کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9141802 1163879 2005 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Proviral integration of an Abelson-murine leukemia virus deregulates BKLF-expression in the hypermutating pre-B cell line 18-81
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
Proviral integration of an Abelson-murine leukemia virus deregulates BKLF-expression in the hypermutating pre-B cell line 18-81
چکیده انگلیسی
The transcription factor BKLF (basic Krüppel-like factor, KLF3) is a member of the Krüppel-like factors (KLF) family. KLF members harbor a characteristic C-terminal zinc-finger DNA-binding domain and bind preferentially to CACCC-motifs. BKLF is highly expressed in haematopoietic and erythoid cells and works either as repressor or activator of transcription in various genes. BKLF-deficient mice display myeloproliferative disorders and abnormalities in haematopoiesis. Other members of the KLF-family such as GKLF and BCL11A have been implicated in tumorigenesis, however, for BKLF such association has not yet been demonstrated. We report here that a single Abelson-murine leukemia virus (A-MuLV) provirus is present in the genome of the hypermutating murine pre-B cell line 18-81. The provirus has integrated into the locus of the transcription factor BKLF. In contrast to other A-MuLV transformed pre-B cell lines, BKLF is highly transcribed in cell line 18-81. BKLF transcripts originate from the retroviral long terminal repeats (LTRs) and BKLF protein can be detected by gel shift retardation assay. We hypothesize on a potential role of BKLF deregulation in tumorigenesis and/or in the induction of somatic hypermutation in cell line 18-81.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 42, Issue 10, June 2005, Pages 1235-1242
نویسندگان
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