The BOB.1 / OBF.1 co-activator is essential for octamer-dependent transcription in B cells

Laumen, Helmut; Nielsen, Peter; Wirth, Thomas

doi:10.1002/1521-4141(200002)30:2<458::aid-immu458>3.0.co;2-5

Cited by 43 publications

(30 citation statements)

References 60 publications

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“…Cells were kept in Iscove's modified Dulbecco's medium (Invitrogen) supplemented with 10% fetal calf serum, penicillin/streptomycin, and 50 M ␤-mercaptoethanol and grown at 37°C and 10% CO 2 . The generation of viruses expressing the BOB.1/ OBF.1-ER fusion protein as well as the infection of BOB.1/OBF.1-deficient Abelson virus-transformed pre-B cells (MB10) with these viruses to establish a BOB.1/OBF.1-deficient cell line stably carrying the BobER gene are described (43).…”

Section: Methodsmentioning

confidence: 99%

“…For luciferase reporter assays, the octamer-dependent reporter plasmids ET1 (43) and the 1ϫ wt (5) were used as internal controls. For in vitro translation of BOB.1/OBF.1, the pMT/PKA-Bob expression vector was used (5).…”

Section: Methodsmentioning

confidence: 99%

“…After separation of RNAs on a 1% formaldehyde agarose gel, Northern blot analyses were performed as described (43).…”

Section: Methodsmentioning

confidence: 99%

“…BobER-In order to identify BOB.1/OBF.1-regulated genes, we used an Abelson virus-transformed bone marrow-derived pre-B cell line from BOB.1/OBF.1-deficient mice (43). These cells were either infected with a retroviral vector expressing an inducible BobER fusion protein, or as a control, they were infected with the parental vector (43).…”

Section: Bob1/obf1 Targets Identified Withmentioning

confidence: 99%

“…These cells were either infected with a retroviral vector expressing an inducible BobER fusion protein, or as a control, they were infected with the parental vector (43). In the BobER-expressing cell line (MB10-K10), octamer-dependent transcription was nondetectable, unless the activity of the BobER protein was induced by treatment of these cells with tamoxifen (OHT).…”

Section: Bob1/obf1 Targets Identified Withmentioning

confidence: 99%

See 4 more Smart Citations

Expression of the Aldehyde Dehydrogenase 2-like Gene Is Controlled by BOB.1/OBF.1 in B Lymphocytes

Brunner

Laumen

Nielsen

et al. 2003

Journal of Biological Chemistry

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…After separation of RNAs on a 1% formaldehyde agarose gel, Northern blot analyses were performed as described (43).…”

Section: Methodsmentioning

confidence: 99%

Section: Bob1/obf1 Targets Identified Withmentioning

confidence: 99%

Section: Bob1/obf1 Targets Identified Withmentioning

confidence: 99%

See 3 more Smart Citations

Expression of the Aldehyde Dehydrogenase 2-like Gene Is Controlled by BOB.1/OBF.1 in B Lymphocytes

Brunner

Laumen

Nielsen

et al. 2003

Journal of Biological Chemistry

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Differential Eµ enhancer activity and expression of BOB.1/OBF.1, Oct2, PU.1, and immunoglobulin in reactive B‐cell populations, B‐cell non‐Hodgkin lymphomas, and Hodgkin lymphomas

Loddenkemper

Anagnostopoulos

Hummel

et al. 2003

The Journal of Pathology

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It has previously been demonstrated that in cultured and in situ tumour cells of classical Hodgkin lymphoma (cHL), the immunoglobulin (Ig) promoter is inactive and its transcription factors Oct2 and/or BOB.1/OBF.1 are down-regulated. In this study, the analysis of these transcription factors has been extended to a broad spectrum of B-cell malignancies and the findings have been related to the situation in normal B-cells of various differentiation stages and to the expression of Ig. Furthermore, an additional Ig transcription factor, PU.1, recently described to be absent from cHL, and a further regulatory element of the Ig gene, the intronic Emu enhancer, have been studied. BOB.1/OBF.1 and Oct2 were present in all B-cells expressing Ig, whereas PU.1 proved to be absent from late B-cell differentiation stages and from a subset of germinal centre B-cells. Interestingly, there were several normal (eg germinal centre centroblasts and monocytoid B-cells) and malignant B-cell populations (eg a proportion of diffuse large B-cell lymphomas, DLBCLs) that were Ig-negative, despite their BOB.1/OBF.1 and Oct2 expression. This study further shows that absence of PU.1 alone, as well as inactivation of the intronic Emu enhancer, is not sufficient to down-regulate Ig transcription. Taken together, the simultaneous absence of PU.1, Oct2, and/or BOB.1/OBF.1 is unique to Hodgkin and Reed-Sternberg (HRS) cells and cannot be detected in normal B-cell subsets or B-cell non-Hodgkin lymphomas (B-NHLs). This supports the concept that the down-regulation of Ig in cHL does not reflect a physiological situation, but a defect probably closely linked to the pathogenesis of cHL.

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Downregulation of internal enhancer activity contributes to abnormally low immunoglobulin expression in the MedB‐1 mediastinal B‐cell lymphoma cell line

Ritz¹,

Leithäuser²,

Hasel³

et al. 2005

The Journal of Pathology

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Primary mediastinal B-cell lymphoma (PMBL) is a highly aggressive tumour with a unique pattern of clinical, morphological, immunological and genetic features distinct from other diffuse large B-cell lymphomas. PMBLs are characterized by a mature B-cell phenotype, but they typically lack immunoglobulin (Ig) gene expression. The PMBL cell line MedB-1 shares many characteristic properties of the primary tumour, including low-level Ig production despite a functionally rearranged IgVH gene and absence of 'crippling' mutations. In this study, a search was undertaken for reasons for downregulated Ig expression. Similar levels of the B-cell-specific transcription factors BOB.1/OBF.1 and PU.1 were found in MedB-1 cells to those in the Ig-producing UM-1 lymphoblastoid cell line. However, MedB-1 lacked the Oct2 transcription factor. Reporter assays showed that Ig-type promoters were active in MedB-1 cells. In contrast, activity of the intronic heavy chain enhancer was dramatically reduced. Ectopic expression of Oct2 was able partially to restore enhancer activity but transcription from the endogenous IgVH gene could not be rescued. Therefore, the role of epigenetic factors in the downregulation of Ig was investigated. Methylated histone 3 lysine 9, a reliable marker of chromatin silencing, was not detected in MedB-1 promoter and enhancer regions. Inhibition of DNA methyltransferase and of histone deacetylases also did not reactivate Ig production. These data suggest the existence of alternative mechanisms of Ig inhibition in MedB-1 cells, different from chromatin silencing and the lack of Oct2.

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The BOB.1 / OBF.1 co-activator is essential for octamer-dependent transcription in B cells

Cited by 43 publications

References 60 publications

Expression of the Aldehyde Dehydrogenase 2-like Gene Is Controlled by BOB.1/OBF.1 in B Lymphocytes

Expression of the Aldehyde Dehydrogenase 2-like Gene Is Controlled by BOB.1/OBF.1 in B Lymphocytes

Differential Eµ enhancer activity and expression of BOB.1/OBF.1, Oct2, PU.1, and immunoglobulin in reactive B‐cell populations, B‐cell non‐Hodgkin lymphomas, and Hodgkin lymphomas

Downregulation of internal enhancer activity contributes to abnormally low immunoglobulin expression in the MedB‐1 mediastinal B‐cell lymphoma cell line

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