Zobrazeno 1 - 10
of 24
pro vyhledávání: '"Michael G, Strainic"'
Autor:
Feng-Qi An, Guangjin Zhou, Micah T. Harland, Wasim Hussain, Michael G. Strainic, Mukesh K. Jain, M. Edward Medof
Publikováno v:
Frontiers in Immunology, Vol 14 (2024)
The transcription factor Kruppel-like factor 4 (KLF4) regulates the expression of immunosuppressive and anti-thrombotic proteins. Despite its importance in maintaining homeostasis, the signals that control its expression and the mechanism of its tran
Externí odkaz:
https://doaj.org/article/2f5772b6e50c4188b8b5cb0536d94249
Autor:
Devin Cao, Michael G. Strainic, Daniel Counihan, Shiva Sridar, Fengqi An, Wasim Hussain, Alvin H. Schmaier, Marvin Nieman, M. Edward Medof
Publikováno v:
Am J Pathol
As per the classical view of the coagulation system, it functions solely in plasma to maintain hemostasis. An experimental approach modeling vascular reconstitution was used to show that vascular endothelial cells (ECs) endogenously synthesize coagul
Autor:
Diane S. Lidke, M. Edward Medof, Christopher C. Valley, Ajay Sammeta, Elliot Pohlmann, Wasim Hussain, Michael G. Strainic
Publikováno v:
FASEB J
How receptor tyrosine kinase (RTK) growth signaling is controlled physiologically is incompletely understood. We have previously provided evidence that the survival and mitotic activities of vascular endothelial cell growth factor receptor-2 (VEGFR2)
Publikováno v:
J Immunol
The involvement of complement in B2 cell responses has been regarded as occurring strictly via complement components in plasma. In this study, we show that Ab production and class switch recombination (CSR) depend on autocrine C3a and C5a receptor (C
Autor:
Andrew Esposito, Fengqi An, M. Edward Medof, Jinbo Liu, Peter S. Heeger, Jörg Hamann, Erin Bailey, Michael G. Strainic
Publikováno v:
American journal of pathology, 189(7), 1386-1401. Elsevier Inc.
Recent studies traced inflammatory bowel disease in some patients to deficiency of CD55 [decay-accelerating factor (DAF)], but the mechanism underlying the linkage remained unclear. Herein, we studied the importance of DAF in enabling processes that
Autor:
Jinbo Liu, Peter S. Heeger, Michael G. Strainic, Weijia Zhang, M. Edward Medof, Zhengzi Yi, Joong Hyuk Sheen
Publikováno v:
The Journal of Immunology. 199:278-291
Induction of proinflammatory T cell immunity is augmented by innate dendritic cell (DC) maturation commonly initiated by TLR signaling. We demonstrate that ligation of TLR3, TLR4, and TLR9 induces murine DC production of complement components and loc
Autor:
Michael G, Strainic, Jinbo, Liu, Fengqi, An, Erin, Bailey, Andrew, Esposito, Jörg, Hamann, Peter S, Heeger, M Edward, Medof
Publikováno v:
Am J Pathol
Recent studies traced inflammatory bowel disease in some patients to deficiency of CD55 [decay-accelerating factor (DAF)], but the mechanism underlying the linkage remained unclear. Herein, we studied the importance of DAF in enabling processes that
Autor:
Diana L. Ramirez-Bergeron, Edward F. Plow, Elzbieta Pluskota, M. Edward Medof, Michael G. Strainic, Ming-Shih Hwang, Hae-Suk Kim, Elliot Pohlmann
Publikováno v:
Journal of cell science. 132(6)
Purified vascular endothelial cell (EC) growth factor receptor-2 (VEGFR2) auto-phosphorylates upon VEGF-A occupation in vitro, arguing that VEGR2 confers its mitotic and viability signaling in and of itself. Herein, we show that, in ECs, VEGFR2 funct
Autor:
Sanjoy Roychowdhury, Megan R. McMullen, M. Edward Medof, Laura E. Nagy, Michael G. Strainic, Dola Das, Rebecca L. McCullough
Background Complement is implicated in the development of alcoholic liver disease. C3 and C5 contribute to ethanol-induced liver injury; however, the role of C5a receptor (C5aR) on myeloid and non-myeloid cells to progression of injury is not known.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6b7a9aa129c4aa7ba3d4021d2ffb1bab
https://europepmc.org/articles/PMC4939119/
https://europepmc.org/articles/PMC4939119/
Publikováno v:
Nature immunology
Signaling through the G protein-coupled receptors for the complement fragments C3a and C5a (C3aR and C5aR, respectively) by dendritic cells and CD4(+) cells provides costimulatory and survival signals to effector T cells. Here we found that when sign