AMINO ACID SEQUENCES OF MOUSE COMPLEMENT C3 DERIVED FROM NUCLEOTIDE SEQUENCES OF CLONED cDNA a

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73374/1/j.1749-6632.1983.tb18118.x.pd

Organization of the Mouse and Human Carbonic Anhydrase II Genes a

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75491/1/j.1749-6632.1984.tb12355.x.pd

Structure and expression of the C3 gene

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46939/1/281_2004_Article_BF00205869.pd

In vitro correction of G.T mispairs to G.C pairs in nuclear extracts from human cells

In differentiated cells, only a specific subset of genes is expressed. Recently, several genes have been shown to be transcriptionally inactivated by methylation of cytosine residues, mainly within their promoter sequences. Spontaneous hydrolytic deamination of 5-methylcytosine to thymine, which has been estimated to generate up to 12 G.T mismatched base pairs in the human genome per day, could have a deleterious effect on the expression of such genes. We recently reported that mammalian cells possess a specific repair pathway, which counteracts the mutagenic effects of this deamination by correcting G.T mismatches almost exclusively to G.C pairs. We show here that, in nuclear extracts from HeLa cells, this repair is mediated by excision of the aberrant thymidine monophosphate residue, followed by gap-filling to generate a G.C pair. We also provide preliminary evidence that the initial step of this process involves a DNA glycosylase