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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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Journal ArticleDOI
T Cells Regulate Peripheral Naive Mature B Cell Survival by Cell-Cell Contact Mediated through SLAMF6 and SAP.
Lihi Radomir,Sivan Cohen,Matthias P. Kramer,Eszter Bakos,Hadas Lewinsky,Avital F. Barak,Ziv Porat,Richard Bucala,Polina Stepensky,Shirly Becker-Herman,Idit Shachar +10 more
TL;DR: It is shown that naive B and T cells interact via the signaling lymphocyte activation molecule (SLAM) family receptor, SLAMF6, which results in an upregulation of the expression of the cytokine migration inhibitory factor in the T cells and augmented expression of its receptor CD74 on the B cell counterparts, consequently enhancing B cell survival.
Journal ArticleDOI
Modeling of both shared and distinct interactions between MIF and its homologue D-DT with their common receptor CD74.
Roberto Meza-Romero,Gil Benedek,Kelley Jordan,Lin Leng,Georgios Pantouris,Elias Lolis,Richard Bucala,Arthur A. Vandenbark +7 more
TL;DR: The D-DT (MIF-2) interaction with CD74 is studied that is mainly defined by three elements scattered throughout the disordered regions of the interacting molecules, which has implications for the manner in which D- DT and MIF compete with each other for binding to the CD74 receptor and for the relative potency of DRa1-MOG-35-55 and RTL1000 for competitive inhibition of D-dopachrome tautomerase.
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The macrophage migration inhibitory factor (MIF)-homologue D-dopachrome tautomerase is a therapeutic target in a murine melanoma model
TL;DR: D-DT and its receptor are expressed in the murine tumors B16F10 and 4T1 and knock-down of D-DT through siRNA or blocking by antibodies reduced proliferation of B 16F10 tumor cells, qualifying D- DT for further evaluation as a therapeutic target.
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Cardiomyocyte d-dopachrome tautomerase protects against heart failure.
Yina Ma,Kevin N. Su,Daniel Pfau,Veena S. Rao,Xiaohong Wu,Xiaoyue Hu,Lin Leng,Xin Du,Marta Piecychna,Kenneth Bedi,Stuart G. Campbell,Anne Eichmann,Jeffrey M. Testani,Kenneth B. Margulies,Richard Bucala,Lawrence H. Young +15 more
TL;DR: Ex vivo endogenous cardiomyocyte DDT has pleiotropic actions that are protective against heart failure.
Journal ArticleDOI
Structural Plasticity in the C-Terminal Region of Macrophage Migration Inhibitory Factor-2 Is Associated with an Induced Fit Mechanism for a Selective Inhibitor
TL;DR: 4-(3-Carboxyphenyl)-2,5-pyridinedicarboxylic acid (4-CPPC) is reported as the first reversible and selective small molecule inhibitor of pro-inflammatory protein macrophage migration inhibitory factor-2 (also known as MIF-2 or d-DT).