ArticleThe EMBO journal1995
Impaired interleukin-3 (IL-3) response of the A/J mouse is caused by a branch point deletion in the IL-3 receptor alpha subunit gene.
Article in The EMBO journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- IL3-Driven T Cell-Basophil Crosstalk Enhances Antitumor Immunity.Cancer immunology research · 2024Article
- Basophils beyond allergic and parasitic diseases.Frontiers in immunology · 2023Review
- Review
- High monocyte to lymphocyte ratio is associated with impaired protection after subcutaneous administration of BCG in a mouse model of tuberculosis.F1000Research · 2018Article
- Deep genome sequencing and variation analysis of 13 inbred mouse strains defines candidate phenotypic alleles, private variation and homozygous truncating mutations.Genome biology · 2016Article
- Transcriptional and Linkage Analyses Identify Loci that Mediate the Differential Macrophage Response to Inflammatory Stimuli and Infection.PLoS genetics · 2015Article
- The genetic basis for individual differences in mRNA splicing and APOBEC1 editing activity in murine macrophages.Genome research · 2014Article
- QTLs for murine red blood cell parameters in LG/J and SM/J F(2) and advanced intercross lines.Mammalian genome : official journal of the International Mammalian Genome Society · 2012Article
- Cytokine receptors and hematopoietic differentiation.Oncogene · 2007Review
- Interleukin-3 receptor in acute leukemia.Leukemia · 2004Review
- Intrinsic and extrinsic control of hemopoietic stem cell numbers: mapping of a stem cell gene.The Journal of experimental medicine · 1997Article
- E-cadherin gene mutations in signet ring cell carcinoma of the stomach.Japanese journal of cancer research : Gann · 1996Article
- Hematopoietic stem cell: self-renewal versus differentiation.Wiley interdisciplinary reviews. Systems biology and medicineReview
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6 authors.
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Abstract
Interleukin-3 (IL-3) alone does not support hematopoietic colony formation of bone marrow cells from the A/J mouse. To elucidate the molecular lesion in A/J mice, we examined expression of the alpha and beta subunits of the IL-3 receptor (IL-3R). While IL-3R beta was normally expressed, IL-3R alpha was not detectable on the surface of A/J-derived cells by antibody staining. Genetic linkage analysis using recombinant inbred mouse strains between A/J and IL-3-responsive C57BL/6 indicated that the IL-3R alpha gene locus was responsible for the impaired IL-3 response in A/J mice. Molecular cloning and characterization of A/J-derived IL-3R alpha cDNA revealed that it lacked the sequence corresponding to exon 8, which encodes 10 amino acid residues in the extracellular domain. The aberrant splicing was due to a 5 base pair deletion at the branch point in intron 7 and was reproduced in heterologous cells by transfecting with an IL-3R alpha minigene carrying the deleterious intron. The A/J-specific abnormal form of IL-3R alpha was localized inside the cells, but not on the cell surface, providing the molecular basis for the impaired IL-3 response in the A/J mouse.
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