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ZNF462 相关综合征的表型描绘。

Phenotype delineation of ZNF462 related syndrome.

机构信息

Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland.

Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, California.

出版信息

Am J Med Genet A. 2019 Oct;179(10):2075-2082. doi: 10.1002/ajmg.a.61306. Epub 2019 Jul 30.

DOI:10.1002/ajmg.a.61306
PMID:31361404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6935050/
Abstract

Zinc finger protein 462 (ZNF462) is a relatively newly discovered vertebrate specific protein with known critical roles in embryonic development in animal models. Two case reports and a case series study have described the phenotype of 10 individuals with ZNF462 loss of function variants. Herein, we present 14 new individuals with loss of function variants to the previous studies to delineate the syndrome of loss of function in ZNF462. Collectively, these 24 individuals present with recurring phenotypes that define a multiple congenital anomaly syndrome. Most have some form of developmental delay (79%) and a minority has autism spectrum disorder (33%). Characteristic facial features include ptosis (83%), down slanting palpebral fissures (58%), exaggerated Cupid's bow/wide philtrum (54%), and arched eyebrows (50%). Metopic ridging or craniosynostosis was found in a third of study participants and feeding problems in half. Other phenotype characteristics include dysgenesis of the corpus callosum in 25% of individuals, hypotonia in half, and structural heart defects in 21%. Using facial analysis technology, a computer algorithm applying deep learning was able to accurately differentiate individuals with ZNF462 loss of function variants from individuals with Noonan syndrome and healthy controls. In summary, we describe a multiple congenital anomaly syndrome associated with haploinsufficiency of ZNF462 that has distinct clinical characteristics and facial features.

摘要

锌指蛋白 462(ZNF462)是一种相对较新发现的脊椎动物特异性蛋白,在动物模型中对胚胎发育具有已知的关键作用。两项病例报告和一项病例系列研究描述了 10 名 ZNF462 功能丧失变异患者的表型。在此,我们向先前的研究报告了 14 名新的功能丧失变异患者,以描绘 ZNF462 功能丧失的综合征。总的来说,这 24 名患者具有反复发作的表型,定义了一种多种先天性异常综合征。大多数患者存在某种形式的发育迟缓(79%),少数患者患有自闭症谱系障碍(33%)。特征性面部特征包括上睑下垂(83%)、下斜的睑裂(58%)、夸大的丘比特弓/宽人中(54%)和拱形眉毛(50%)。三分之一的研究参与者存在额骨嵴或颅缝早闭,一半存在喂养问题。其他表型特征包括 25%的个体存在胼胝体发育不全、一半存在张力减退和 21%存在结构性心脏缺陷。使用面部分析技术,一种应用深度学习的计算机算法能够准确地区分 ZNF462 功能丧失变异患者与 Noonan 综合征患者和健康对照者。总之,我们描述了一种与 ZNF462 杂合不足相关的多种先天性异常综合征,具有独特的临床特征和面部特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be11/6935050/84be75b8e8dc/nihms-1063502-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be11/6935050/d7a68a5f2e5a/nihms-1063502-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be11/6935050/84be75b8e8dc/nihms-1063502-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be11/6935050/d7a68a5f2e5a/nihms-1063502-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be11/6935050/84be75b8e8dc/nihms-1063502-f0002.jpg

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本文引用的文献

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2
ZNF462 and KLF12 are disrupted by a de novo translocation in a patient with syndromic intellectual disability and autism spectrum disorder.在一名患有综合征性智力障碍和自闭症谱系障碍的患者中,ZNF462和KLF12因新发易位而被破坏。
Eur J Med Genet. 2018 Jul;61(7):376-383. doi: 10.1016/j.ejmg.2018.02.002. Epub 2018 Feb 7.
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Haploinsufficiency of ZNF462 is associated with craniofacial anomalies, corpus callosum dysgenesis, ptosis, and developmental delay.
分析两例 Weiss-Kruszka 综合征家系的临床表型和遗传变异。
BMC Med Genomics. 2024 Nov 5;17(1):261. doi: 10.1186/s12920-024-02035-x.
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Common variants increase risk for congenital diaphragmatic hernia within the context of de novo variants.常见变异在新生变异的背景下增加先天性膈疝的风险。
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