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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 期刊论文

编号：

950bdacf-5cf6-44ad-8980-98f421a0a140
作者：

FingerleRowson, Guenter#^[2]Kaleswarapu, Dayananda Rao^[2];Schlander, Corinna^[4];Kabgani, Nazanin^[2];Brocks, Tania^[2];Reinart, Nina^[2];Busch, Raymonde^[3];Schuetz, Anke^[5];Lue, Hongqi^[5];Du, Xin;Liu, Aihua(柳爱华)^[6]Xiong, Huabao^[7];Chen, Yibang^[7];Nemajerova, Alice^[8];Hallek, Michael^[2];Bernhagen, Juergen^[5];Leng, Lin;Bucala, Richard*^[1]
语种：

英文
期刊：

MOLECULAR AND CELLULAR BIOLOGY ISSN：0270-7306 2009 年 29 卷 7 期 (1922 - 1932) ; APR 1
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摘要：

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 address the functional role of the MIF tautomerase activity in vivo, we created a knock-in mouse in which the endogenous mif gene was replaced by one encoding a tautomerase-null, Pro1 -> Gly1 MIF protein (P1G-MIF). While P1G-MIF is completely inactive catalytically, it maintains significant, albeit reduced, binding to its cell surface receptor (CD74) and to the intracellular binding protein JAB1/CSN5. P1G-MIF knock-in mice (mif(P1G/P1G)) and cells derived from these mice show a phenotype in assays of growth control and tumor induction that is intermediate between those of the wild type (mif(+/+)) and complete MIF deficiency (mif(-/-)). These data provide genetic evidence that MIF's intrinsic tautomerase activity is dispensable for this cytokine's growth-regulatory properties and support a role for the N-terminal region in protein-protein interactions.
推荐引用方式
GB/T 7714：

Fingerle-Rowson Guenter,Kaleswarapu Dayananda Rao,Schlander Corinna, et al. 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 [J].MOLECULAR AND CELLULAR BIOLOGY,2009,29(7):1922-1932.
APA：

Fingerle-Rowson Guenter,Kaleswarapu Dayananda Rao,Schlander Corinna,Kabgani Nazanin,&Bucala Richard.(2009).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,29(7):1922-1932.
MLA：

Fingerle-Rowson Guenter, et al. "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 29,7(2009):1922-1932.
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