M
M. Silva
Researcher at University of Texas Southwestern Medical Center
Publications - 12
Citations - 8697
M. Silva is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Tumor necrosis factor alpha & TLR4. The author has an hindex of 11, co-authored 12 publications receiving 8436 citations. Previous affiliations of M. Silva include Howard Hughes Medical Institute.
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Journal ArticleDOI
Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene
Alexander Poltorak,Xiaolong He,Irina Smirnova,Mu Ya Liu,Christophe Van Huffel,Xin Du,Dale Birdwell,E. Alejos,M. Silva,Chris Galanos,Marina Freudenberg,Paola Ricciardi-Castagnoli,Betsy Layton,Bruce Beutler +13 more
TL;DR: The mammalian Tlr4 protein has been adapted primarily to subserve the recognition of LPS and presumably transduces the LPS signal across the plasma membrane.
Journal ArticleDOI
Genetic and physical mapping of the Lps locus: identification of the toll-4 receptor as a candidate gene in the critical region.
Alexander Poltorak,Irina Smirnova,Xiaolong He,Mu Ya Liu,Christophe Van Huffel,Dale Birdwell,E. Alejos,M. Silva,Xin Du,Patricia A. Thompson,Edward K. L. Chan,Jessica Ledesma,Bruce A. Roe,Sandra W. Clifton,Stefanie N. Vogel,Bruce Beutler +15 more
TL;DR: To identify gene candidates, nearly 40,000 sequencing runs were performed across the critical region, and Selective hybridization and exon trapping were also employed to identify genes throughout the "zero" region.
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Prolonged and effective blockade of tumor necrosis factor activity through adenovirus-mediated gene transfer
TL;DR: Adenovirus-mediated transfer of a gene encoding a TNF inhibitor offers a practical means of imposing effective, long-term blockade of TNF activity in vivo for investigational and therapeutic purposes.
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Analysis of Tlr4-Mediated LPS Signal Transduction in Macrophages by Mutational Modification of the Receptor
TL;DR: Findings support the view that Tlr4 is an integral component of a solitary pathway for LPS signal transduction in macrophages and permit inferences related to the mechanism of signaling and its blockade.
Journal ArticleDOI
A reporter transgene indicates renal-specific induction of tumor necrosis factor (TNF) by shiga-like toxin. Possible involvement of TNF in hemolytic uremic syndrome.
TL;DR: It is concluded that shigatoxin acts to induce TNF synthesis within the kidney, and at the same time increases renal sensitivity to the toxic effects of TNF.