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一个66个碱基对的插入片段连接了导致β地中海贫血小鼠模型的缺失区域。

A 66-base pair insert bridges the deletion responsible for a mouse model of beta-thalassemia.

作者信息

Goldberg S Z, Kuebbing D, Trauber D, Schafer M P, Lewis S E, Popp R A, Anderson W F

出版信息

J Biol Chem. 1986 Sep 15;261(26):12368-74.

PMID:3017971
Abstract

The breakpoints of the deletion responsible for the Hbb(th-1) mouse model of beta-thalassemia have been isolated. A 3709 (+/- 2)-base pair (bp) region, including the entire beta major globin gene and 2 kilobases of 5' flanking region, is deleted. A novel 66 (+/- 2)-bp sequence, ending in a stretch of 25 dA:dT base pairs, was found to bridge the deletion. A region of the normal murine genome, containing the first 43 bp of the deletion-associated insert (DAI), but lacking the 25-bp dA:dT sequence, was isolated. All normal mice tested contain this DAI-like element and several inbred strains contain an additional DAI-like element. The sequence spanning the Hbb(th-1) deletion may be a reverse transcript of this region.

摘要

导致β地中海贫血Hbb(th-1)小鼠模型的缺失断点已被分离出来。一个3709(±2)碱基对(bp)的区域被删除,该区域包括整个β-珠蛋白基因和2千碱基对的5'侧翼区域。发现一个新的66(±2)bp序列,以一段25个dA:dT碱基对结尾,用于连接该缺失区域。分离出了正常小鼠基因组的一个区域,该区域包含缺失相关插入片段(DAI)的前43 bp,但缺少25 bp的dA:dT序列。所有测试的正常小鼠都含有这种DAI样元件,几个近交系还含有另一种DAI样元件。跨越Hbb(th-1)缺失区域的序列可能是该区域的逆转录产物。

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