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2
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本文引用的文献

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The secretory phospholipase A2 gene is a candidate for the Mom1 locus, a major modifier of ApcMin-induced intestinal neoplasia.分泌型磷脂酶A2基因是Mom1位点的一个候选基因,Mom1位点是ApcMin诱导的肠道肿瘤形成的主要修饰因子。
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Suppression of intestinal neoplasia by DNA hypomethylation.DNA低甲基化对肠道肿瘤的抑制作用。
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DNA fingerprints applied to gene introgression in breeding programs.应用于育种计划中基因渐渗的DNA指纹图谱。
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A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse.一种导致小鼠发生多发性肠道肿瘤的显性突变。
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7
The Min (multiple intestinal neoplasia) mutation: its effect on gut epithelial cell differentiation and interaction with a modifier system.Min(多发性肠道肿瘤)突变:其对肠道上皮细胞分化的影响以及与修饰系统的相互作用。
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Using markers in gene introgression breeding programs.在基因渐渗育种计划中使用标记。
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9
A genetic map of the mouse suitable for typing intraspecific crosses.一张适用于种内杂交分型的小鼠遗传图谱。
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Mom1是Min/+小鼠肠道腺瘤大小和数量的半显性修饰基因。

Mom1 is a semi-dominant modifier of intestinal adenoma size and multiplicity in Min/+ mice.

作者信息

Gould K A, Dietrich W F, Borenstein N, Lander E S, Dove W F

机构信息

McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706, USA.

出版信息

Genetics. 1996 Dec;144(4):1769-76. doi: 10.1093/genetics/144.4.1769.

DOI:10.1093/genetics/144.4.1769
PMID:8978062
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1207726/
Abstract

The intestinal tumor multiplicity in mice heterozygous for ApcMin is strongly modulated by genetic background. On the sensitive C57BL/6J (B6) background, mice develop large numbers of intestinal adenomas. The AKR/J (AKR) strain carries alleles that correlate with a strong reduction in tumor multiplicity. To study the effect of one of these modifiers, Mom1, we have generated a mouse line in which the AKR allele of Mom1 is carried on the sensitive B6 genetic background. This strain was produced by using a marker-assisted selection method to eliminate unlinked AKR alleles more rapidly. The application and efficiency of this method are discussed. We used this strain to determine that Mom1 affects both tumor multiplicity and tumor size in a semi-dominant fashion.

摘要

ApcMin杂合子小鼠的肠道肿瘤多发性受到遗传背景的强烈调控。在敏感的C57BL/6J(B6)背景下,小鼠会产生大量肠道腺瘤。AKR/J(AKR)品系携带的等位基因与肿瘤多发性的显著降低相关。为了研究其中一个修饰基因Mom1的作用,我们培育了一个小鼠品系,其Mom1的AKR等位基因位于敏感的B6遗传背景上。该品系是通过使用标记辅助选择方法更快地消除不连锁的AKR等位基因而产生的。本文讨论了该方法的应用及效率。我们使用这个品系确定Mom1以半显性方式影响肿瘤多发性和肿瘤大小。