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首页> 外文期刊>Cell cycle >From top to bottom: the two faces of HIPK2 for regulation of the hypoxic response.
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From top to bottom: the two faces of HIPK2 for regulation of the hypoxic response.

机译：从上到下：HIPK2的两个面，用于调节缺氧反应。

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摘要

Oxygen deprivation (hypoxia) triggers a complex network of signaling pathways that result in changed gene expression patterns in order to cope with this challenge. Recent work has identified the serine/threonine kinase HIPK2 as a novel regulatory protein participating in hypoxic gene regulation. HIPK2 can affect apical as well as downstream events during the hypoxic response. Under normoxic conditions, HIPK2-mediated phosphorylation of the ubiquitin E3 ligase Siah2 weakens mutual binding and destabilizes the phosphorylated E3 ligase. Low oxygen levels result in strongly increased HIPK2/Siah2 interactions that lead to efficient polyubiquitylation and proteasomal degradation of the kinase. At the apical level, the Siah2 inhibiting phosphorylations are lost, thus allowing Siah2-dependent proteolysis of dioxygenases which in turn allows for activation of transcription factor HIF. Downstream events of the hypoxic response are affected by the proteasomal elimination of HIPK2 from gene repressing complexes, an event that allows for full induction of gene expression. Thus HIPK2 can regulate a subset of HIF-dependent and -independent genes during the hypoxic response.
机译：缺氧（缺氧）会触发复杂的信号通路网络，从而导致基因表达模式发生变化，以应对这一挑战。最近的工作已确定丝氨酸/苏氨酸激酶HIPK2为参与缺氧基因调控的新型调控蛋白。 HIPK2可以影响低氧反应过程中的顶端以及下游事件。在常氧条件下，HIPK2介导的泛素E3连接酶Siah2磷酸化会削弱相互结合，并使磷酸化的E3连接酶不稳定。低氧水平导致HIPK2 / Siah2相互作用大大增加，从而导致有效的多泛素化和激酶的蛋白酶体降解。在顶端水平，Siah2抑制性磷酸化丢失，从而使Siah2依赖的双加氧酶发生蛋白水解，进而激活转录因子HIF。缺氧反应的下游事件受到蛋白酶抑制基因抑制复合物中HIPK2的影响，该事件可完全诱导基因表达。因此，HIPK2可以在缺氧反应中调节HIF依赖性和非依赖性基因的子集。

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