ArticleInternational immunology2009
The effects of c-Abl mutation on developing B cell differentiation and survival.
Article in International immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Tyrosine kinase c-Abl regulates the survival of plasma cells.Scientific reports · 2017Article
- Arg Deficiency Does not Influence the Course of Myelin Oligodendrocyte Glycoprotein (MOG35-55)-induced Experimental Autoimmune Encephalomyelitis.Journal of clinical & cellular immunology · 2016Article
- Critical role of actin-associated proteins in smooth muscle contraction, cell proliferation, airway hyperresponsiveness and airway remodeling.Respiratory research · 2015Review
- C-Abl tyrosine kinase mediates neurotoxic prion peptide-induced neuronal apoptosis via regulating mitochondrial homeostasis.Molecular neurobiology · 2014Article
- Orchestrating B cell lymphopoiesis through interplay of IL-7 receptor and pre-B cell receptor signalling.Nature reviews. Immunology · 2014Review
- Role of Abl in airway hyperresponsiveness and airway remodeling.Respiratory research · 2013Article
- Article
- Functional mechanisms and roles of adaptor proteins in abl-regulated cytoskeletal actin dynamics.Journal of signal transduction · 2012Article
- ABL tyrosine kinases: evolution of function, regulation, and specificity.Science signaling · 2010Review
- Interferon-γ regulates cell malignant growth via the c-Abl/HDAC2 signaling pathway in mammary epithelial cells.Journal of Zhejiang University. Science. BArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
c-Abl is a widely expressed Src family protein tyrosine kinase that is activated by chromosomal translocation in certain human leukemias. While shown in various experimental systems to regulate cell division and stress responses, its biological functions remain poorly understood. Although expressed at similar levels throughout B cell development, we found that the fraction of phosphorylated, active c-Abl peaks at the pro-B stage. We went on to perform a detailed analysis of B cell development in c-Abl-deficient mice. We confirmed a striking but variable decrease in pro- and pre-B cell numbers, a decrease in pre-B cell growth and an increase in pre-B cell apoptosis. This phenotype was not rescued by transgenic expression of a functional IgHC transgene and only partially rescued by the anti-apoptosis gene Bcl-x. Unlike their wild-type counterparts, c-Abl-deficient pre-B cells show a defect in Ca(2+) flux upon cross-linking of CD19, a co-receptor known to be involved in pre-B cell receptor signaling and failed to express CD25 on the cell surface. Despite these pre-B cell-signaling defects, selection for in-frame heavy-chain rearrangements was intact in the mutant mice. Remarkably, we were able to rescue the proliferative defect by culturing cells in vitro with large amounts of rIL-7. We conclude that c-Abl is required for normal B cell differentiation and survival.
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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.