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首页> 外文期刊>Genomics >Neuronatin gene: Imprinted and misfolded. Studies in Lafora disease, diabetes and cancer may implicate NNAT-aggregates as a common downstream participant in neuronal loss
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Neuronatin gene: Imprinted and misfolded. Studies in Lafora disease, diabetes and cancer may implicate NNAT-aggregates as a common downstream participant in neuronal loss

机译：神经阴性基因：印迹和错误折叠。 Lafora病，糖尿病和癌症的研究可能将NNAT-作为神经元损失的常见下游参与者致癌

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Neuronatin (NNAT) is a ubiquitous and highly conserved mammalian gene involved in brain development. Its mRNA isoforms, chromosomal location, genomic DNA structure and regulation have been characterized. More recently there has been rapid progress in the understanding of its function in physiology and human disease. In particular there is fairly direct evidence implicating neuronatin in the causation of Lafora disease and diabetes. Neuronatin protein has a strong predisposition to misfold and form cellular aggregates that cause cell death by apoptosis. Aggregation of Neuronatin within cortical neurons and resulting cell death is the hallmark of Lafora disease, a progressive and fatal neurodegenerative disease. Under high glucose conditions simulating diabetes, neuronatin protein also accumulates and destroys pancreatic beta cells.The neuronatin gene is imprinted and only the paternal allele is normally expressed in the adult. However, changes in DNA methylation may cause the maternal allele to lose imprinting and trigger cell proliferation and metastasis. Neuronatin has also been shown to be translated peripherally within the dendrites of neurons, a finding of relevance in synaptic plasticity. The current understanding of the function of neuronatin raises the possibility that this gene may participate in the common downstream mechanisms associated with aberrant neuronal growth and death. A better understanding of these mechanisms may open new therapeutic targets to help modify the progression of devastating neurodegenerative conditions such as Alzheimer's and anterior horn cell disease.
机译：Neuronatin（NNAT）是患有脑发育的普遍存在和高度保守的哺乳动物基因。其mRNA同种型，染色体位置，基因组DNA结构和调节已经表征。最近，在理解其在生理学和人类疾病中的功能方面存在迅速进展。特别是存在相当直接的证据，暗示神经大生在Lafora病和糖尿病的原因中。神经大素蛋白具有强烈的易感性，并形成细胞聚集体，使细胞凋亡引起细胞死亡。皮质神经元内神经大麻素的聚集，并导致细胞死亡是Lafora病的标志，一种渐进和致命的神经变性疾病。在高葡萄糖条件下，模拟糖尿病，神经大素蛋白也积聚并破坏胰腺β细胞。神经阴性基因被印记，并且仅在成人中仅表达父母等位基因。然而，DNA甲基化的变化可能导致母体等位基因失去印记和触发细胞增殖和转移。 Neuronatin还被证明在神经元的树突内翻译，在突触可塑性中的相关性。目前对神经约素功能的理解提出了该基因可以参与与异常神经元生长和死亡相关的共同下游机制的可能性。更好地理解这些机制可以打开新的治疗目标，以帮助改变毁灭性神经退行性条件的进展，例如阿尔茨海默氏症和前骨细胞疾病。

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