小鼠突变体多指名古屋（Pdn）定义了锌指基因Gli3的一个新等位基因。 - Suppr

Suppr

超能文献

The mouse mutant Polydactyly Nagoya (Pdn) defines a novel allele of the zinc finger gene Gli3.

作者信息

Schimmang T, Oda S I, Rüther U

机构信息

European Molecular Biology Laboratory, Heidelberg, Germany.

出版信息

Mamm Genome. 1994 Jun;5(6):384-6. doi: 10.1007/BF00356560.

DOI:10.1007/BF00356560

PMID:8043956

Abstract

摘要

相似文献

The mouse mutant Polydactyly Nagoya (Pdn) defines a novel allele of the zinc finger gene Gli3.小鼠突变体多指名古屋（Pdn）定义了锌指基因Gli3的一个新等位基因。

Mamm Genome. 1994 Jun;5(6):384-6. doi: 10.1007/BF00356560.

The mouse mutation Pdn (Polydactyly Nagoya) is caused by the integration of a retrotransposon into the Gli3 gene.

Mamm Genome. 1999 Mar;10(3):205-9. doi: 10.1007/s003359900973.

Birth defects caused by mutations in human GLI3 and mouse Gli3 genes.人类GLI3基因和小鼠Gli3基因突变导致的出生缺陷。

Congenit Anom (Kyoto). 2010 Mar;50(1):1-7. doi: 10.1111/j.1741-4520.2009.00266.x.

Expression of the zinc finger gene Gli3 is affected in the morphogenetic mouse mutant extra-toes (Xt).锌指基因Gli3的表达在形态发生的小鼠突变体多趾（Xt）中受到影响。

Development. 1992 Nov;116(3):799-804. doi: 10.1242/dev.116.3.799.

Molecular linkage of the morphogenetic mutation add and the zinc finger gene Gli3.形态发生突变add与锌指基因Gli3的分子连锁

Mamm Genome. 1993;4(5):276-7. doi: 10.1007/BF00417435.

Zfp-51, a murine zinc finger encoding gene mapping to the t-complex region of chromosome 17, encodes 19 contiguous zinc fingers and is ubiquitously expressed.锌指蛋白51（Zfp-51）是一种小鼠锌指编码基因，定位于17号染色体的t复合区域，编码19个连续的锌指结构，且在全身广泛表达。

Mamm Genome. 1994 Jun;5(6):387-9. doi: 10.1007/BF00356561.

Point mutations throughout the GLI3 gene cause Greig cephalopolysyndactyly syndrome.GLI3基因上的点突变会导致Greig头多指（趾）综合征。

Hum Mol Genet. 1999 Sep;8(9):1769-77. doi: 10.1093/hmg/8.9.1769.

Exencephaly induction by valproic acid in the genetic polydactyly/arhinencephaly mouse, Pdn/Pdn.丙戊酸在遗传性多指/无脑小鼠Pdn/Pdn中诱导无脑畸形

Congenit Anom (Kyoto). 2005 Dec;45(4):132-6. doi: 10.1111/j.1741-4520.2005.00082.x.

Neuro-glial neurotrophic interaction in the S-100 beta retarded mutant mouse (Polydactyly Nagoya). III. Transplantation study.

Brain Res. 1996 Oct 28;738(1):15-23. doi: 10.1016/0006-8993(96)00758-5.

Gli3 expression is affected in the morphogenetic mouse mutants add and Xt.Gli3基因的表达在形态发生小鼠突变体add和Xt中受到影响。

Prog Clin Biol Res. 1993;383A:153-61.

引用本文的文献

Identification and functional characterization of novel transcriptional enhancers involved in regulating human GLI3 expression during early development.早期发育过程中参与调控人类GLI3表达的新型转录增强子的鉴定与功能表征

Dev Growth Differ. 2015 Oct;57(8):570-80. doi: 10.1111/dgd.12239. Epub 2015 Oct 14.

