首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Wildtype Elk-1, but not a SUMOylation mutant, represses egr-1 expression in SH-SY5Y neuroblastomas.
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Wildtype Elk-1, but not a SUMOylation mutant, represses egr-1 expression in SH-SY5Y neuroblastomas.

机译:野生型Elk-1(而非SUMOylation突变体)抑制SH-SY5Y神经母细胞瘤中egr-1的表达。

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摘要

Elk-1, an ETS domain transcription factor of the TCF (ternary complex factor) subfamily, is known to be involved in the regulation of immediate-early genes such as c-fos upon mitogen activation, and thus commonly implied in cell proliferation. Early growth response-1, Egr-1, which was known to be an immediate-early gene, has recently been shown to be pro-apoptotic for SH-SY5Y neuroblastoma cells. In that respect, it was not clear whether Elk-1 would activate or repress from this promoter, since Elk-1 is mostly associated with proliferation and not apoptosis. In this study, we wanted to address whether Elk-1 activates or represses egr-1 promoter in neuroblastoma cells, and using a combination of RNA interference and reporter analyses, we present evidence that egr-1 gene is repressed by Elk-1 in normally cycling SH-SY5Y neuroblastoma cell line in a SUMO (small ubiquitin-related modifier)-dependent manner, a potential mechanism used by these cells to bypass apoptosis.
机译:Elk-1是TCF(三元复合因子)亚家族的ETS结构域转录因子,已知参与有丝分裂原活化后对早期基因(例如c-fos)的调控,因此通常暗示细胞增殖。早期生长应答-1,Egr-1,已知是一种立即早期的基因,最近已显示出对SH-SY5Y神经母细胞瘤细胞具有促凋亡作用。在这方面,尚不清楚Elk-1是否会从该启动子激活或抑制,因为Elk-1主要与增殖相关,与凋亡无关。在这项研究中,我们想解决Elk-1是否激活或抑制神经母细胞瘤细胞中的egr-1启动子,并结合RNA干扰和记者分析,我们提供证据证明Elr-1在正常情况下会抑制egr-1基因。以SUMO(小泛素相关修饰物)依赖性方式循环SH-SY5Y神经母细胞瘤细胞系,这是这些细胞绕过凋亡的潜在机制。

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