Abelson virus potentiates long-term growth of mature B lymphocytes.

Serunian, Leslie A.; Rosenberg, Naomi

doi:10.1128/mcb.6.1.183

Cited by 22 publications

(17 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent cell fractionation studies also suggest that the major target of transformation by Abelson virus is a very primitive cell (Tidmarsh et al, 1989). In vitro transformation of normal B lymphocytes by Abelson virus requires prolonged culture with mitogenic lipopolysaccharide and is highly inefficient (Serunian and Rosenberg, 1986). The primary target may be lineage committed, or a bipotential cell able to generate a T or pre-B lymphoma depending on its microenvironment.…”

Section: Discussionmentioning

confidence: 99%

An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

et al. 1990

View full text Add to dashboard Cite

To clarify how the v‐abl oncogene of Abelson murine leukemia virus contributes to lymphoid tumorigenesis, we introduced the gene linked to an immunoglobulin heavy chain enhancer (E mu) into the mouse germline. Although lymphoid development was not detectably affected in young E mu‐v‐abl mice, three transgenic lines shared a high predisposition to develop clonal plasmacytomas that secreted IgA or IgG. The unexpected absence of pre‐B lymphomas suggests that Abelson virus generates such tumors by infecting an early lymphoid progenitor cell that has not yet activated the heavy chain enhancer. Most plasmacytomas bore a rearranged c‐myc gene, apparently as a result of spontaneous translocation to the Igh locus. Moreover, progeny of a cross with analogous E mu‐myc mice rapidly developed oligoclonal plasmacytomas. Thus, the collusion of v‐abl with c‐myc is stage specific, efficiently transforming plasma cells but not pre‐B cells or B cells.

show abstract

Section: Discussionmentioning

confidence: 99%

An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

et al. 1990

View full text Add to dashboard Cite

show abstract

“…220-8 cells (53) were cultured at 37°C with 5% CO 2 in 10% RPMI medium. Apoptosis was induced by using two different protocols: (i) irradiation for 5 min with UV-B (0.5 mW/cm 2 ) in PBS followed by incubation at 37°C with 5% CO 2 in 10% RPMI medium for 24 h or (ii) incubation at 37°C with 5% CO 2 in 10% RPMI medium supplemented with 2 g of etoposide per ml (Sigma) for 48 h. Cell death by apoptosis was confirmed by ethidium bromide visualization of internucleosomal DNA cleavage on 0.7% agarose gels.…”

mentioning

confidence: 99%

Pro-B-Cell-Specific Transcription and Proapoptotic Function of Protein Kinase Cη

Morrow

Muljo

Zhang

et al. 1999

Molecular and Cellular Biology

View full text Add to dashboard Cite

Using a subtractive cloning scheme on cDNA prepared from primary pro-B and pre-B cells, we identified several genes whose products regulate apoptosis. We further characterized one of these genes, encoding protein kinase C (PKC). PKC transcripts were readily detected in pro-B cells but were absent in pre-B cells. Although both a full-length and a truncated form of PKC were detectable in bone marrow pro-B cells, transition to the pre-B-cell stage was associated with increased relative levels of truncated PKC. We found that PKC is proteolyzed in apoptotic lymphocytes, generating a kinase-active fragment identical to the truncated form which is capable of inducing apoptosis when expressed in a pro-B cell line. Caspase-3 can generate an identical PKC cleavage product in vitro, and caspase inhibitors prevent the generation of this product during apoptosis in transfected cell lines. Inducible overexpression of either the full-length or truncated form of PKC results in cell cycle arrest at the G 1 /S transition. These results suggest that the expression and proteolytic activation of PKC play an important role in the regulation of cell division and cell death during early B-cell development.

show abstract

“…All of the mature membrane Ig+ cell lines used in this study were generated by infection of LPS-treated BALB/c adult murine BM cells with Ab-MuLV and Moloney murine leukemia virus (Mo-MLV) as previously described [26].…”

Section: Ig Analysismentioning

confidence: 99%

“…We have been studying a mature B cell line, C3a, derived using Abelson murine leukemia virus (Ab-MLV) and LPS [26]. C3a contains cells that synthesize exclusively y.1 H chains and a second population that synthesizes both y3 and Y2b H chains.…”

Section: Introductionmentioning

confidence: 99%

Allelic exclusion of membrane but not secreted immunoglobulin in a mature B cell line

1991

View full text Add to dashboard Cite

Although many B lymphocytes contain two completely rearranged immunoglobulin (Ig) heavy (H) chain genes, only one of the alleles specifies a protein product. This phenomenon is termed allelic exclusion and is controlled in part by the membrane portion of Ig H chains. We have identified a mature B cell line derived from murine bone marrow that expresses two H chain proteins, gamma 3 and gamma 2b. Proteins of appropriate size for the membrane and secreted forms of both H chains are produced and both IgG3 and IgG2b are secreted from the cells. However, only IgG3 is expressed on the membrane. Detailed restriction mapping of the H chain genes indicates that both are rearranged, one containing a VHJ558 gene linked to the gamma 3 constant region and the other a VHS107 gene linked to the gamma 2b constant region. Primer extension sequencing of the RNA reveals that the gamma 2b RNA is transcribed from the allele containing VHS107 sequences while the gamma 3 RNA is transcribed from the allele containing VHJ558 sequences. Thus, this mature B cell line secretes two distinct antibody molecules but is allelically excluded at the level of surface Ig expression. This cell line provides a model system to study factors, in addition to aberrant rearrangement, that influence allelic exclusion.

show abstract

Abelson virus potentiates long-term growth of mature B lymphocytes.

Cited by 22 publications

References 47 publications

An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

Pro-B-Cell-Specific Transcription and Proapoptotic Function of Protein Kinase Cη

Allelic exclusion of membrane but not secreted immunoglobulin in a mature B cell line

Contact Info

Product

Resources

About