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扩展 KIF4A 相关表型。

Expanding the KIF4A-associated phenotype.

机构信息

Medical Genetics, Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Switzerland.

Department of Clinical Research, University Hospital Basel, Basel, Switzerland.

出版信息

Am J Med Genet A. 2021 Dec;185(12):3728-3739. doi: 10.1002/ajmg.a.62443. Epub 2021 Aug 3.

Abstract

Kinesin super family (KIF) genes encode motor kinesins, a family of evolutionary conserved proteins, involved in intracellular trafficking of various cargoes. These proteins are critical for various physiological processes including neuron function and survival, ciliary function and ciliogenesis, and cell-cycle progression. Recent evidence suggests that alterations in motor kinesin genes can lead to a variety of human diseases, including monogenic disorders. Neuropathies, impaired higher brain functions, structural brain abnormalities and multiple congenital anomalies (i.e., renal, urogenital, and limb anomalies) can result from pathogenic variants in many KIF genes. We expand the phenotype associated with KIF4A variants from developmental delay and intellectual disability with or without epilepsy to a congenital anomaly phenotype with hydrocephalus and various brain anomalies at the more severe end of phenotypic manifestations. Additional anomalies of the kidneys and urinary tract, congenital lymphedema, eye, and dental anomalies seem to be variably associated and overlap with clinical signs observed in other kinesinopathies. Caution still applies to missense variants, but hopefully, future work will further establish genotype-phenotype correlations in a larger number of patients and functional studies may give further insights into the complex function of KIF4A.

摘要

驱动蛋白超家族(KIF)基因编码马达驱动蛋白,这是一类进化上保守的蛋白质,参与各种货物的细胞内运输。这些蛋白质对各种生理过程至关重要,包括神经元功能和存活、纤毛功能和纤毛发生以及细胞周期进程。最近的证据表明,驱动蛋白基因的改变可能导致多种人类疾病,包括单基因疾病。许多 KIF 基因的致病性变异可导致多种神经病、大脑高级功能受损、结构性脑异常和多种先天性异常(即肾、泌尿生殖和肢体异常)。我们将 KIF4A 变异相关的表型从伴或不伴癫痫的发育迟缓和智力残疾扩展到更严重表现形式的伴有脑积水和各种脑异常的先天性异常表型。肾脏和泌尿道、先天性淋巴水肿、眼睛和牙齿异常的其他异常似乎与其他驱动蛋白病观察到的临床体征存在可变性关联和重叠。对错义变异仍需谨慎,但希望未来的工作将在更多患者中进一步建立基因型-表型相关性,功能研究可能会进一步深入了解 KIF4A 的复杂功能。

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