Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Pierrette Andre"'
Autor:
Michelle E. Page, Li Bao, Pierrette Andre, Joshua Pelta-Heller, Emily Sluzas, Pedro Gonzalez-Alegre, Alexey Bogush, Loren E. Khan, Lorraine Iacovitti, Margaret E. Rice, Michelle E. Ehrlich
Publikováno v:
Neurobiology of Disease, Vol 39, Iss 3, Pp 318-326 (2010)
Early onset torsion dystonia is an autosomal dominant movement disorder of variable penetrance caused by a glutamic acid, i.e. ΔE, deletion in DYT1, encoding the protein TorsinA. Genetic and structural data implicate basal ganglia dysfunction in dys
Externí odkaz:
https://doaj.org/article/4816615fc72d4c10bd0cda7356777982
Publikováno v:
Platelets. 27(5)
Platelet outside-in signaling regulates important morphological changes such as cell spreading and retraction. A role for FcγRIIa in outside-in signaling has been recently described. Using murine platelets expressing human transgenic FcγRIIa we exp
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::167da8993227b646baadf7890921ae45
https://pubmed.ncbi.nlm.nih.gov/26809427
https://pubmed.ncbi.nlm.nih.gov/26809427
Autor:
Joshua Pelta-Heller, Pedro Gonzalez-Alegre, Loren E. Khan, Alexey Bogush, Li Bao, Lorraine Iacovitti, Pierrette Andre, Michelle E. Ehrlich, Emily Sluzas, Margaret E. Rice, Michelle E. Page
Publikováno v:
Neurobiology of Disease, Vol 39, Iss 3, Pp 318-326 (2010)
Early onset torsion dystonia is an autosomal dominant movement disorder of variable penetrance caused by a glutamic acid, i.e. ΔE, deletion in DYT1 , encoding the protein TorsinA. Genetic and structural data implicate basal ganglia dysfunction in dy
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4ea2bf52b7d9683ef8ffc62ee4712ab1
http://www.sciencedirect.com/science/article/pii/S0969996110001324
http://www.sciencedirect.com/science/article/pii/S0969996110001324
Autor:
Shaji Abraham, Yuhang Zhou, Alexander Y. Tsygankov, Satya P. Kunapuli, Leonard C. Edelstein, Steven E. McKenzie, Paul F. Bray, Carol Dangelmaier, Chad A. Shaw, Pierrette Andre
Publikováno v:
Blood. 126(26)
Fc receptor for IgG IIA (FcγRIIA)-mediated platelet activation is essential in heparin-induced thrombocytopenia (HIT) and other immune-mediated thrombocytopenia and thrombosis disorders. There is considerable interindividual variation in platelet Fc
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::49912d9a2f88929cf1224b636e5107e1
https://pubmed.ncbi.nlm.nih.gov/26705343
https://pubmed.ncbi.nlm.nih.gov/26705343
Autor:
Pierrette Andre, Moritz Stolla, Wolfgang Bergmeier, Steven E. McKenzie, Michael P. Reilly, Lucia Stefanini, Timothy Daniel Ouellette
Platelet activation via Fcγ receptor IIA (FcγRIIA) is a critical event in immune-mediated thrombocytopenia and thrombosis syndromes (ITT). We recently identified signaling by the guanine nucleotide exchange factor CalDAG-GEFI and the adenosine diph
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::01284e41f292e7e65901718b2d922cab
https://europepmc.org/articles/PMC3148161/
https://europepmc.org/articles/PMC3148161/
Autor:
Pierrette Andre, Wolfgang Bergmeier, Nisha Nanda, Francis DeGuzman, Uma Sinha, Anjali Pandey, Scott M. Taylor, Moritz Stolla, Yvonne Pak, Steven E. McKenzie, Michael P. Reilly
Publikováno v:
Blood. 117(7)
Heparin-induced thrombocytopenia (HIT) is a major cause of morbidity and mortality resulting from the associated thrombosis. Extensive studies using our transgenic mouse model of HIT have shown that antibodies reactive with heparin-platelet factor 4
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a2aee89e21dad0ba6979e4001cb37fb2
https://pubmed.ncbi.nlm.nih.gov/21330480
https://pubmed.ncbi.nlm.nih.gov/21330480
Autor:
Steven E. McKenzie, Michael P. Reilly, Andrew R. Crow, Pierrette Andre, Shuhua Ma, Sara J. Suppa, Seng Song, Alan H. Lazarus
Publikováno v:
Blood. 117(3)
To explore the potential for monoclonal antibodies as a treatment for immune thrombocytopenia (ITP) and to further explore their mechanisms of action, we tested 8 monoclonal CD44 antibodies in murine ITP and found 4 antibodies that could successfully
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::147fe21496be9061afaf9b6f4a93f983
https://pubmed.ncbi.nlm.nih.gov/21045192
https://pubmed.ncbi.nlm.nih.gov/21045192
Autor:
Satya P. Kunapuli, Yuhang Zhou, Shaji Abraham, Steven E. McKenzie, Leonard C. Edelstein, Chad A. Shaw, Pierrette Andre, Paul F. Bray, Alexander Y. Tsygankov
Publikováno v:
Blood. 124:337-337
FcγRIIA-mediated platelet activation is important in the pathogenesis of heparin-induced thrombocytopenia (HIT) and other immune-mediated thrombocytopenia and thrombosis disorders. FcgRIIa is also the major transmembrane signaling adapter for the hu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::ec2c26d450bf7584c2dfa74e47891b45
https://doi.org/10.1182/blood.v124.21.337.337
https://doi.org/10.1182/blood.v124.21.337.337
Autor:
Chad A. Shaw, Shaji Abraham, Alexander Y. Tsygankov, Steven E. McKenzie, Carol T Dangelmaier, Paul F. Bray, Pierrette Andre, Leonard C. Edelstein, Satya P. Kunapuli, Xianguo Kong
Publikováno v:
Blood. 124:2761-2761
Platelet FcγRIIA is central to the pathophysiology of immune-mediated thrombocytopenia and thrombosis syndromes, such as heparin-induced thrombocytopenia (HIT). FcγRIIA is also the major transmembrane signaling adapter for αIIbβ3 outside-in signa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7c65495ec8ceeb9b9c4ac25d113aaf1f
https://doi.org/10.1182/blood.v124.21.2761.2761
https://doi.org/10.1182/blood.v124.21.2761.2761
Publikováno v:
Blood. 122:3514-3514
Platelet FcγRIIa is an important component of heparin-induced thrombocytopenia and other immune-mediated thrombocytopenia and thrombosis syndromes. Platelet FcγRIIa, an ITAM receptor, signals not only to cause aggregation and secretion, but also to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::0ca7d3535a59fdbcd10a31c042acaeab
https://doi.org/10.1182/blood.v122.21.3514.3514
https://doi.org/10.1182/blood.v122.21.3514.3514