• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Evolutionary genomics of human intellectual disability.人类智力残疾的进化基因组学
Evol Appl. 2010 Jan;3(1):52-63. doi: 10.1111/j.1752-4571.2009.00098.x. Epub 2009 Sep 7.
2
Molecular diversity and phenotypic pleiotropy of ancient genomic regulatory loci derived from human endogenous retrovirus type H (HERVH) promoter LTR7 and HERVK promoter LTR5_Hs and their contemporary impacts on pathophysiology of Modern Humans.源自人类内源性逆转录病毒 H 型(HERVH)启动子 LTR7 和 HERVK 启动子 LTR5_Hs 的古老基因组调控位点的分子多样性和表型多效性及其对现代人类病理生理学的当代影响。
Mol Genet Genomics. 2022 Nov;297(6):1711-1740. doi: 10.1007/s00438-022-01954-7. Epub 2022 Sep 19.
3
Understanding the Landscape of X-linked Variants Causing Intellectual Disability in Females Through Extreme X Chromosome Inactivation Skewing.通过极端 X 染色体失活偏斜理解导致女性智力障碍的 X 连锁变异景观。
Mol Neurobiol. 2020 Sep;57(9):3671-3684. doi: 10.1007/s12035-020-01981-8. Epub 2020 Jun 20.
4
Deep sequencing reveals 50 novel genes for recessive cognitive disorders.深度测序揭示 50 个隐性认知障碍的新基因。
Nature. 2011 Sep 21;478(7367):57-63. doi: 10.1038/nature10423.
5
Next-Generation Sequencing Reveals Novel Mutations in X-linked Intellectual Disability.下一代测序揭示X连锁智力障碍中的新突变。
OMICS. 2017 May;21(5):295-303. doi: 10.1089/omi.2017.0009.
6
Network Profiling of Brain-Expressed X-Chromosomal MicroRNA Genes Implicates Shared Key MicroRNAs in Intellectual Disability.脑表达 X 染色体微小 RNA 基因的网络分析提示智力障碍中存在共享关键微小 RNA。
J Mol Neurosci. 2019 Feb;67(2):295-304. doi: 10.1007/s12031-018-1235-7. Epub 2019 Jan 3.
7
X-linked intellectual disability related genes disrupted by balanced X-autosome translocations.因平衡X-常染色体易位而中断的X连锁智力障碍相关基因。
Am J Med Genet B Neuropsychiatr Genet. 2015 Dec;168(8):669-77. doi: 10.1002/ajmg.b.32355. Epub 2015 Aug 20.
8
Non-syndromic X linked intellectual disability: Current knowledge in light of the recent advances in molecular and functional studies.X 连锁非综合征性智力障碍:分子和功能研究新进展的现状。
Clin Genet. 2020 May;97(5):677-687. doi: 10.1111/cge.13698. Epub 2020 Jan 9.
9
The neurobiology of X-linked intellectual disability.X 连锁智力障碍的神经生物学
Neuroscientist. 2013 Oct;19(5):541-52. doi: 10.1177/1073858413493972. Epub 2013 Jul 2.
10
Pathogenesis of Börjeson-Forssman-Lehmann syndrome: Insights from PHF6 function.博耶森-福斯曼-莱曼综合征的发病机制:来自PHF6功能的见解。
Neurobiol Dis. 2016 Dec;96:227-235. doi: 10.1016/j.nbd.2016.09.011. Epub 2016 Sep 12.

引用本文的文献

1
Physical-intellectual badminton teaching intervention for children with intellectual disabilities.针对智障儿童的身心-智力羽毛球教学干预
Front Psychol. 2025 Mar 11;16:1445620. doi: 10.3389/fpsyg.2025.1445620. eCollection 2025.
2
Intellectual disability associated with craniofacial dysmorphism due to POLR3B mutation and defect in spliceosomal machinery.由于 POLR3B 突变和剪接体机制缺陷导致的伴有颅面畸形的智力残疾。
BMC Med Genomics. 2022 Apr 18;15(1):89. doi: 10.1186/s12920-022-01237-5.
3
Impaired oxidative stress response characterizes HUWE1-promoted X-linked intellectual disability.HUWE1 促进的 X 连锁智力障碍的特征是氧化应激反应受损。
Sci Rep. 2017 Nov 8;7(1):15050. doi: 10.1038/s41598-017-15380-y.
4
Evolutionary applications summer 2011.《进化应用》2011年夏季刊
Evol Appl. 2011 Sep;4(5):617-20. doi: 10.1111/j.1752-4571.2011.00205.x.
5
Dolphin genome provides evidence for adaptive evolution of nervous system genes and a molecular rate slowdown.海豚基因组为神经系统基因的适应性进化和分子速率减缓提供了证据。
Proc Biol Sci. 2012 Sep 22;279(1743):3643-51. doi: 10.1098/rspb.2012.0869. Epub 2012 Jun 27.

