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Expression and differential splicing of the mouse TSC2 homolog.

作者信息

Olsson P G, Schofield J N, Edwards Y H, Frischauf A M

机构信息

Imperial Cancer Research Fund, London, UK.

出版信息

Mamm Genome. 1996 Mar;7(3):212-5. doi: 10.1007/s003359900057.

DOI:10.1007/s003359900057
PMID:8833243
Abstract
摘要

相似文献

1
Expression and differential splicing of the mouse TSC2 homolog.小鼠TSC2同源物的表达与差异剪接
Mamm Genome. 1996 Mar;7(3):212-5. doi: 10.1007/s003359900057.
2
Comparative analysis and genomic structure of the tuberous sclerosis 2 (TSC2) gene in human and pufferfish.
Hum Mol Genet. 1996 Jan;5(1):131-7. doi: 10.1093/hmg/5.1.131.
3
The GAP-related domain of tuberin, the product of the TSC2 gene, is a target for missense mutations in tuberous sclerosis.结节性硬化症中，TSC2基因产物结节蛋白的GAP相关结构域是错义突变的靶点。
Hum Mol Genet. 1997 Oct;6(11):1991-6. doi: 10.1093/hmg/6.11.1991.
4
Alternative splicing of the tuberous sclerosis 2 (TSC2) gene in human and mouse tissues.
Genomics. 1995 Jun 10;27(3):475-80. doi: 10.1006/geno.1995.1079.
5
Expression of the tuberous sclerosis 2 gene product, tuberin, in adult and developing nervous system tissues.结节性硬化症2基因产物结节蛋白在成人及发育中的神经系统组织中的表达。
Neurobiol Dis. 1996 Apr;3(2):111-20. doi: 10.1006/nbdi.1996.0011.
6
Identification of cDNAs induced by the tumor suppressor Tsc2 gene using a conditional expression system in Tsc2 mutant (Eker) rat renal carcinoma cells.在Tsc2突变（Eker）大鼠肾癌细胞中使用条件表达系统鉴定由肿瘤抑制基因Tsc2诱导的cDNA。
Biochem Biophys Res Commun. 1998 Jun 29;247(3):728-33. doi: 10.1006/bbrc.1998.8853.
7
Cloning, developmental expression, and evidence for alternative splicing of the murine tuberous sclerosis (TSC2) gene product.
Cell Mol Biol Res. 1995;41(6):515-26.
8
Identification of tuberous sclerosis 2 messenger RNA splice variants that are conserved and differentially expressed in rat and human tissues.结节性硬化症2信使核糖核酸剪接变体的鉴定，这些变体在大鼠和人类组织中保守且差异表达。
Cell Growth Differ. 1995 Sep;6(9):1185-91.
9
Cloning and evaluation of RALGDS as a candidate for the tuberous sclerosis gene TSC1.将RALGDS作为结节性硬化症基因TSC1候选基因的克隆与评估
Ann Hum Genet. 1997 Jul;61(Pt 4):299-305. doi: 10.1046/j.1469-1809.1997.6140299.x.
10
Characterisation of a novel TSC2 missense mutation in the GAP related domain associated with minimal clinical manifestations of tuberous sclerosis.与结节性硬化症最小临床表现相关的GAP相关结构域中一种新型TSC2错义突变的特征分析
J Med Genet. 2004 May;41(5):e64. doi: 10.1136/jmg.2003.010835.

引用本文的文献

1
Variants Within TSC2 Exons 25 and 31 Are Very Unlikely to Cause Clinically Diagnosable Tuberous Sclerosis.TSC2基因第25和31外显子内的变异极不可能导致临床可诊断的结节性硬化症。
Hum Mutat. 2016 Apr;37(4):364-70. doi: 10.1002/humu.22951. Epub 2016 Jan 12.
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Rho-associated kinase connects a cell cycle-controlling anchorage signal to the mammalian target of rapamycin pathway.Rho 相关激酶将细胞周期调控的锚定信号与哺乳动物雷帕霉素靶蛋白通路连接起来。
J Biol Chem. 2011 Jul 1;286(26):23132-41. doi: 10.1074/jbc.M110.209114. Epub 2011 May 11.
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Growth controls connect: interactions between c-myc and the tuberous sclerosis complex-mTOR pathway.

