-
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.
PMID: 3021337 [PubMed - indexed for MEDLINE]
-
Cited by 75 PubMed Central articles
-
ReviewTreatment for chronic myelogenous leukemia: the long road to imatinib.
Hunter T.
J Clin Invest. 2007 Aug; 117(8):2036-43.
[J Clin Invest. 2007]
-
Enhanced phosphorylation of Nbs1, a member of DNA repair/checkpoint complex Mre11-RAD50-Nbs1, can be targeted to increase the efficacy of imatinib mesylate against BCR/ABL-positive leukemia cells.
Rink L, Slupianek A, Stoklosa T, Nieborowska-Skorska M, Urbanska K, Seferynska I, Reiss K, Skorski T.
Blood. 2007 Jul 15; 110(2):651-60. Epub 2007 Apr 12.
[Blood. 2007]
-
The extreme carboxyl terminus of v-Abl is required for lymphoid cell transformation by Abelson virus.
Warren D, Griffin DS, Mainville C, Rosenberg N.
J Virol. 2003 Apr; 77(8):4617-25.
[J Virol. 2003]
- » See all...