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ATAR是一种新型肿瘤坏死因子受体家族成员,通过TRAF2和TRAF5发出信号。

ATAR, a novel tumor necrosis factor receptor family member, signals through TRAF2 and TRAF5.

作者信息

Hsu H, Solovyev I, Colombero A, Elliott R, Kelley M, Boyle W J

机构信息

Department of Cell Biology, Amgen Inc., Thousand Oaks, California 91320, USA.

出版信息

J Biol Chem. 1997 May 23;272(21):13471-4. doi: 10.1074/jbc.272.21.13471.

Abstract

Members of tumor necrosis factor receptor (TNFR) family signal largely through interactions with death domain proteins and TRAF proteins. Here we report the identification of a novel TNFR family member ATAR. Human and mouse ATAR contain 283 and 276 amino acids, respectively, making them the shortest known members of the TNFR superfamily. The receptor is expressed mainly in spleen, thymus, bone marrow, lung, and small intestine. The intracellular domains of human and mouse ATAR share only 25% identity, yet both interact with TRAF5 and TRAF2. This TRAF interaction domain resides at the C-terminal 20 amino acids. Like most other TRAF-interacting receptors, overexpression of ATAR activates the transcription factor NF-kappaB. Co-expression of ATAR with TRAF5, but not TRAF2, results in synergistic activation of NF-kappaB, suggesting potentially different roles for TRAF2 and TRAF5 in post-receptor signaling.

摘要

肿瘤坏死因子受体(TNFR)家族成员主要通过与死亡结构域蛋白和TRAF蛋白相互作用来传递信号。在此,我们报告了一种新型TNFR家族成员ATAR的鉴定。人类和小鼠的ATAR分别包含283和276个氨基酸,这使它们成为TNFR超家族中已知最短的成员。该受体主要在脾脏、胸腺、骨髓、肺和小肠中表达。人类和小鼠ATAR的胞内结构域仅有25%的同源性,但二者均与TRAF5和TRAF2相互作用。这种TRAF相互作用结构域位于C末端的20个氨基酸处。与大多数其他与TRAF相互作用的受体一样,ATAR的过表达会激活转录因子NF-κB。ATAR与TRAF5(而非TRAF2)共表达会导致NF-κB的协同激活,这表明TRAF2和TRAF5在受体后信号传导中可能具有不同的作用。

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