Matthew J. Fenton
Affiliations: | Boston University, Boston, MA, United States |
Area:
Molecular Biology, Cell Biology, Microbiology BiologyGoogle:
"Matthew Fenton"Children
Sign in to add trainee| Sylvia Marecki | grad student | 2000 | Boston University |
| Terry K. Means | grad student | 2000 | Boston University |
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Publications
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| Trova S, Lin F, Lomada S, et al. (2023) Pathogen and human NDPK-proteins promote AML cell survival via monocyte NLRP3-inflammasome activation. Plos One. 18: e0288162 |
| Chandran SS, Verhoeven D, Teijaro JR, et al. (2009) TLR2 engagement on dendritic cells promotes high frequency effector and memory CD4 T cell responses. Journal of Immunology (Baltimore, Md. : 1950). 183: 7832-41 |
| Shoenfelt J, Mitkus RJ, Zeisler R, et al. (2009) Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter. Journal of Leukocyte Biology. 86: 303-12 |
| Laird MH, Rhee SH, Perkins DJ, et al. (2009) TLR4/MyD88/PI3K interactions regulate TLR4 signaling. Journal of Leukocyte Biology. 85: 966-77 |
| Medvedev AE, Piao W, Shoenfelt J, et al. (2007) Role of TLR4 tyrosine phosphorylation in signal transduction and endotoxin tolerance. The Journal of Biological Chemistry. 282: 16042-53 |
| Basu S, Kang TJ, Chen WH, et al. (2007) Role of Bacillus anthracis spore structures in macrophage cytokine responses. Infection and Immunity. 75: 2351-8 |
| Toshchakov VY, Fenton MJ, Vogel SN. (2007) Cutting Edge: Differential inhibition of TLR signaling pathways by cell-permeable peptides representing BB loops of TLRs. Journal of Immunology (Baltimore, Md. : 1950). 178: 2655-60 |
| Shoenfelt JL, Fenton MJ. (2006) TLR2- and TLR4-dependent activation of STAT1 serine phosphorylation in murine macrophages is protein kinase C-delta-independent. Journal of Endotoxin Research. 12: 231-40 |
| Yu M, Wang H, Ding A, et al. (2006) HMGB1 signals through toll-like receptor (TLR) 4 and TLR2. Shock (Augusta, Ga.). 26: 174-9 |
| Scheibner KA, Lutz MA, Boodoo S, et al. (2006) Hyaluronan fragments act as an endogenous danger signal by engaging TLR2. Journal of Immunology (Baltimore, Md. : 1950). 177: 1272-81 |