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首页> 外文期刊>Genomics >Disruption of Apc10/Doc1 in three alleles of oligosyndactylism.
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Disruption of Apc10/Doc1 in three alleles of oligosyndactylism.

机译:Apc10 / Doc1在寡聚寡核苷酸的三个等位基因中的破坏。

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摘要

Oligosyndactylism (Os) is a radiation-induced mouse mutation associated with recessive lethality and a dominant effect on limb and kidney development. The lethal effect of the mutation is due to a cell-autonomous block in the transition from metaphase to anaphase. We have previously characterized two transgene-induced mutations, 94-A and 94-K, which are allelic with Os. These mutations facilitated the identification of genomic segments and transcribed sequences in the affected region. One of the transcripts in this region corresponds to the mouse homolog of the anaphase-promoting complex component APC10/DOC1. The disruption of this gene can explain the mitotic arrest phenotype of all three alleles of Os. Copyright 2001 Academic Press.
机译:少突触症(Os)是一种辐射诱发的小鼠突变,与隐性致死率相关,对肢体和肾脏发育起主要作用。突变的致死作用是由于从中期到后期的过渡过程中的细胞自主阻滞。我们以前已经表征了两个转基因诱导的突变,即94-A和94-K,它们与Os等位基因相同。这些突变有助于在受影响区域中鉴定基因组片段和转录序列。该区域中的转录物之一对应于后期促进复杂成分APC10 / DOC1的小鼠同源物。该基因的破坏可以解释Os所有三个等位基因的有丝分裂停滞表型。版权所有2001学术出版社。

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