ArticleMolecular and cellular biology2003
Interleukin-3 stimulation of mcl-1 gene transcription involves activation of the PU.1 transcription factor through a p38 mitogen-activated protein kinase-dependent pathway.
Article in Molecular and cellular biology, 2003. 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
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
26 citing papers in PubMed, 82 citations in OpenAlex.
- Myeloid-derived MANF ameliorates ethanol-induced liver injury by enhancing microRNA-223 expression.Journal of gastroenterology · 2025Article
- Deregulation of apoptotic proteins by induction ofIranian journal of basic medical sciences · 2023Article
- Ferulic Acid Induces Apoptosis of HeLa and Caski Cervical Carcinoma Cells by Down-Regulating the Phosphatidylinositol 3-Kinase (PI3K)/Akt Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Immunomodulatory germline variation associated with the development of multiple primary melanoma (MPM).Scientific reports · 2019Article
- 3-Chloroplumbagin Induces Cell Death in Breast Cancer Cells Through MAPK-Mediated Mcl-1 Inhibition.Frontiers in pharmacology · 2019Article
- Myeloid cell leukemia 1 (MCL-1), an unexpected modulator of protein kinase signaling during invasion.Cell adhesion & migration · 2018Review
- Identification of Interleukin-1 by Functional Screening as a Key Mediator of Cellular Expansion and Disease Progression in Acute Myeloid Leukemia.Cell reports · 2017Article
- PTBP1 modulation of MCL1 expression regulates cellular apoptosis induced by antitubulin chemotherapeutics.Cell death and differentiation · 2016Article
- Regulation of Mcl-1 by constitutive activation of NF-κB contributes to cell viability in human esophageal squamous cell carcinoma cells.BMC cancer · 2014Article
- Notch signaling regulates expression of Mcl-1 and apoptosis in PPD-treated macrophages.Cellular & molecular immunology · 2013Article
- Sorafenib and its derivative SC-49 sensitize hepatocellular carcinoma cells to CS-1008, a humanized anti-TNFRSF10B (DR5) antibody.British journal of pharmacology · 2013Article
- Ets-1 mediates upregulation of Mcl-1 downstream of XBP-1 in human melanoma cells upon ER stress.Oncogene · 2011Article
- T cell lineage commitment: identity and renunciation.Journal of immunology (Baltimore, Md. : 1950) · 2011Review
- The molecular mechanisms of glucocorticoids-mediated neutrophil survival.Current drug targets · 2011Review
- Molecular and cellular pathobiology of Ehrlichia infection: targets for new therapeutics and immunomodulation strategies.Expert reviews in molecular medicine · 2011Review
- CEBPD reverses RB/E2F1-mediated gene repression and participates in HMDB-induced apoptosis of cancer cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Article
- TRAIL-activated stress kinases suppress apoptosis through transcriptional upregulation of MCL-1.Cell death and differentiation · 2010Article
- Article
- 5-Lipoxygenase inhibitors potentiate 1alpha,25-dihydroxyvitamin D3-induced monocytic differentiation by activating p38 MAPK pathway.Molecular and cellular biochemistry · 2009Article
- Lipopolysaccharide-dependent interaction between PU.1 and c-Jun determines production of lipocalin-type prostaglandin D synthase and prostaglandin D2 in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously demonstrated that the antiapoptotic gene mcl-1 is activated by interleukin-3 (IL-3) in Ba/F3 pro-B cells through two promoter elements designated the CRE-2 and SIE motifs. While the CRE-2-binding complex contains the CREB protein and is activated by IL-3 through the phosphatidylinositol 3-kinase/Akt-dependent pathway, the identity and cytokine activation pathway of the SIE-binding complex remains unclear. In this report, we demonstrated that PU.1 is one component of the SIE-binding complex. A chromatin immunoprecipitation assay further confirmed that PU.1 binds to the mcl-1 promoter region containing the SIE motif in vivo. While IL-3 stimulation does not significantly alter the SIE-binding activity of PU.1, it markedly increases PU.1's transactivation activity. The latter effect coincides with the increased phosphorylation of PU.1 following IL-3 activation of a p38 mitogen-activated protein kinase (p38(MAPK))-dependent pathway. A serine-to-alanine substitution at position 142 significantly weakens PU.1's ability to be phosphorylated by the p38(MAPK) immunocomplex. Furthermore, this S142A mutant is impaired in the ability to be further stimulated by IL-3 to transactivate the mcl-1 reporter through the SIE motif. Taken together, our results demonstrate that IL-3 stimulation of mcl-1 gene transcription through the SIE motif involves phosphorylation of PU.1 at serine 142 by a p38(MAPK)-dependent pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.