| Literature DB >> 8327517 |
Q Ma1, H Alder, K K Nelson, D Chatterjee, Y Gu, T Nakamura, E Canaani, C M Croce, L D Siracusa, A M Buchberg.
Abstract
A series of translocation break points found in a subset of human acute leukemias have one of the breaks on human chromosome 11q23. This region has recently been cloned and a large gene, ALL-1, with homology to the Drosophila trithorax gene has been identified. This paper describes the cloning, sequencing, and mapping of the mouse homolog of ALL-1. We have found a motif present in All-1 that shows homology to the zinc-binding domain of DNA (cytosine-5) methyltransferases (EC 2.1.1.63). Sequence analysis of the murine All-1 gene has identified distinct regions of homology with the human ALL-1 gene; these highly conserved domains may define regions of functional significance in mammals. In addition, we have identified alternatively spliced forms of All-1 within one of the zinc-finger domains, suggesting that there may be different targets and/or functions for All-1 proteins. Finally, we report that All-1 resides in the proximal portion of mouse chromosome 9 and is a candidate for a mutation that results in skeletal transformations during embryonic development.Entities:
Mesh:
Substances:
Year: 1993 PMID: 8327517 PMCID: PMC46926 DOI: 10.1073/pnas.90.13.6350
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205