作者: C A Klug , S J Gerety , P C Shah , Y Y Chen , N R Rice
DOI: 10.1101/GAD.8.6.678
关键词: Abelson murine leukemia virus 、 Tyrosine kinase 、 Biology 、 Transcription (biology) 、 NFKB1 、 Transcription factor 、 Molecular biology 、 Kinase 、 Enhancer 、 Cell culture
摘要: Transformation of B-lineage precursors by the Abelson murine leukemia virus appears to arrest development at pre-B stage. Abelson-transformed cell lines generally retain transcriptionally inactive, unrearranged immunoglobulin K alleles. We demonstrate that nontransformed cells expanded from mouse bone marrow efficiently transcribe In addition, they contain activated complexes NF-KB/RCI transcription factor family, in contrast with their counterparts. Using conditionally transformed lines, we show v-abl viral transforming protein, a tyrosine kinase, blocks germ-line gene and negatively regulates activity. An active \-abI kinase specifically inhibits NF-KB/Rel-dependent intron enhancer, which is implicated promoting both rearrangement locus, \-abl state via post-translational mechanism results increased stability inhibitory subunit IKBU. This analysis suggests molecular pathway locus