Biomedical subjects

E Shtivelman

Publications and source records attributed to E Shtivelman.

21 records · Page 2Linked to original sources

PubMed1986

Alternative splicing of RNAs transcribed from the human abl gene and from the bcr-abl fused gene.

The primary structure of normal abl protein was determined by sequencing the coding region of its cDNA. abl contains two alternative 5' exons spliced to a common set of 3' exons to yield the two major abl RNA transcripts. These transcripts initiate in different promoter regions and give rise to proteins that vary in their N-termini. In the human cell line K562, abl is translocated from chromosome 9 to within the bcr gene on chromosome 22. Within the fused bcr-abl gene, abl exon II alternatively splices to two adjacent bcr exons. This phenomenon is seen in many patients with chronic myeloid leukemia.

Abelson murine leukemia virus↗

PubMed1984

Frequent generation of nonrescuable reorganized Moloney murine sarcoma viral genomes.

Nonproducer transformants infected with wild-type Moloney murine sarcoma virus were screened for the generation of variants with reorganized genomes. Seven of 20 lines contained such viral genomes, 5 of which were found to be nonrescuable. Blotting analysis indicated that viral RNA molecules transcribed from these variant genomes could not be encapsidated into virions. The nonrescuable genomes were molecularly cloned and all were found to have suffered deletions or deletions/inversions involving the 5' long terminal repeat as well as some adjacent sequences. Nucleotide sequence analysis suggested that the long terminal repeat or the tetranucleotides G-G-T-C and G-A-C-C (or both) were involved in the generation of these mutants. Transfection studies showed that the cloned DNAs of the 5 mutants transformed NIH/3T3 monolayers. Removal of the 3' long terminal repeat from the genomes that lacked the 5' long terminal repeat or carried it in an inverted orientation abolished or considerably reduced the transforming activity.

Chromosome Deletion↗

PubMedDate not supplied

Fused transcript of abl and bcr genes in chronic myelogenous leukaemia.

Human chronic myelogenous leukaemia is characterized by a reciprocal translocation between chromosomes 9 and 22 resulting in an abbreviated form of chromosome 22 and the transfer of the abl cellular oncogene from chromosome 9 into the bcr gene of chromosome 22. Characterization of an 8-kilobase RNA specific to chronic myelogenous leukaemia shows it to be a fused transcript of the two genes. The fused protein that would be produced is probably involved in the malignant process.

Base Sequence↗