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P53 gene deficiency does not enhance instability of mouse minisatellites in somatic cells of normal tissues.P53基因缺陷不会增强正常组织体细胞中小鼠微卫星的不稳定性。
Jpn J Cancer Res. 1996 Jul;87(7):696-701. doi: 10.1111/j.1349-7006.1996.tb00280.x.
2
Two mouse hypervariable minisatellites: chromosomal location and simultaneous mutation.两种小鼠高变微卫星：染色体定位与同步突变
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Minisatellites show rare and simple intra-allelic instability in the mouse germ line.微卫星在小鼠生殖系中表现出罕见且简单的等位基因内不稳定性。
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Somatic versus germline mutation processes at minisatellite CEB1 (D2S90) in humans and transgenic mice.人类和转基因小鼠中微小卫星CEB1（D2S90）的体细胞与种系突变过程
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p53 deficiency does not affect mutation rate in the mouse germline.p53基因缺陷不影响小鼠种系的突变率。
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p53 wild-type and p53 nullizygous Big Blue transgenic mice have similar frequencies and patterns of observed mutation in liver, spleen and brain.p53野生型和p53纯合缺失的大蓝转基因小鼠在肝脏、脾脏和大脑中观察到的突变频率和模式相似。
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Spontaneous mutation at the hypervariable mouse minisatellite locus Ms6-hm: flanking DNA sequence and analysis of germline and early somatic mutation events.高变小鼠微卫星位点Ms6-hm的自发突变：侧翼DNA序列及种系和早期体细胞突变事件分析
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本文引用的文献

1
Accumulation of p53 protein in human esophageal precancerous lesions: a possible early biomarker for carcinogenesis.人食管癌前病变中p53蛋白的积累：一种可能的癌变早期生物标志物。
Cancer Res. 1993 Apr 15;53(8):1783-7.
2
The p53 tumor suppressor gene as a common cellular target in human carcinogenesis.p53肿瘤抑制基因作为人类致癌过程中的常见细胞靶点。
Am J Gastroenterol. 1993 Feb;88(2):174-86.
3
Spontaneous and carcinogen-induced tumorigenesis in p53-deficient mice.p53基因缺陷小鼠的自发及致癌物诱导的肿瘤发生
Nat Genet. 1993 Nov;5(3):225-9. doi: 10.1038/ng1193-225.
4
Two mouse hypervariable minisatellites: chromosomal location and simultaneous mutation.两种小鼠高变微卫星：染色体定位与同步突变
J Biochem. 1993 Aug;114(2):292-6. doi: 10.1093/oxfordjournals.jbchem.a124169.
5
2-Hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine induction of recombinational mutations in mammalian cell lines as detected by DNA fingerprinting.通过DNA指纹图谱检测2-羟基氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶在哺乳动物细胞系中诱导的重组突变。
Mol Carcinog. 1994 Feb;9(2):67-70. doi: 10.1002/mc.2940090203.
6
Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis.p53肿瘤抑制基因的突变：癌症病因学和分子发病机制的线索
Cancer Res. 1994 Sep 15;54(18):4855-78.
7
p53 tumor suppressor gene mutation in early esophageal precancerous lesions and carcinoma among high-risk populations in Henan, China.中国河南高危人群早期食管前病变和癌组织中p53抑癌基因突变情况
Cancer Res. 1994 Aug 15;54(16):4342-6.
8
Cell cycle control and cancer.细胞周期调控与癌症。
Science. 1994 Dec 16;266(5192):1821-8. doi: 10.1126/science.7997877.
9
A genetic map of the mouse with 4,006 simple sequence length polymorphisms.一张具有4006个简单序列长度多态性的小鼠遗传图谱。
Nat Genet. 1994 Jun;7(2 Spec No):220-45. doi: 10.1038/ng0694supp-220.
10
Enhanced proliferative potential in culture of cells from p53-deficient mice.p53基因缺陷型小鼠细胞在培养中的增殖潜能增强。
Oncogene. 1993 Dec;8(12):3313-22.

P53基因缺陷不会增强正常组织体细胞中小鼠微卫星的不稳定性。

P53 gene deficiency does not enhance instability of mouse minisatellites in somatic cells of normal tissues.

作者信息

Ohashi M, Hatakeyama K, Aizawa S, Kominami R

机构信息

First Department of Biochemistry, Niigata University School of Medicine.

出版信息

Jpn J Cancer Res. 1996 Jul;87(7):696-701. doi: 10.1111/j.1349-7006.1996.tb00280.x.

DOI:10.1111/j.1349-7006.1996.tb00280.x
PMID:8698618
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5921163/
Abstract

The effect of p53-deficiency on somatic mutation of minisatellites in normal tissues was examined using p53-deficient (-/-) mice. In total, 248 mice consisting of three different genotypes, +/+, +/ -and -/-, were obtained and DNA from their embryos was probed with two minisatellites, Pc-1 and Pc-2. The somatic mutation was detected by Southern blot hybridization as the presence of a third nonparental band reflecting mosaicism in tissues. Mutation frequency of Pc-1 for (+/+) and (+/-) was 1.3% and 1.4%, respectively, which is consistent with previous studies. On the other hand, none of the mice lacking the p53 gene (-/-) exhibited mutation. The Pc-2 probe did not show any somatic mutation in the three groups. These results suggest that the p53 deficiency does not enhance the genomic instability of the minisatellite loci in normal somatic cells.

摘要

利用p53基因缺陷型（-/-）小鼠，研究了p53基因缺陷对正常组织中微卫星体细胞突变的影响。总共获得了248只具有三种不同基因型（+/+、+/-和-/-）的小鼠，并用两种微卫星Pc-1和Pc-2对其胚胎DNA进行检测。通过Southern印迹杂交检测体细胞突变，以反映组织中嵌合体的第三条非亲本条带的存在。（+/+）和（+/-）小鼠中Pc-1的突变频率分别为1.3%和1.4%，这与先前的研究结果一致。另一方面，缺乏p53基因的小鼠（-/-）均未表现出突变。Pc-2探针在三组中均未显示任何体细胞突变。这些结果表明，p53基因缺陷不会增强正常体细胞中微卫星位点的基因组不稳定性。