ArticleBlood2007
Abnormal hematopoiesis in Gab2 mutant mice.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Current Views on the Interplay between Tyrosine Kinases and Phosphatases in Chronic Myeloid Leukemia.Cancers · 2021Review
- Gab2 and Gab3 Redundantly Suppress Colitis by Modulating Macrophage and CD8Frontiers in immunology · 2019Article
- Inhibition of the Gab2/PI3K/mTOR signaling ameliorates myeloid malignancy caused by Ptpn11 (Shp2) gain-of-function mutations.Leukemia · 2017Article
- Article
- Changes in Gab2 phosphorylation and interaction partners in response to interleukin (IL)-2 stimulation in T-lymphocytes.Scientific reports · 2016Article
- Functional screen identifies regulators of murine hematopoietic stem cell repopulation.The Journal of experimental medicine · 2016Article
- Structure and function of Gab2 and its role in cancer (Review).Molecular medicine reports · 2015Review
- Stat5 Exerts Distinct, Vital Functions in the Cytoplasm and Nucleus of Bcr-Abl+ K562 and Jak2(V617F)+ HEL Leukemia Cells.Cancers · 2015Article
- Gain-of-function of Stat5 leads to excessive granulopoiesis and lethal extravasation of granulocytes to the lung.PloS one · 2013Article
- Gab2 signaling in chronic myeloid leukemia cells confers resistance to multiple Bcr-Abl inhibitors.Leukemia · 2013Article
- Gab docking proteins in cardiovascular disease, cancer, and inflammation.International journal of inflammation · 2013Article
- GAB2--a scaffolding protein in cancer.Molecular cancer research : MCR · 2012Review
- Novel mechanism for Fc{epsilon}RI-mediated signal transducer and activator of transcription 5 (STAT5) tyrosine phosphorylation and the selective influence of STAT5B over mast cell cytokine production.The Journal of biological chemistry · 2012Article
- 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
- Spry1 is expressed in hemangioblasts and negatively regulates primitive hematopoiesis and endothelial cell function.PloS one · 2011Article
- Article
- Gab1 mediates hepatocyte growth factor-stimulated mitogenicity and morphogenesis in multipotent myeloid cells.Journal of cellular biochemistry · 2010Article
- Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Gab2 is an important adapter molecule for cytokine signaling. Despite its major role in signaling by receptors associated with hematopoiesis, the role of Gab2 in hematopoiesis has not been addressed. We report that despite normal numbers of peripheral blood cells, bone marrow cells, and c-Kit(+)Lin(-)Sca-1(+) (KLS) cells, Gab2-deficient hematopoietic cells are deficient in cytokine responsiveness. Significant reductions in the number of colony-forming units in culture (CFU-C) in the presence of limiting cytokine concentrations were observed, and these defects could be completely corrected by retroviral complementation. In earlier hematopoiesis, Gab2-deficient KLS cells isolated in vitro responded poorly to hematopoietic growth factors, resulting in an up to 11-fold reduction in response to a cocktail of stem cell factor, flt3 ligand, and thrombopoietin. Gab2-deficient c-Kit(+)Lin(-) cells also demonstrate impaired activation of extracellular signal-regulated kinase (ERK) and S6 in response to IL-3, which supports defects in activating the phosphatidylinositol-3 kinase (PI-3K) and mitogen-associated protein kinase (MAPK) signaling cascades. Associated with the early defects in cytokine response, competitive transplantation of Gab2(-/-) bone marrow cells resulted in defective long-term multilineage repopulation. Therefore, we demonstrate that Gab2 adapter function is intrinsically required for hematopoietic cell response to early-acting cytokines, resulting in defective hematopoiesis in Gab2-deficient mice.
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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.