Ectodomain shedding of the EGF-receptor ligand epigen is mediated by ADAM17
Ectodomain shedding of the EGF-receptor ligand epigen is mediated by ADAM17
复制标题
DOI：
10.1016/j.febslet.2006.11.074
复制
发表时间：
2007-01-09
期刊：
影响因子：
3.5
通讯作者：
Blobel, Carl P.
中科院分区：
文献类型：
--
作者：
Sahin, Umut;Blobel, Carl P.
表皮生长因子受体（EGFR）的所有配体都是跨膜前体，在发育和疾病中起重要作用。蛋白水解加工的亚当斯（解整合素和金属蛋白酶）调节的生物利用度的几个EGFR配体，但很少有人知道的酶负责处理最近确定的EGFR配体，epigen。在这里，我们表明，epigen的胞外结构域脱落需要ADAM 17，它可以被佛波醇酯，磷酸酶抑制剂和钙内流刺激。这些结果表明，ADAM17可能是一个很好的目标，以阻止释放的生物活性epigen，一个高度有丝分裂的配体的表皮生长因子受体，其中涉及伤口愈合和癌症。(c)2006年欧洲生物化学学会联合会。Elsevier B.V.出版，保留所有权利。
All ligands of the epidermal growth factor receptor (EGFR), which has important roles in development and disease, are made as transmembrane precursors. Proteolytic processing by ADAMs (a disintegrin and metalloprotease) regulates the bioavailability of several EGFR-ligands, yet little is known about the enzyme responsible for processing the recently identified EGFR ligand, epigen. Here we show that ectodomain shedding of epigen requires ADAM 17, which can be stimulated by phorbol esters, phosphatase inhibitors and calcium influx. These results suggest that ADAM17 might be a good target to block the release of bioactive epigen, a highly mitogenic ligand of the EGFR which has been implicated in wound healing and cancer. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.