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HSD17B10:一个通过异亮氨酸代谢和神经活性甾体参与认知功能的基因。

HSD17B10: a gene involved in cognitive function through metabolism of isoleucine and neuroactive steroids.

作者信息

Yang Song-Yu, He Xue-Ying, Miller David

机构信息

Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA.

出版信息

Mol Genet Metab. 2007 Sep-Oct;92(1-2):36-42. doi: 10.1016/j.ymgme.2007.06.001. Epub 2007 Jul 6.

Abstract

The HSD17B10 gene maps on chromosome Xp11.2, a region highly associated with X-linked mental retardation. This gene encodes HSD10, a mitochondrial multifunctional enzyme that plays a significant part in the metabolism of neuroactive steroids and the degradation of isoleucine. The HSD17B10 gene is composed of six exons and five introns. Its exon 5 is an alternative exon such that there are several HSD17B10 mRNA isoforms in brain. A silent mutation (c.605C-->A) and three missense mutations (c.395C-->G; c.419C-->T; c.771A-->G), respectively, cause the X-linked mental retardation, choreoathetosis, and abnormal behavior (MRXS10) and the hydroxyacyl-CoA dehydrogenase II deficiency. The latter condition seems to be a multifactorial disease due to the disturbance of more than one metabolic pathway by the HSD10 deficiency. HSD10 inactivates the positive modulators of GABAA receptors, and plays a role in the maintenance of GABAergic neuronal function. This working model may account for the mental retardation of these patients. The dehydrogenase activity is slightly inhibited by the binding of amyloid-beta peptide to the loop D of HSD10. Elevated levels of HSD10 were observed in hippocampi of Alzheimer disease patients so this multifunctional enzyme may be related to Alzheimer disease pathogenesis; however, the molecular mechanism of its involvement remains to be ascertained.

摘要

HSD17B10基因定位于Xp11.2染色体上,该区域与X连锁智力障碍高度相关。该基因编码HSD10,一种线粒体多功能酶,在神经活性甾体的代谢和异亮氨酸的降解中起重要作用。HSD17B10基因由六个外显子和五个内含子组成。其外显子5是一个可变外显子,因此大脑中有几种HSD17B10 mRNA异构体。一个沉默突变(c.605C→A)和三个错义突变(c.395C→G;c.419C→T;c.771A→G)分别导致X连锁智力障碍、舞蹈手足徐动症和异常行为(MRXS10)以及羟酰基辅酶A脱氢酶II缺乏症。后一种情况似乎是一种多因素疾病,因为HSD10缺乏会干扰多种代谢途径。HSD10使GABAA受体的正性调节剂失活,并在维持GABA能神经元功能中起作用。这个工作模型可能解释了这些患者的智力障碍。淀粉样β肽与HSD10的环D结合会轻微抑制脱氢酶活性。在阿尔茨海默病患者的海马体中观察到HSD10水平升高,因此这种多功能酶可能与阿尔茨海默病的发病机制有关;然而,其参与的分子机制仍有待确定。

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