通过cAMP信号传导至不依赖PKA的ERK对PC12细胞分化的调控：所有联系都合理吗？
Regulation of PC12 cell differentiation by cAMP signaling to ERK independent of PKA: do all the connections add up?
作者信息
Gerdin Matthew J, Eiden Lee E
机构信息
Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institutes of Health, Bethesda, MD 20892, USA.
出版信息
Sci STKE. 2007 Apr 17;2007(382):pe15. doi: 10.1126/stke.3822007pe15.
Abstract
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide that elevates adenosine 3',5'-monophosphate (cyclic AMP, also abbreviated cAMP) to elicit neuritogenesis in PC12 cells. This effect appears to be independent of cAMP-dependent protein kinase (PKA) yet dependent on cAMP, leading to the conclusion that another cAMP-binding protein and subsequent signaling pathway must exist to mediate this PKA-independent signaling mechanism. Such a protein was identified as exchange protein directly activated by cAMP (EPAC). Although EPAC may play an indirect role in PACAP-mediated neuritogenesis, it does not serve as the only PKA-independent link from cAMP that leads to neuritogenesis. Thus, the challenge remains to construct a signaling network that incorporates the known mediators, working independently of PKA, that are ultimately responsible for PACAP-mediated neuritogenesis.
摘要
垂体腺苷酸环化酶激活多肽（PACAP）是一种神经肽，它可提高3',5'-单磷酸腺苷（环磷酸腺苷，也缩写为cAMP）水平，从而在PC12细胞中引发神经突生成。这种效应似乎独立于cAMP依赖性蛋白激酶（PKA），但依赖于cAMP，由此得出结论，必然存在另一种cAMP结合蛋白和后续信号通路来介导这种不依赖PKA的信号传导机制。这样一种蛋白被鉴定为直接由cAMP激活的交换蛋白（EPAC）。尽管EPAC可能在PACAP介导的神经突生成中发挥间接作用，但它并不是cAMP介导神经突生成的唯一不依赖PKA的联系。因此，构建一个包含已知介质的信号网络仍然是一个挑战，这些介质独立于PKA发挥作用，最终负责PACAP介导的神经突生成。
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