Article
A tautomerase-null macrophage migration-inhibitory factor (MIF) gene knock-in mouse model reveals that protein interactions and not enzymatic activity mediate MIF-dependent growth regulation.
Molecular and cellular biology - 1 Apr 2009
Fingerle-Rowson Günter, Kaleswarapu Dayananda Rao, Schlander Corinna, Kabgani Nazanin, Brocks Tania, Reinart Nina, Busch Raymonde, Schütz Anke, Lue Hongqi, Du Xin, Liu Aihua, Xiong Huabao, Chen Yibang, Nemajerova Alice, Hallek Michael, Bernhagen Jürgen, Leng Lin, Bucala Richard
Abstract excerpt
Macrophage migration-inhibitory factor (MIF) is an upstream regulator of innate immunity and a potential molecular link between inflammation and cancer. The unusual structural homology between MIF and certain tautomerases, which includes both a conserved substrate-binding pocket and a catalytic N-terminal proline (Pro1), has fueled speculation that an enzymatic reaction underlies MIF's biologic function. To...
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