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Richard Bucala

Researcher at Yale University

Publications -  622
Citations -  58697

Richard Bucala is an academic researcher from Yale University. The author has contributed to research in topics: Macrophage migration inhibitory factor & Cytokine. The author has an hindex of 119, co-authored 595 publications receiving 54607 citations. Previous affiliations of Richard Bucala include École Polytechnique Fédérale de Lausanne & Rockefeller University.

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Age-associated elevation in TLR5 leads to increased inflammatory responses in the elderly.

TL;DR: A multivariable mixed effect model is used to report a highly significant increase in TLR5‐induced production of IL‐8 from monocytes of older individuals, which may provide a critical mechanism to enhance immune responsiveness in older individuals.
Journal Article

De novo renal expression of macrophage migration inhibitory factor during the development of rat crescentic glomerulonephritis

TL;DR: Data provide the first demonstration that renal epithelial cells are a major source of MIF in both normal and diseased kidney and the up-regulation of Mif expression may play an important role in macrophage accumulation and progressive renal injury in rat crescentic glomerulonephritis.
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Evolving complexity of MIF signaling.

TL;DR: D-dopachrome tautomerase (D-DT or MIF-2) was recognized to be a structural and functional homolog of MIF, which could exert overlapping effects, raising further the complexity of canonical MIF signaling pathways.
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Cloning and characterization of the gene for mouse macrophage migration inhibitory factor (mif)

TL;DR: The cloned mouse MIF gene is cloned and potential regulatory sequences present within the 5'-proximal promoter region are identified, including both inflammatory/growth factor-related elements and sites associated with the genes for certain peptide hormones.
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Role of cyclophilin A in the uptake of HIV-1 by macrophages and T lymphocytes

TL;DR: It is reported that HIV-1 infection of primary peripheral blood mononuclear cells can be inhibited by an excess of exogenously added CyPA; a CsA analogue unable to enter the cells; and neutralizing antibodies to CyPA.