Functional Subsets of Murine and Human B Lymphocyte Cell Lines

Ralph, Peter

doi:10.1111/j.1600-065x.1979.tb00300.x

Cited by 77 publications

(29 citation statements)

References 44 publications

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“…The decline in the GFP ϩ ICN1 population occurred more rapidly in V9 cells than in 70Z cells, although by 5 days after transduction, there were very few GFP ϩ cells present in either cell population ( Figure 1A). Similar results were obtained in the murine B-cell lymphoma line WEHI-231 24 (data not shown).…”

Section: Activated Notch1 Inhibits B-cell But Not T-cell Growthsupporting

confidence: 77%

Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies

Zweidler‐McKay

et al. 2005

Blood

181

166

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[3][4][5] Many potential targets of Notch signaling have been identified in various cell contexts, and several members of the Hairy/Enhancer of Split (Hes) family of basic helix-loophelix (bHLH) proteins are direct Notch/CSL targets, including Hes1. 6,7 Notch signaling has multiple functions during normal hematolymphoid development. These include regulation of T-cell commitment from a multipotential precursor, regulation of ␣␤ T-cell development, and marginal zone B-cell development. 8 Notch signaling is tightly controlled, and failure to maintain this regulation can lead to transformation. 9 Within the hematolymphoid compartment, constitutive Notch signaling causes T-cell malignancy in multiple species, and recent data identified Notchactivating mutations as the most frequent event in human T-cell leukemia. 10 In malignant T cells, Notch signaling influences proliferation, differentiation, and survival.Although Notch receptor expression is widespread throughout the hematolymphoid compartment, its transforming potential seems to be restricted to developing T cells. For personal use only. on March 27, 2019. by guest www.bloodjournal.org From with less dramatic effects on the cell cycle. In a second study, Romer et al 12 showed that Notch signaling enhanced apoptosis in a murine B-cell lymphoma line after B-cell antigen receptor (BCR) crosslinking. In the third study, Nefedova et al 13 found that Notch activation induced growth arrest in 4 human myeloma-derived cell lines.In contrast, 3 studies suggest that Notch signaling promotes proliferation of malignant B cells. Hubmann et al 14 reported that Notch2 induced CD23a expression in a pre-B acute lymphoblastic leukemia (ALL) cell line, and both Notch2 and CD23a are expressed at high levels in chronic lymphocytic leukemia (CLL) samples, suggesting a potential role for Notch2 in CD23a-mediated proliferation. In 2 publications that used Jagged1-expressing cells to induce Notch signaling, Jundt et al 15,16 demonstrated that 5 Hodgkin and 3 myeloma-derived cell lines increased thymidine incorporation after 48 hours of ligand signaling, suggesting a proliferative effect on these cell lines. This result is in contrast to that of Nefedova et al 13 who observed decreased thymidine incorporation in 2 of the same cell lines tested.These conflicting results reveal the need to reevaluate the effects of Notch signaling in B-cell malignancies. Given the variety of effects in a range of different B-cell malignancies, we sought to address 3 topics: (1) whether Notch signaling had a consistent effect on different types of B-cell malignancies, (2) whether different Notch receptors differentially affected the B-cell response, and (3) to determine the transcriptional targets of Notch signaling that mediate the B-cell effect. To establish the effects of Notch signaling in B cells, we investigated the effects of constitutive Notch signaling in transformed murine B cells. We found that, in contrast to T cells, murine B-cell lines underwent caspasedependent apoptosis and growth inhibition...

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Section: Activated Notch1 Inhibits B-cell But Not T-cell Growthsupporting

confidence: 77%

Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies

Zweidler‐McKay

et al. 2005

Blood

181

166

View full text Add to dashboard Cite

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“…Anti-IgM causes irreversible growth inhibition of WEHI-231 cells (4,15,29). After 24 h of treatment with anti-IgM, most of the cells have arrested in the G1 phase of the cell cycle (31), and the cell volume has decreased to less than half that of untreated cells (12).…”

mentioning

confidence: 99%

Antigen receptor-induced cell cycle arrest in WEHI-231 B lymphoma cells depends on the duration of signaling before the G1 phase restriction point.

Page

DeFranco

1990

Mol. Cell. Biol.

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“…WEHI 231 is a murine lymphoma cell line that has been characterized as an early B cell on the basis of surface markers and biological properties (28). Although these cells are transformed, the c-myc genes are unrearranged in this line, and these cells remain capable of responding to various immunological stimuli in a manner reminiscent of that of nontransformed cells.…”

mentioning

confidence: 99%

Transcriptional and posttranscriptional control of c-myc gene expression in WEHI 231 cells.

Levine¹,

McCormack²,

Buckler³

et al. 1986

Mol. Cell. Biol.

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Incubation of WEHI 231 cells, derived from a murine B-cell lymphoma, with antisera directed against its surface immunoglobulin results in the inhibition of growth within 24 h. Previously, we demonstrated that this treatment selectively affects cytoplasmic levels of c-myc mRNA (J. E. McCormack, V. H. Pepe, R. B. Kent, M. Dean, A. Marshak-Rothstein, and G. E. Sonenshein, Proc. Natl. Acad. Sci. USA 81: [5546][5547][5548][5549][5550] 1984). An initial increase in the cytoplasmic mRNA level is followed by a precipitous drop. We now show that the early increase results from a dramatic increase in the rate of c-myc gene transcription, as well as from partial stabilization of the mRNA in the cytoplasm. The later decrease results from a shutdown in transcription of the c-myc gene and a return to the normal lability of the cytoplasmic c-myc mRNA. Treatment with phorbol ester, like treatment with anti-immunoglobulin sera, inhibited WEHI 231 cell growth and caused similar changes in cytoplasmic c-myc mRNA levels, which can also be related to alterations in c-myc gene transcription. These results indicate that the control of c-myc gene expression in B cells is effected through regulation at multiple levels.

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Functional Subsets of Murine and Human B Lymphocyte Cell Lines

Cited by 77 publications

References 44 publications

Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies

Notch signaling is a potent inducer of growth arrest and apoptosis in a wide range of B-cell malignancies

Antigen receptor-induced cell cycle arrest in WEHI-231 B lymphoma cells depends on the duration of signaling before the G1 phase restriction point.

Transcriptional and posttranscriptional control of c-myc gene expression in WEHI 231 cells.

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