ArticleMolecular and cellular biology2003
Gab3-deficient mice exhibit normal development and hematopoiesis and are immunocompetent.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 50 citations in OpenAlex.
- Silencing Asian Seabass gab3 Inhibits Nervous Necrosis Virus Replication.Marine biotechnology (New York, N.Y.) · 2022Article
- Identification of a ceRNA Network in Lung Adenocarcinoma Based on Integration Analysis of Tumor-Associated Macrophage Signature Genes.Frontiers in cell and developmental biology · 2021Article
- Article
- PI3Kδ Forms Distinct Multiprotein Complexes at the TCR Signalosome in Naïve and Differentiated CD4Frontiers in immunology · 2021Article
- Article
- Behavioral analysis in mice deficient for GAREM2 (Grb2-associated regulator of Erk/MAPK subtype2) that is a subtype of highly expressing in the brain.Molecular brain · 2019Article
- Gab3 is required for IL-2- and IL-15-induced NK cell expansion and limits trophoblast invasion during pregnancy.Science immunology · 2019Article
- Gab2 and Gab3 Redundantly Suppress Colitis by Modulating Macrophage and CD8Frontiers in immunology · 2019Article
- Increased levels of Gab1 and Gab2 adaptor proteins skew interleukin-4 (IL-4) signaling toward M2 macrophage-driven pulmonary fibrosis in mice.The Journal of biological chemistry · 2017Article
- Gab3 overexpression in human glioma mediates Akt activation and tumor cell proliferation.PloS one · 2017Article
- Changes in Gab2 phosphorylation and interaction partners in response to interleukin (IL)-2 stimulation in T-lymphocytes.Scientific reports · 2016Article
- Essential roles of Gab1 tyrosine phosphorylation in growth factor-mediated signaling and angiogenesis.International journal of cardiology · 2015Review
- CSF-1 receptor signaling in myeloid cells.Cold Spring Harbor perspectives in biology · 2014Review
- A brain-specific Grb2-associated regulator of extracellular signal-regulated kinase (Erk)/mitogen-activated protein kinase (MAPK) (GAREM) subtype, GAREM2, contributes to neurite outgrowth of neuroblastoma cells by regulating Erk signaling.The Journal of biological chemistry · 2013Article
- Gab docking proteins in cardiovascular disease, cancer, and inflammation.International journal of inflammation · 2013Article
- Gab adapter proteins as therapeutic targets for hematologic disease.Advances in hematology · 2012Article
- Gab2 promotes colony-stimulating factor 1-regulated macrophage expansion via alternate effectors at different stages of development.Molecular and cellular biology · 2011Article
- Grb2-associated binding (Gab) proteins in hematopoietic and immune cell biology.American journal of blood research · 2011Article
- Function, regulation and pathological roles of the Gab/DOS docking proteins.Cell communication and signaling : CCS · 2009Article
- Gab family proteins are essential for postnatal maintenance of cardiac function via neuregulin-1/ErbB signaling.The Journal of clinical investigation · 2007Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Gab proteins are intracellular scaffolding and docking molecules involved in signaling pathways mediated by various growth factor, cytokine, or antigen receptors. Gab3 has been shown to act downstream of the macrophage colony-stimulating factor receptor, c-Fms, and to be important for macrophage differentiation. To analyze the physiological role of Gab3, we used homologous recombination to generate mice deficient in Gab3. Gab3(-/-) mice develop normally, are visually indistinguishable from their wild-type littermates, and are healthy and fertile. To obtain a detailed expression pattern of Gab3, we generated Gab3-specific monoclonal antibodies. Immunoblotting revealed a predominant expression of Gab3 in lymphocytes and bone marrow-derived macrophages. However, detailed analysis demonstrated that hematopoiesis in mice lacking Gab3 is not impaired and that macrophages develop in normal numbers and exhibit normal function. The lack of Gab3 expression during macrophage differentiation is not compensated for by increased levels of Gab1 or Gab2 mRNA. Furthermore, Gab3-deficient mice have no major immune deficiency in T- and B-lymphocyte responses to protein antigens or during viral infection. In addition, allergic responses in Gab3-deficient mice appeared to be normal. Together, these data demonstrate that loss of Gab3 does not result in detectable defects in normal mouse development, hematopoiesis, or immune system function.
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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.