Activation of transcription factor NF-kappaB requires ELKS, an IkappaB kinase regulatory subunit.
Activation of transcription factor NF-kappaB requires ELKS, an IkappaB kinase regulatory subunit.
复制标题
DOI：
--
复制
发表时间：
2004
期刊：
影响因子：
56.9
通讯作者：
Jeanette L Ducut Sigala;Virginie Bottero;David B. Young;Andrej Shevchenko;Frank Mercurio;I. M. Verma
中科院分区：
文献类型：
--
作者：
Jeanette L Ducut Sigala;Virginie Bottero;David B. Young;Andrej Shevchenko;Frank Mercurio;I. M. Verma
核因子-κ B（NF-κ B）家族的转录因子在炎症、细胞凋亡、发育和癌症中起着重要作用。响应于不同信号的NF-κ B介导的基因表达的调节由IkappaB激酶（IKK）复合物协调。我们确定了ELKS，IKK复合物的一个重要调节亚基。通过RNA干扰沉默ELKS表达阻断了NF-κ B靶基因的诱导表达，包括NF-κ B抑制剂IkappaB α和促炎基因，如环氧合酶2和白细胞介素8。这些细胞也没有被保护免于响应于细胞因子的凋亡。ELKS可能通过将IkappaB α募集到IKK复合物中而发挥作用，因此对IKK激活起调节作用。
The nuclear factor-kappa B (NF-kappaB) family of transcription factors plays a seminal role in inflammation, apoptosis, development, and cancer. Modulation of NF-kappaB-mediated gene expression in response to diverse signals is coordinated by the IkappaB kinase (IKK) complex. We identified ELKS, an essential regulatory subunit of the IKK complex. Silencing ELKS expression by RNA interference blocked induced expression of NF-kappaB target genes, including the NF-kappaB inhibitor IkappaBalpha and proinflammatory genes such as cyclo-oxygenase 2 and interleukin 8. These cells were also not protected from apoptosis in response to cytokines. ELKS likely functions by recruiting IkappaBalpha to the IKK complex and thus serves a regulatory function for IKK activation.