ArticleThe Journal of experimental medicine1997
The thrombopoietin receptor can mediate proliferation without activation of the Jak-STAT pathway.
Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 59 citations in OpenAlex.
- Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome.Nature communications · 2025Article
- In Silico Evaluation of Coding and Non-Coding nsSNPs in the Thrombopoietin Receptor (Current issues in molecular biology · 2023Article
- CD110 promotes pancreatic cancer progression and its expression is correlated with poor prognosis.Journal of cancer research and clinical oncology · 2019Article
- Two patterns of thrombopoietin signaling suggest no coupling between platelet production and thrombopoietin reactivity in thrombocytopenia-absent radii syndrome.Haematologica · 2012Article
- Article
- An ENU-induced recessive mutation in Mpl leads to thrombocytopenia with overdominance.Experimental hematology · 2009Article
- Expansion of multipotent and lymphoid-committed human progenitors through intracellular dimerization of Mpl.Blood · 2008Article
- A rationally designed agonist antibody fragment that functionally mimics thrombopoietin.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Interleukin-6-induced proliferation of human myeloma cells associated with CD45 molecules.International journal of hematology · 2003Review
- Article
- Molecular control of megakaryopoiesis and thrombopoiesis.International journal of hematology · 2002Review
- Dissection of the cytoplasmic domains of cytokine receptors involved in STAT and Ras dependent proliferation.Oncogene · 2002Article
- The carboxy-terminal fragment of nucleolin interacts with the nucleocapsid domain of retroviral gag proteins and inhibits virion assembly.Journal of virology · 2000Article
- The role of STATs in myeloid differentiation and leukemia.Oncogene · 2000Review
- Regulatory and signaling properties of the Vav family.Molecular and cellular biology · 2000Review
- Involvement of Shc and Cbl-PI 3-kinase in Lyn-dependent proliferative signaling pathways for G-CSF.Oncogene · 2000Article
- c-Abl-induced apoptosis, but not cell cycle arrest, requires mitogen-activated protein kinase kinase 6 activation.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Article
- Direct interaction of Jak1 and v-Abl is required for v-Abl-induced activation of STATs and proliferation.Molecular and cellular biology · 1998Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokine receptors of the hematopoietic receptor superfamily lack intrinsic tyrosine kinase domains for the intracellular transmission of their signals. Instead all members of this family associate with Jak family nonreceptor tyrosine kinases. Upon ligand stimulation of the receptors, Jaks are activated to phosphorylate target substrates. These include STAT (signal transducers and activators of transcription) proteins, which after phosphorylation translocate to the nucleus and modulate gene expression. The exact role of the Jak-STAT pathway in conveying growth and differentiation signals remains unclear. Here we describe a deletion mutant of the thrombopoietin receptor (c-mpl) that has completely lost the capacity to activate Jaks and STATs but retains its ability to induce proliferation. This mutant still mediates TPO-induced phosphorylation of Shc, Vav, mitogen-activated protein kinase (MAPK) and Raf-1 as well as induction of c-fos and c-myc, although at somewhat reduced levels. Furthermore, we show that both wild-type and mutant receptors activate phosphatidylinositol (PI) 3-kinase upon thrombopoietin stimulation and that thrombopoietin-induced proliferation is inhibited in the presence of the PI 3-kinase inhibitor wortmannin. These results demonstrate that the Jak-STAT pathway is dispensable for the generation of mitogenic signals by a cytokine receptor.
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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.