ArticleProceedings of the National Academy of Sciences of the United States of America1995
Membrane-associated and soluble granulocyte/macrophage-colony-stimulating factor receptor alpha subunits are independently regulated in HL-60 cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed, 33 citations in OpenAlex.
- Proteasomal regulation of betac signaling reveals a novel mechanism for cytokine receptor heterotypic desensitization.The Journal of clinical investigation · 2001Article
- Orf virus encodes a novel secreted protein inhibitor of granulocyte-macrophage colony-stimulating factor and interleukin-2.Journal of virology · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The effects of granulocyte/macrophage-colony-stimulating factor (GM-CSF) are mediated by interaction with its composite receptor (GMR), which consists of a unique alpha subunit (GMR alpha) and a beta subunit (GMR beta) that is common to the receptors for GM-CSF, interleukin 3, and interleukin 5. GMR beta is required for high-affinity binding, cell proliferation, and protein phosphorylation but has no intrinsic GM-CSF-binding activity. GMR alpha in isolation binds to GM-CSF with low affinity and can signal for increased glucose uptake. In addition to the membrane-bound receptor (mGMR alpha), there is a naturally occurring soluble isoform (sGMR alpha) that is released free into the pericellular milieu. Analysis of genomic sequences reveals that the soluble GMR alpha isoform comes about by alternative mRNA splicing. To examine GMR alpha expression, we developed a quantitative reverse transcription-polymerase chain reaction assay based on serial dilutions of in vitro transcribed GMR alpha RNA. This assay provides a strict log-log measure of GMR alpha RNA expression, distinguishes transcripts related to the soluble and membrane-associated isoforms, and quantitatively detects 0.1 fg of GMR alpha-related mRNA. There was little or no GMR alpha expression in two human lymphoid cell lines and in the erythroblastic leukemia cell line K562, but all myeloid cell lines tested expressed both the membrane-associated and soluble isoforms of GMR alpha. Baseline level of expression of both isoforms varied > 20-fold among the myeloid cell lines studied. Differentiation of HL-60 cells to neutrophils with dimethyl sulfoxide led to a 2-fold downregulation of sGMR alpha and a 20-fold upregulation of mGMR alpha. These differentiation-induced transcriptional changes were unrelated to changes in mRNA stability. These findings indicate that sGMR alpha is differentially expressed from mGMR alpha in human hematopoietic cells and that programmed downregulation of sGMR alpha may be important in myeloid maturation.
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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.