ArticleProceedings of the National Academy of Sciences of the United States of America1996
Activation of Stat 5b in erythroid progenitors correlates with the ability of ErbB to induce sustained cell proliferation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 38 citations in OpenAlex.
- Productive parvovirus B19 infection of primary human erythroid progenitor cells at hypoxia is regulated by STAT5A and MEK signaling but not HIFα.PLoS pathogens · 2011Article
- Article
- Antiapoptotic activity of Stat5 required during terminal stages of myeloid differentiation.Genes & development · 2000Article
- The fibroblast growth factor receptor FGFR-4 acts as a ligand dependent modulator of erythroid cell proliferation.Oncogene · 1999Article
- TGF-beta cooperates with TGF-alpha to induce the self-renewal of normal erythrocytic progenitors: evidence for an autocrine mechanism.The EMBO journal · 1999Article
- Leukemic transformation by the v-ErbA oncoprotein entails constitutive binding to and repression of an erythroid enhancer in vivo.The EMBO journal · 1998Article
- Transformation of hematopoietic cells by the Ski oncoprotein involves repression of retinoic acid receptor signaling.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Mammalian granulocyte-macrophage colony-stimulating factor receptor expressed in primary avian hematopoietic progenitors: lineage-specific regulation of proliferation and differentiation.The Journal of cell biology · 1998Article
- Activation of different Stat5 isoforms contributes to cell-type-restricted signaling in response to interferons.Molecular and cellular biology · 1996Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Self renewal of normal erythroid progenitors is induced by the receptor tyrosine kinase c-ErbB, whereas other receptors (c-Kit/Epo-R) regulate erythroid differentiation. To address possible mechanisms that could explain this selective activity of c-ErbB, we analyzed the ability of these receptors to activate the different members of the Stat transcription factor family. Ligand activation of c-ErbB induced the tyrosine phosphorylation, DNA-binding, and reporter gene transcription of Stat 5b in erythroblasts. In contrast, ligand activation of c-Kit was unable to induce any of these effects in the same cells. Activation of the erythropoietin receptor caused specific DNA-binding of Stat 5b, but failed to induce reporter gene transcription. These biochemical findings correlate perfectly with the selective ability of c-ErbB to cause sustained self renewal in erythroid progenitors.
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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.