School of Medicine, New Haven, Connecticuten_US
dc.contributor.affiliationotherWashington University School of Medicine, St. Louis, Missourien_US
dc.contributor.affiliationumcampusAnn Arboren_US
dc.identifier.pmid20112357en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/65006/1/Scatizzi - Arthritis Rheum vol. 62 pg. 441-451.pdf
dc.identifier.doi10.1002/art.27198
dc.identifier.sourceArthritis & Rheumatismen_US
dc.owningcollnameRheumatology, Division of


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