tailieunhanh - báo cáo hóa học:" Regulation of FeLV-945 by c-Myb binding and CBP recruitment to the LTR"

Tuyển tập các báo cáo nghiên cứu về hóa học được đăng trên tạp chí sinh học đề tài : Regulation of FeLV-945 by c-Myb binding and CBP recruitment to the LTR | BioMed Central Virology Journal Research Open Access Regulation of FeLV-945 by c-Myb binding and CBP recruitment to the LTR Samantha L Finstad1 Sudha Prabhu1 Karen R Rulli1 2 and Laura S Levy 1 Address department of Microbiology and Immunology Program in Molecular and Cellular Biology and Tulane Cancer Center Tulane University Health Sciences Center New Orleans Louisiana USA and 2Science Applications International Corporation Frederick Maryland USA Email Samantha L Finstad - sfinsta1@ Sudha Prabhu - sndprabhu@ Karen R Rulli - rullik@ Laura S Levy - llevy@ Corresponding author Published 03 September 2004 Received 06 July 2004 Accepted 03 September 2004 Virology Journal 2004 1 3 doi 1743-422X-1-3 This article is available from http content 1 1 3 2004 Finstad et al licensee BioMed Central Ltd. This is an open-access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Feline leukemia virus FeLV induces degenerative proliferative and malignant hematologic disorders in its natural host the domestic cat. FeLV-945 is a viral variant identified as predominant in a cohort of naturally infected animals. FeLV-945 contains a unique sequence motif in the long terminal repeat LTR comprised of a single copy of transcriptional enhancer followed by a 21-bp sequence triplicated in tandem. The LTR is precisely conserved among independent cases of multicentric lymphoma myeloproliferative disease and anemia in animals from the cohort. The 21-bp triplication was previously shown to act as a transcriptional enhancer preferentially in hematopoietic cells and to confer a replicative advantage. The objective of the present study was to examine the molecular mechanism by which the 21-bp triplication exerts its influence and