Human intronic enhancers control distinct sub-domains of Gli3 expression during mouse CNS and limb development.人类内含子增强子在小鼠中枢神经系统和肢体发育过程中控制Gli3表达的不同亚结构域。

BMC Dev Biol. 2010 Apr 28;10:44. doi: 10.1186/1471-213X-10-44.

Human GLI3 intragenic conserved non-coding sequences are tissue-specific enhancers.人类 GLI3 基因内保守的非编码序列是组织特异性增强子。

PLoS One. 2007 Apr 11;2(4):e366. doi: 10.1371/journal.pone.0000366.

The phenotypic spectrum of GLI3 morphopathies includes autosomal dominant preaxial polydactyly type-IV and postaxial polydactyly type-A/B; No phenotype prediction from the position of GLI3 mutations.GLI3形态病变的表型谱包括常染色体显性遗传的IV型轴前多指畸形和A/B型轴后多指畸形；无法根据GLI3突变的位置预测表型。

Am J Hum Genet. 1999 Sep;65(3):645-55. doi: 10.1086/302557.

本文引用的文献

Molecular linkage of the morphogenetic mutation add and the zinc finger gene Gli3.形态发生突变add与锌指基因Gli3的分子连锁

Mamm Genome. 1993;4(5):276-7. doi: 10.1007/BF00417435.

Mutations in the paired domain of the human PAX3 gene cause Klein-Waardenburg syndrome (WS-III) as well as Waardenburg syndrome type I (WS-I).人类PAX3基因配对结构域中的突变会导致克莱因-瓦尔登堡综合征（WS-III）以及I型瓦尔登堡综合征（WS-I）。

Am J Hum Genet. 1993 Mar;52(3):455-62.

A mouse model of greig cephalopolysyndactyly syndrome: the extra-toesJ mutation contains an intragenic deletion of the Gli3 gene.格里格头多指综合征的小鼠模型：额外脚趾J突变包含Gli3基因的基因内缺失。

Nat Genet. 1993 Mar;3(3):241-6. doi: 10.1038/ng0393-241.

Polydactyly Nagoya, Pdn: A new mutant gene in the mouse.多指（趾）名古屋型，Pdn：小鼠中的一个新突变基因。

Jikken Dobutsu. 1980 Oct;29(4):391-5. doi: 10.1538/expanim1978.29.4_391.

Occurrences and linkage relations of the mutant "extra-toes" in the mouse.

Genet Res. 1967 Jun;9(3):383-5. doi: 10.1017/s0016672300010673.

Extra-toes: anew mutant gene causing multiple abnormalities in the mouse.

J Embryol Exp Morphol. 1967 Jun;17(3):543-81.

Greig cephalopolysyndactyly syndrome: a possible mouse homologue (Xt-extra toes).格雷格头多指（趾）综合征：一种可能的小鼠同源物（Xt-额外脚趾）

Am J Med Genet. 1988 Dec;31(4):793-8. doi: 10.1002/ajmg.1320310411.

Developmental brain abnormalities accompanied with the retarded production of S-100 beta protein in genetic polydactyly mice.遗传性多指畸形小鼠中伴有S-100β蛋白产生延迟的发育性脑异常。

Brain Res Dev Brain Res. 1990 Feb 1;51(2):253-8. doi: 10.1016/0165-3806(90)90283-5.

GLI3 encodes a 190-kilodalton protein with multiple regions of GLI similarity.GLI3编码一种190千道尔顿的蛋白质，具有多个与GLI相似的区域。

Mol Cell Biol. 1990 Oct;10(10):5408-15. doi: 10.1128/mcb.10.10.5408-5415.1990.

Evidence for allelism of the recessive insertional mutation add and the dominant mouse mutation extra-toes (Xt).

Development. 1990 Dec;110(4):1153-7. doi: 10.1242/dev.110.4.1153.

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