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Publication : Disruption of Apc10/Doc1 in three alleles of oligosyndactylism.

First Author  Pravtcheva DD Year  2001
Journal  Genomics Volume  72
Issue  1 Pages  78-87
PubMed ID  11247669 Mgi Jnum  J:81567
Mgi Id  MGI:2449564 Doi  10.1006/geno.2001.6474
Citation  Pravtcheva DD, et al. (2001) Disruption of Apc10/Doc1 in three alleles of oligosyndactylism. Genomics 72(1):78-87
abstractText  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.
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