The data suggest that proviral insertions near Cyl-1 in mouse lymphomas are functionally equivalent to the BCL1 translocations that activate cyclin D1 expression in human B-cell malignancies.
CYL2 is considered to encode a D-type cyclin because (i) there is cross hybridization with CYL1 (a murine homolog of human cyclin D1) and the encoded protein has 64% amino acid sequence identity with CYL1 and (ii) murine erythroleukemia cell-derived CYL2 contains an amino acid sequence identical to that previously reported for the C-terminal portion of a partially sequenced CYL2.
As there is no intervening CpG island, proviral insertions at Fis-1 could influence the expression of Cyl-1 and we describe two virally induced tumours in which this appears to be the case.
CYL2 is considered to encode a D-type cyclin because (i) there is cross hybridization with CYL1 (a murine homolog of human cyclin D1) and the encoded protein has 64% amino acid sequence identity with CYL1 and (ii) murine erythroleukemia cell-derived CYL2 contains an amino acid sequence identical to that previously reported for the C-terminal portion of a partially sequenced CYL2.
CYL2 is considered to encode a D-type cyclin because (i) there is cross hybridization with CYL1 (a murine homolog of human cyclin D1) and the encoded protein has 64% amino acid sequence identity with CYL1 and (ii) murine erythroleukemia cell-derived CYL2 contains an amino acid sequence identical to that previously reported for the C-terminal portion of a partially sequenced CYL2.