本文引用的文献

1
The genetic landscape of intellectual disability arising from chromosome X.由X染色体引发的智力残疾的遗传图谱。
Trends Genet. 2009 Jul;25(7):308-16. doi: 10.1016/j.tig.2009.05.002. Epub 2009 Jun 24.
2
Haploinsufficiency of DNA Damage Response Genes and their Potential Influence in Human Genomic Disorders.DNA 损伤反应基因单倍不足及其在人类基因组疾病中的潜在影响。
Curr Genomics. 2008 May;9(3):137-46. doi: 10.2174/138920208784340795.
3
Brca1 is required for embryonic development of the mouse cerebral cortex to normal size by preventing apoptosis of early neural progenitors.通过防止早期神经祖细胞凋亡,Brca1对于小鼠大脑皮质胚胎发育至正常大小是必需的。
Development. 2009 Jun;136(11):1859-68. doi: 10.1242/dev.033498. Epub 2009 Apr 29.
4
A systematic, large-scale resequencing screen of X-chromosome coding exons in mental retardation.一项针对智力障碍中X染色体编码外显子的系统性大规模重测序筛查。
Nat Genet. 2009 May;41(5):535-43. doi: 10.1038/ng.367. Epub 2009 Apr 19.
5
Genetic foundations of human intelligence.人类智力的遗传基础。
Hum Genet. 2009 Jul;126(1):215-32. doi: 10.1007/s00439-009-0655-4. Epub 2009 Mar 18.
6
Mutations of CASK cause an X-linked brain malformation phenotype with microcephaly and hypoplasia of the brainstem and cerebellum.CASK基因的突变会导致一种X连锁的脑畸形表型,伴有小头畸形以及脑干和小脑发育不全。
Nat Genet. 2008 Sep;40(9):1065-7. doi: 10.1038/ng.194.
7
Replication independent ATR signalling leads to G2/M arrest requiring Nbs1, 53BP1 and MDC1.不依赖复制的ATR信号传导导致G2/M期阻滞,这需要Nbs1、53BP1和MDC1。
Hum Mol Genet. 2008 Oct 15;17(20):3247-53. doi: 10.1093/hmg/ddn220. Epub 2008 Jul 28.
8
Role of Fanconi DNA repair pathway in neural stem cell homeostasis.范可尼DNA修复途径在神经干细胞稳态中的作用。
Cell Cycle. 2008 Jul 1;7(13):1911-5. doi: 10.4161/cc.7.13.6235. Epub 2008 May 5.
9
Tissue-specific accelerated aging in nucleotide excision repair deficiency.核苷酸切除修复缺陷中的组织特异性加速衰老。
Mech Ageing Dev. 2008 Jul-Aug;129(7-8):408-15. doi: 10.1016/j.mad.2008.04.010. Epub 2008 May 1.
10
Cognitive functioning and survival in the elderly: the SSADH C538T polymorphism.老年人的认知功能与生存:SSADH基因C538T多态性
Ann Hum Genet. 2008 Sep;72(Pt 5):630-5. doi: 10.1111/j.1469-1809.2008.00450.x. Epub 2008 May 23.

人类智力残疾的进化基因组学

Evolutionary genomics of human intellectual disability.

作者信息

Crespi Bernard, Summers Kyle, Dorus Steve

机构信息

Department of Biosciences, Simon Fraser University Burnaby, BC, Canada.

Department of Biology, East Carolina University Greenville, NC, USA.

出版信息

Evol Appl. 2010 Jan;3(1):52-63. doi: 10.1111/j.1752-4571.2009.00098.x. Epub 2009 Sep 7.

DOI:10.1111/j.1752-4571.2009.00098.x
PMID:25567903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3352458/
Abstract

Previous studies have postulated that X-linked and autosomal genes underlying human intellectual disability may have also mediated the evolution of human cognition. We have conducted the first comprehensive assessment of the extent and patterns of positive Darwinian selection on intellectual disability genes in humans. We report three main findings. First, as noted in some previous reports, intellectual disability genes with primary functions in the central nervous system exhibit a significant concentration to the X chromosome. Second, there was no evidence for a higher incidence of recent positive selection on X-linked than autosomal intellectual disability genes, nor was there a higher incidence of selection on such genes overall, compared to sets of control genes. However, the X-linked intellectual disability genes inferred to be subject to recent positive selection were concentrated in the Rho GTP-ase pathway, a key signaling pathway in neural development and function. Third, among all intellectual disability genes, there was evidence for a higher incidence of recent positive selection on genes involved in DNA repair, but not for genes involved in other functions. These results provide evidence that alterations to genes in the Rho GTP-ase and DNA-repair pathways may play especially-important roles in the evolution of human cognition and vulnerability to genetically-based intellectual disability.

摘要

先前的研究推测,导致人类智力残疾的X连锁基因和常染色体基因可能也介导了人类认知能力的进化。我们首次对人类智力残疾基因上正向达尔文选择的程度和模式进行了全面评估。我们报告了三个主要发现。第一,正如之前一些报告所指出的,在中枢神经系统中具有主要功能的智力残疾基因在X染色体上显著富集。第二,没有证据表明X连锁智力残疾基因比常染色体智力残疾基因有更高的近期正向选择发生率,与对照基因集相比,这类基因总体上也没有更高的选择发生率。然而,推断受到近期正向选择的X连锁智力残疾基因集中在Rho GTP酶途径,这是神经发育和功能中的一个关键信号通路。第三,在所有智力残疾基因中,有证据表明参与DNA修复的基因有更高的近期正向选择发生率,但参与其他功能的基因则没有。这些结果提供了证据,表明Rho GTP酶和DNA修复途径中的基因改变可能在人类认知能力的进化以及对基于基因的智力残疾的易感性方面发挥特别重要的作用。