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首页> 外文期刊>Cell cycle >Merlin's tumor suppression linked to inhibition of the E3 ubiquitin ligase CRL4 (DCAF1).
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Merlin's tumor suppression linked to inhibition of the E3 ubiquitin ligase CRL4 (DCAF1).

机译：Merlin的肿瘤抑制作用与E3泛素连接酶CRL4（DCAF1）的抑制作用有关。

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摘要

The mechanism by which the FERM domain protein Merlin, encoded by the tumor suppressor NF2, restrains cell proliferation is poorly understood. Prior studies have suggested that Merlin exerts its antimitogenic effect by interacting with multiple signaling proteins located at or close to the plasma membrane. We have recently observed that Merlin translocates into the nucleus and binds to and inhibits the E3 ubiquitin ligase CRL4 (DCAF1) . Genetic evidence indicates that inactivation of Merlin induces oncogenic gene expression, hyperproliferation, and tumorigenicity by unleashing the activity of CRL4 (DCAF1) . In addition to providing a potential explanation for the diverse effects that loss of Merlin exerts in multiple cell types, these findings suggest that compounds inhibiting CRL4 (DCAF1) may display therapeutic efficacy in Neurofibromatosis type 2 and other cancers driven by Merlin inactivation.
机译：对由肿瘤抑制因子NF2编码的FERM域蛋白Merlin抑制细胞增殖的机制了解甚少。先前的研究表明，Merlin通过与位于或接近质膜的多种信号蛋白相互作用来发挥其抗有丝分裂作用。我们最近观察到，Merlin易位到细胞核中并结合并抑制E3泛素连接酶CRL4（DCAF1）。遗传学证据表明，通过释放CRL4（DCAF1）的活性，Merlin的失活可诱导致癌基因表达，过度增殖和致瘤性。除了提供可能的解释Merlin在多种细胞类型中发挥多种作用的可能解释外，这些发现还表明抑制CRL4（DCAF1）的化合物可能在2型神经纤维瘤病和其他由Merlin失活驱动的癌症中显示出治疗功效。

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