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首页> 外文期刊>Cellular Signalling >Differential activity of c-KIT splice forms is controlled by extracellular peptide insert length
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Differential activity of c-KIT splice forms is controlled by extracellular peptide insert length

机译：c-KIT剪接形式的差异活性受细胞外肽插入片段长度的控制

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摘要

Understanding receptor activation is important for disease intervention. Activation of the receptor tyrosine kinase c-KIT is involved in numerous diseases including melanoma, mastocytosis, multiple myeloma and gastrointestinal stromal tumors. To better understand the regulation of activation, we studied the two c-KIT isoforms, c-KIT(-) and c-KIT(+), which differ by a tetrapeptide insert GNNK, located in the extracellular juxtamembrane domain of the c-KIT(+) isoform. This region is important for regulating receptor activation. Here we show that the consecutive elimination of one amino acid at a time from the GNNK tetrapeptide insert gradually increases receptor tyrosine phosphorylation, ubiquitination, internalization and downstream MAP kinase-ERK activation. Successively decreasing the insert length progressively improves cell survival during drug treatment. Our results indicate that the length of the tetrapeptide fine-tunes receptor activity, thus providing deeper insight into c-KIT activation.
机译：了解受体激活对于疾病干预很重要。受体酪氨酸激酶c-KIT的激活涉及多种疾病，包括黑素瘤，肥大细胞增多症，多发性骨髓瘤和胃肠道间质瘤。为了更好地理解激活的调控，我们研究了两个c-KIT同工型c-KIT（-）和c-KIT（+），它们的区别在于位于c-KIT胞外近膜结构域中的四肽插入物GNNK。 （+）同工型。该区域对于调节受体激活很重要。在这里，我们显示从GNNK四肽插入片段中一次连续消除一个氨基酸逐渐增加了受体酪氨酸的磷酸化，泛素化，内在化和下游MAP激酶-ERK激活。连续减小插入物长度逐渐改善了药物治疗期间的细胞存活率。我们的结果表明，四肽的长度可以微调受体的活性，从而提供对c-KIT激活的更深入了解。

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