ArticleProceedings of the National Academy of Sciences of the United States of America1996
Increased sensitivity to apoptotic stimuli in c-abl-deficient progenitor B-cell lines.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Anti-apoptotic HAX-1 suppresses cell apoptosis by promoting c-Abl kinase-involved ROS clearance.Cell death & disease · 2022Article
- Sept4/ARTS is required for stem cell apoptosis and tumor suppression.Genes & development · 2010Article
- Regulation of cell migration and morphogenesis by Abl-family kinases: emerging mechanisms and physiological contexts.Journal of cell science · 2009Article
- The effects of c-Abl mutation on developing B cell differentiation and survival.International immunology · 2009Article
- c-Abl-deficient mice exhibit reduced numbers of peritoneal B-1 cells and defects in BCR-induced B cell activation.International immunology · 2009Article
- T cell survival and function requires the c-Abl tyrosine kinase.Cell cycle (Georgetown, Tex.) · 2008Article
- Distinct roles of c-Abl and Atm in oxidative stress response are mediated by protein kinase C delta.Genes & development · 2004Article
- Imatinib sensitizes CLL lymphocytes to chlorambucil.Leukemia · 2004Article
- Article
- Specific association of Type I c-Abl with Ran GTPase in lipopolysaccharide-mediated differentiation.Oncogene · 2001Article
- JAK-STAT signaling activated by Abl oncogenes.Oncogene · 2000Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protooncogene c-abl encodes a nonreceptor tyrosine kinase whose cellular function is unknown. To study the possible involvement of c-Abl in proliferation, differentiation, and cell cycle regulation of early B cells, long-term lymphoid bone marrow cultures were established from c-abl-deficient mice and their wild-type littermates. Interleukin 7-dependent progenitor B-cell clones and lines expressing B220 and CD43 could be generated from both mutant and wild-type mice. The mutant and wild-type lines displayed no difference in their proliferative capacity as measured by thymidine incorporation in response to various concentrations of interleukin 7. Similarly, c-abl deficiency did not interfere with the ability of mutant clones to differentiate into surface IgM-positive cells in vitro. Analysis of cultures after growth factor deprivation, however, revealed a strikingly accelerated rate of cell death in c-abl mutant cells, due to apoptosis as confirmed by terminal deoxynucleotidyltransferase-mediated UTP nick end labeling analysis. Furthermore, a greater susceptibility to apoptotic cell death in c-abl mutant cells was also observed after glucocorticoid treatment. These results suggest that mutant c-Abl renders the B-cell progenitors more sensitive to apoptosis, and may account for some of the phenotypes observed in c-abl-deficient animals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.