ArticleProceedings of the National Academy of Sciences of the United States of America1997
A proliferation switch for genetically modified cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 107 citations in OpenAlex.
- Synthetic Biology: Emerging Concepts to Design and Advance Adeno-Associated Viral Vectors for Gene Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Human Cord Blood and Bone Marrow CD34+ Cells Generate Macrophages That Support Erythroid Islands.PloS one · 2017Article
- Towards in vivo amplification: Overcoming hurdles in the use of hematopoietic stem cells in transplantation and gene therapy.World journal of stem cells · 2015Review
- Engineering macrophages to control the inflammatory response and angiogenesis.Experimental cell research · 2015Article
- Article
- In vivo regulation of erythropoiesis by chemically inducible dimerization of the erythropoietin receptor intracellular domain.PloS one · 2015Article
- An inducible, ligand-independent receptor activator of NF-κB gene to control osteoclast differentiation from monocytic precursors.PloS one · 2013Article
- Combination of Sleeping Beauty transposition and chemically induced dimerization selection for robust production of engineered cells.Nucleic acids research · 2012Article
- Long-term regulation of genetically modified primary hematopoietic cells in dogs.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- Regulated expansion of human pancreatic beta-cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- Genetic control of mammalian T-cell proliferation with synthetic RNA regulatory systems.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Cell vehicle targeting strategies.Gene therapy · 2008Review
- Using gene transfer to circumvent off-target effects.Gene therapy · 2008Review
- Expansion of multipotent and lymphoid-committed human progenitors through intracellular dimerization of Mpl.Blood · 2008Article
- Engineering the melanocortin-4 receptor to control constitutive and ligand-mediated G(S) signaling in vivo.PloS one · 2007Article
- Article
- Molecular imaging of drug-modulated protein-protein interactions in living subjects.Cancer research · 2004Article
- In vivo selective expansion of gene-modified hematopoietic cells in a nonhuman primate model.Gene therapy · 2002Article
- JAK2, complemented by a second signal from c-kit or flt-3, triggers extensive self-renewal of primary multipotential hemopoietic cells.The EMBO journal · 2002Article
- Hematopoietic stem cell gene therapy.International journal of hematology · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Receptor dimerization is the key signaling event for many cytokines, including erythropoietin. A system has been recently developed that permits intracellular protein dimerization to be reversibly activated in response to a lipid-soluble dimeric form of the drug FK506, called FK1012. FK1012 is used as a pharmacological mediator of dimerization to bring together FK506 binding domains, taken from the endogenous protein FKBP12. In experiments reported herein, FK1012-induced dimerization of a fusion protein containing the intracellular portion of the erythropoietin receptor allowed cells normally dependent on interleukin 3 to proliferate in its absence. FK506 competitively reversed the proliferative effect of FK1012 but had no influence on the proliferative effect of interleukin 3. Signaling pathways activated by FK1012 mimicked those activated by erythropoietin, because both JAK2 and STAT5 were phosphorylated in response to FK1012. This approach may provide a means to specifically and reversibly stimulate the proliferation of genetically modified cell populations in vitro or 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.