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LRRK2 在 B-2 细胞中表达而不在 B-1 B 细胞中表达,并且细胞活化可使其下调。

LRRK2 is expressed in B-2 but not in B-1 B cells, and downregulated by cellular activation.

机构信息

Division of Clinical Immunology, Graduate School of Medical Sciences, Kitasato University, Minami-ku, Sagamihara, Kanagawa, Japan.

出版信息

J Neuroimmunol. 2010 Dec 15;229(1-2):123-8. doi: 10.1016/j.jneuroim.2010.07.021. Epub 2010 Aug 21.

Abstract

LRRK2, the causal molecule of familial Parkinson's disease, is expressed strongly by one of the B cell subsets, B-2 cells, but not by the other subset, B-1 cells, in the mouse peritoneal cavity, spleen, and peripheral blood. Bone marrow pre-B cells or T cells exhibited little LRRK2 expression. LRRK2 expression was dramatically downregulated upon activation of B-2 cells with various types of stimulation. These results suggest that LRRK2, whose true function has not yet been clarified, may play some important role(s) in the development and function of B cells, particularly the maintenance of B-2 cells in a resting status.

摘要

LRRK2,家族性帕金森病的致病分子,在小鼠腹腔、脾脏和外周血中的 B 细胞亚群 B-2 细胞中强烈表达,但在另一个亚群 B-1 细胞中不表达。骨髓前 B 细胞或 T 细胞表达很少的 LRRK2。用各种刺激物激活 B-2 细胞后,LRRK2 的表达显著下调。这些结果表明,LRRK2 的真正功能尚未阐明,它可能在 B 细胞的发育和功能中发挥某些重要作用,特别是维持 B-2 细胞的静息状态。

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