Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A recent work published in Molecular Immunology examined the editing activity of activation-induced deaminase (AID) in yeast (Krause, K., Marcu, K.B., Greeve, J., 2006. The cytidine deaminases AID and APOBEC-1 exhibit distinct functional properties in a novel yeast selectable system.
Mol
. Immunol.). It was proposed that expression of AID in yeast is not sufficient for the generation of point mutations in a highly transcribed gene due to the lack of cofactors for AID-induced somatic hypermutation, which are unique to B cells. It was suggested that, on its own, AID does not have an intrinsic specificity for its target sequences. However, it has been shown previously that expression of the human AID gene in yeast was moderately mutagenic in a wild-type strain and highly mutagenic in an ung1 uracil-DNA glycosylase-deficient strain (Mayorov, V.I., Rogozin, I.B., Adkison, L.R., Frahm, C.R., Kunkel T.A., Pavlov Y. I., 2005. Expression of human AID in yeast induces mutations in context similar to the context of somatic hypermutation at G-C pairs in immunoglobulin genes.
BMC
Immunol. 6, 10; Poltoratsky, V.P., Wilson, S.H., Kunkel, T.A., Pavlov, Y.I., 2004. Recombinogenic phenotype of human activation-induced cytosine deaminase. J. Immunol. 172, 4308-4313). The vast majority of mutations were at G-C pairs. Mutations showed a clear DNA sequence context specificity which resembled the specificity of somatic hypermutation at G-C pairs in immunoglobulin genes and AID mutation specificity in vitro. The inability to detect mutator effects of AID by Krause et al. is likely to be caused by the use of the wild-type yeast strain and a small sample of clones examined for the presence of mutations. In addition, we show that non-uniformity of the mutation hotspot distribution is a factor potentially decreasing the chances of detecting mutations.
Mol
Immunol 2006 Mar
PMID:The cytidine deaminase AID exhibits similar functional properties in yeast and mammals. 1633 70
BMC
Mol
Biol 2005 Oct 19
PMID:Pseudouridine modification in Caenorhabditis elegans spliceosomal snRNAs: unique modifications are found in regions involved in snRNA-snRNA interactions. 1623 71
BMC
Mol
Biol 2005 Nov 17
PMID:Evaluation of potential reference genes in real-time RT-PCR studies of Atlantic salmon. 1629 92
BMC
Mol
Biol 2005 Dec 01
PMID:SiteFind: a software tool for introducing a restriction site as a marker for successful site-directed mutagenesis. 1632 Nov 47
BMC
Mol
Biol 2006 Jan 13
PMID:Competition between the DNA unwinding and strand pairing activities of the Werner and Bloom syndrome proteins. 1641 21
BMC
Mol
Biol 2006 Jan 25
PMID:The Tgif2 gene contains a retained intron within the coding sequence. 1643 15
BMC
Mol
Biol 2006 Jan 31
PMID:The RIN: an RNA integrity number for assigning integrity values to RNA measurements. 1644 64
BMC
Mol
Biol 2006 Feb 07
PMID:Regulation of the human LAT gene by the Elf-1 transcription factor. 1646 44
BMC
Mol
Biol 2006 Feb 16
PMID:The in vitro real-time oscillation monitoring system identifies potential entrainment factors for circadian clocks. 1648 73
BMC
Mol
Biol 2006 Feb 17
PMID:Length-dependent degradation of single-stranded 3' ends by the Werner syndrome protein (WRN): implications for spatial orientation and coordinated 3' to 5' movement of its ATPase/helicase and exonuclease domains. 1650 84
<< Previous
1
2
3
4
5
6
7
8
9
10