微管相关蛋白2（MAP2）的磷酸化及其与调节神经元细胞骨架功能的相关性。,Progress in Neurobiology

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微管相关蛋白2（MAP2）的磷酸化及其与调节神经元细胞骨架功能的相关性。
Progress in Neurobiology ( IF 6.7 ) Pub Date : 2000-03-08 , DOI: 10.1016/s0301-0082(99)00046-5
C Sánchez ₁ , J Díaz-Nido , J Avila

Affiliation

神经元是神经系统的基本信息处理单元，其特征是复杂的极性形态，这对它们的功能至关重要。为了获得其精确的形态，神经元以高度调控的方式扩展了细胞质过程（轴突和树突）并建立了突触连接。另外，神经元在成年期也经历小的塑性变化，以调节突触传递。神经元发育的每个步骤都受到内源性决定簇以及包括细胞间接触，细胞外基质和扩散信号在内的环境信号的遗传控制。细胞骨架成分是响应大多数最终决定神经元形态的细胞外信号而修饰的主要蛋白质靶标之一。控制神经元细胞骨架的主要机制之一是通过改变神经元内蛋白激酶和磷酸酶的相对活性来改变细胞骨架蛋白的磷酸化状态。特别是，微管相关蛋白2（MAP2）家族是大量的细胞骨架成分，主要在神经元中表达，并充当神经元中大多数蛋白激酶和磷酸酶的底物。MAP2磷酸化似乎控制着它与细胞骨架的联系，并且受到发育的调节。此外，MAP2可能执行许多功能，包括微管（可能还有微丝）的成核和稳定化，轴突和树突内细胞器运输的调节，以及调节蛋白（例如蛋白激酶）的锚定，这可能对信号转导很重要。还提出了MAP2的这些假定功能在神经元过程的生长，突触可塑性和神经元细胞死亡中起重要作用。因此，MAP2构成了一个有趣的案例，以了解通过响应不同的细胞外信号改变细胞骨架蛋白的磷酸化状态来调节神经元功能。在这里，我们将回顾有关通过磷酸化/去磷酸化调控MAP2功能的最新知识，以及其在神经元功能的更广泛背景下的相关性。还提出了MAP2的这些假定功能在神经元过程的生长，突触可塑性和神经元细胞死亡中起重要作用。因此，MAP2构成了一个有趣的案例，以了解通过响应不同的细胞外信号改变细胞骨架蛋白的磷酸化状态来调节神经元功能。在这里，我们将回顾有关通过磷酸化/去磷酸化调控MAP2功能的最新知识，以及其在神经元功能的更广泛背景下的相关性。还提出了MAP2的这些假定功能在神经元过程的生长，突触可塑性和神经元细胞死亡中起重要作用。因此，MAP2构成了一个有趣的案例，以了解通过响应不同的细胞外信号改变细胞骨架蛋白的磷酸化状态来调节神经元功能。在这里，我们将回顾有关通过磷酸化/去磷酸化调控MAP2功能的最新知识，以及其在神经元功能的更广泛背景下的相关性。

"点击查看英文标题和摘要"

Phosphorylation of microtubule-associated protein 2 (MAP2) and its relevance for the regulation of the neuronal cytoskeleton function.

Neurons, the basic information processing units of the nervous system, are characterized by a complex polar morphology which is essential for their function. To attain their precise morphology, neurons extend cytoplasmatic processes (axons and dendrites) and establish synaptic connections in a highly regulated way. Additionally, neurons are also subjected to small plastic changes at the adult stage which serve to regulate synaptic transmission. Every step of neuronal development is genetically controlled by endogenous determinants, as well as by environmental signals including intercellular contacts, extracellular matrix and diffusible signals. Cytoskeletal components are among the main protein targets modified in response to most of those extracellular signals which ultimately determine neuronal morphology. One of the major mechanisms controlling the neuronal cytoskeleton is the modification of the phosphorylation state of cytoskeletal proteins via changes in the relative activities of protein kinases and phosphatases within neurons. In particular, the microtubule-associated protein 2 (MAP2) family of proteins is an abundant group of cytoskeletal components which are predominantly expressed in neurons and serve as substrates for most of protein kinases and phosphatases present in neurons. MAP2 phosphorylation seems to control its association with the cytoskeleton and it is developmentally regulated. Moreover, MAP2 may perform many functions including the nucleation and stabilization of microtubules (and maybe microfilaments), the regulation of organelle transport within axons and dendrites, as well as the anchorage of regulatory proteins such as protein kinases which may be important for signal transduction. These putative functions of MAP2 have also been proposed to play important roles in the outgrowth of neuronal processes, synaptic plasticity and neuronal cell death. Thus, MAP2 constitutes an interesting case to understand the regulation of neuronal function by the alteration of the phosphorylation state of cytoskeletal proteins in response to different extracellular signals. Here we will review the current knowledge about the regulation of MAP2 function through phosphorylation/dephosphorylation and its relevance in the broader context of neuronal functions.

更新日期：2019-11-01

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