本文引用的文献

1
Identification of a ten-amino acid proline-rich SH3 binding site.鉴定一个富含脯氨酸的十氨基酸SH3结合位点。
Science. 1993 Feb 19;259(5098):1157-61. doi: 10.1126/science.8438166.
2
Spontaneous and radiation-induced renal tumors in the Eker rat model of dominantly inherited cancer.在显性遗传癌症的埃克大鼠模型中自发和辐射诱导的肾肿瘤。
Proc Natl Acad Sci U S A. 1993 Jan 1;90(1):327-31. doi: 10.1073/pnas.90.1.327.
3
Identification and characterization of the tuberous sclerosis gene on chromosome 16.16号染色体上结节性硬化症基因的鉴定与特征分析
生长调控相互关联：c-myc与结节性硬化症复合物-mTOR信号通路之间的相互作用
Cell Cycle. 2009 May 1;8(9):1344-51. doi: 10.4161/cc.8.9.8215. Epub 2009 May 18.
4
Survey of somatic mutations in tuberous sclerosis complex (TSC) hamartomas suggests different genetic mechanisms for pathogenesis of TSC lesions.结节性硬化症（TSC）错构瘤体细胞突变的调查表明TSC病变发病机制存在不同的遗传机制。
Am J Hum Genet. 2001 Sep;69(3):493-503. doi: 10.1086/321972. Epub 2001 Jul 20.
5
Identification of a leader exon and a core promoter for the rat tuberous sclerosis 2 (Tsc2) gene and structural comparison with the human homolog.
Mamm Genome. 1997 Aug;8(8):554-8. doi: 10.1007/s003359900502.
6
Intragenic Tsc2 somatic mutations as Knudson's second hit in spontaneous and chemically induced renal carcinomas in the Eker rat model.基因内Tsc2体细胞突变作为克努森二次打击，出现在埃克大鼠模型的自发性和化学诱导性肾癌中。
Jpn J Cancer Res. 1997 Mar;88(3):254-61. doi: 10.1111/j.1349-7006.1997.tb00375.x.
7
Transgenic rescue from embryonic lethality and renal carcinogenesis in the Eker rat model by introduction of a wild-type Tsc2 gene.通过导入野生型Tsc2基因对Eker大鼠模型中的胚胎致死性和肾致癌作用进行转基因拯救。
Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3990-3. doi: 10.1073/pnas.94.8.3990.
Cell. 1993 Dec 31;75(7):1305-15. doi: 10.1016/0092-8674(93)90618-z.
4
Allelic loss at the predisposing gene locus in spontaneous and chemically induced renal cell carcinomas in the Eker rat.Eker大鼠自发性和化学诱导性肾细胞癌中易感基因座的等位基因缺失。
Cancer Res. 1994 May 15;54(10):2633-5.
5
Predisposition to renal carcinoma in the Eker rat is determined by germ-line mutation of the tuberous sclerosis 2 (TSC2) gene.艾克大鼠患肾癌的易感性由结节性硬化症2（TSC2）基因的种系突变决定。
Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11413-6. doi: 10.1073/pnas.91.24.11413.
6
The molecular genetics of tuberous sclerosis.
Hum Mol Genet. 1994;3 Spec No:1477-80. doi: 10.1093/hmg/3.suppl_1.1477.
7
9q34 loss of heterozygosity in a tuberous sclerosis astrocytoma suggests a growth suppressor-like activity also for the TSC1 gene.结节性硬化星形细胞瘤中9号染色体长臂34区杂合性缺失表明TSC1基因也具有类似生长抑制因子的活性。
Hum Mol Genet. 1994 Oct;3(10):1829-32. doi: 10.1093/hmg/3.10.1829.
8
The mouse homologue of the tuberin gene (TSC2) maps to a conserved synteny group between mouse chromosome 17 and human 16p13.3.结节性硬化症2基因（TSC2）的小鼠同源基因定位于小鼠17号染色体与人类16p13.3之间的一个保守同线群。
Genomics. 1995 Jan 1;25(1):339-40. doi: 10.1016/0888-7543(95)80159-j.
9
A germline insertion in the tuberous sclerosis (Tsc2) gene gives rise to the Eker rat model of dominantly inherited cancer.结节性硬化症（Tsc2）基因中的种系插入导致了显性遗传癌症的埃克大鼠模型。
Nat Genet. 1995 Jan;9(1):70-4. doi: 10.1038/ng0195-70.
10
cDNA structure, alternative splicing and exon-intron organization of the predisposing tuberous sclerosis (Tsc2) gene of the Eker rat model.埃克大鼠模型中结节性硬化症易感基因（Tsc2）的cDNA结构、可变剪接及外显子-内含子组织形式
Nucleic Acids Res. 1995 Jul 25;23(14):2608-13. doi: 10.1093/nar/23.14.2608.