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鉴定 APBB1 为间变性淋巴瘤激酶的底物。

Identification of APBB1 as a substrate for anaplastic lymphoma kinase.

机构信息

Department of Integrative Physiology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.

Department of Biochemistry, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.

出版信息

J Biochem. 2024 Nov 4;176(5):395-403. doi: 10.1093/jb/mvae055.

Abstract

Anaplastic lymphoma kinase (ALK) is a well-known oncogene involved in various malignancies such as anaplastic large cell lymphoma, lung cancer and neuroblastoma. Several substrates for fused ALK have been identified and their biological functions have been described. However, the lack of a comprehensive identification of ALK substrates limits our understanding of the biological roles of receptor ALK. Thus, this study aimed to identify novel ALK substrates and characterize their biological functions. We screened the interactors of the kinase domain of receptor ALK using proximity-dependent biotin identification and identified 43 interactors. We narrowed down the candidates by evaluating whether these interactors were downstream of ALK in a neuroblastoma cell line, NB-1. Amongst these, we identified amyloid beta precursor protein-binding family B member 1 (APBB1) as an ALK downstream molecule involved in NB-1 cell viability. Finally, we assessed the kinase-substrate relationship between ALK and APBB1 and found that ALK phosphorylated multiple tyrosine residues in APBB1 both in-cell and in-tube assays, with tyrosine 269 as a major target. In conclusion, we successfully identified a new substrate for receptor ALK. Our results may help further elucidate the molecular mechanism of ALK downstream signalling in neuroblastoma.

摘要

间变性淋巴瘤激酶(ALK)是一种众所周知的癌基因,参与多种恶性肿瘤,如间变大细胞淋巴瘤、肺癌和神经母细胞瘤。已经鉴定出几种融合 ALK 的底物,并描述了它们的生物学功能。然而,缺乏对 ALK 底物的全面鉴定限制了我们对受体 ALK 生物学作用的理解。因此,本研究旨在鉴定新的 ALK 底物并表征其生物学功能。我们使用邻近依赖性生物素鉴定筛选了受体 ALK 激酶结构域的相互作用蛋白,鉴定出 43 个相互作用蛋白。我们通过评估这些相互作用蛋白是否是神经母细胞瘤细胞系 NB-1 中 ALK 的下游分子,从而缩小了候选者的范围。其中,我们鉴定出淀粉样前体蛋白结合家族 B 成员 1(APBB1)是一种参与 NB-1 细胞活力的 ALK 下游分子。最后,我们评估了 ALK 和 APBB1 之间的激酶-底物关系,发现 ALK 在细胞内和试管内实验中均可磷酸化 APBB1 的多个酪氨酸残基,酪氨酸 269 是主要靶点。总之,我们成功鉴定了受体 ALK 的一个新底物。我们的结果可能有助于进一步阐明神经母细胞瘤中 ALK 下游信号转导的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a82b/11954158/fbac82bc8b15/mvae055ga.jpg

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