The biological functions and signaling mechanisms of the p75 neurotrophin receptor.
The biological functions and signaling mechanisms of the p75 neurotrophin receptor.
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DOI：
10.1007/978-3-642-45106-5_6
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发表时间：
2014-01-01
影响因子：
--
通讯作者：
Carter, B D
中科院分区：
文献类型：
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作者：
Kraemer, B R;Yoon, S O;Carter, B D
p75神经营养因子受体（p75（NTR））调节广泛的细胞功能，包括程序性细胞死亡、轴突生长和变性、细胞增殖、髓鞘形成和突触可塑性。受受体支配的细胞功能的多样性源于与p75（NTR）缔合并调节其信号传导的各种配体和共受体。P75（NTR）通过与Trk受体的相互作用促进存活，通过与Nogo受体（Nogo-R）和Lingo-1的伙伴关系抑制轴突再生，并通过与分拣蛋白的结合促进细胞凋亡。这些相互作用的下游信号通过p75（NTR）的调节性膜内蛋白水解（RIP）以及与许多胞质伴侣的相互作用而进一步调节。在这一章中，我们将讨论p75（NTR）的复杂的信号机制，强调这些信号是如何差异调节介导这些不同的细胞功能。
The p75 neurotrophin receptor (p75(NTR)) regulates a wide range of cellular functions, including programmed cell death, axonal growth and degeneration, cell proliferation, myelination, and synaptic plasticity. The multiplicity of cellular functions governed by the receptor arises from the variety of ligands and co-receptors which associate with p75(NTR) and regulate its signaling. P75(NTR) promotes survival through interactions with Trk receptors, inhibits axonal regeneration via partnerships with Nogo receptor (Nogo-R) and Lingo-1, and promotes apoptosis through association with Sortilin. Signals downstream of these interactions are further modulated through regulated intramembrane proteolysis (RIP) of p75(NTR) and by interactions with numerous cytosolic partners. In this chapter, we discuss the intricate signaling mechanisms of p75(NTR), emphasizing how these signals are differentially regulated to mediate these diverse cellular functions.