ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Early growth response genes regulate B cell development, proliferation, and immune response.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Trial
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- Impaired B-cell function inFrontiers in immunology · 2024Article
- Inferring gene regulatory network from single-cell transcriptomes with graph autoencoder model.PLoS genetics · 2023Article
- Iguratimod attenuated fibrosis in systemic sclerosis via targeting early growth response 1 expression.Arthritis research & therapy · 2023Article
- Single-cell biological network inference using a heterogeneous graph transformer.Nature communications · 2023Article
- EGFR is a master switch between immunosuppressive and immunoactive tumor microenvironment in inflammatory breast cancer.Science advances · 2022Article
- Early growth response 1 transcription factor is essential for the pathogenic properties of human endometriotic epithelial cells.Reproduction (Cambridge, England) · 2022Article
- Comprehensive analysis of spatial architecture in primary liver cancer.Science advances · 2021Article
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- Early growth response 1 (EGR1) activation in initial stages of host-pathogen interactions.Molecular biology reports · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Egr-1 (early growth response gene-1) is an immediate early gene encoding a zinc finger motif-containing transcription factor. Upon cross-linking of BCR, mature B cells undergo proliferation with an increase in Egr-1 message. Immature B lymphoma cells that express Egr-1 message and protein constitutively are growth inhibited when Egr-1 is down-regulated by negative signals from BCR or by antisense oligonucleotides. To test the hypothesis that Egr-1 is important for B cell development, we examined B cells from primary and secondary lymphoid organs in Egr-1(-/-) mice. Marginal zone B cell development was arrested in these mice, whereas the B cells in all other compartments were increased. To test the hypothesis that Egr-1 function may be partially compensated by other Egr family members, we developed transgenic mice expressing a dominant negative form of Egr-1, which lacks the trans activation domain but retains the DNA-binding domain, in a B cell-specific manner. There was a decrease in B lymphopoiesis in the bone marrow accompanied by a reduction in splenic immature and mature B cells as well as marginal zone B cells in the transgenic mice. Moreover, transgenic mice respond poorly to BCR cross-linking in vitro and T-independent and T-dependent Ags in vivo.
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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.