ArticleMolecular and cellular biology1994
The novel primary response gene MyD118 and the proto-oncogenes myb, myc, and bcl-2 modulate transforming growth factor beta 1-induced apoptosis of myeloid leukemia cells.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
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Who cites it
60 citing papers in PubMed, 185 citations in OpenAlex.
- Growth arrest and DNA damage-inducible 45: a new player on inflammatory diseases.Frontiers in immunology · 2025Review
- Berberine and Oligomeric Proanthocyanidins Exhibit Synergistic Efficacy Through Regulation of PI3K-Akt Signaling Pathway in Colorectal Cancer.Frontiers in oncology · 2022Article
- Gadd45 Proteins in Immunity 2.0.Advances in experimental medicine and biology · 2022Article
- GADD45 in Stress Signaling, Cell Cycle Control, and Apoptosis.Advances in experimental medicine and biology · 2022Article
- Gadd45 in Normal Hematopoiesis and Leukemia.Advances in experimental medicine and biology · 2022Article
- Fluorescent labeling of CRISPR/Cas9 RNP for gene knockout in HSPCs and iPSCs reveals an essential role for GADD45b in stress response.Blood advances · 2019Article
- Endometrial mesenchymal stem cells isolated from menstrual blood repaired epirubicin-induced damage to human ovarian granulosa cells by inhibiting the expression of Gadd45b in cell cycle pathway.Stem cell research & therapy · 2019Article
- Loss of Gadd45b accelerates BCR-ABL-driven CML.Oncotarget · 2018Article
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- DNA-damage response gene GADD45A induces differentiation in hematopoietic stem cells without inhibiting cell cycle or survival.Stem cells (Dayton, Ohio) · 2016Article
- Early transcriptional responses of internalization defective Brucella abortus mutants in professional phagocytes, RAW 264.7.BMC genomics · 2013Article
- GADD45 proteins: central players in tumorigenesis.Current molecular medicine · 2012Review
- Gadd45 proteins: relevance to aging, longevity and age-related pathologies.Ageing research reviews · 2012Review
- B-MYB positively regulates serine-threonine kinase receptor-associated protein (STRAP) activity through direct interaction.The Journal of biological chemistry · 2011Article
- Roles of inflammatory and anabolic cytokines in cartilage metabolism: signals and multiple effectors converge upon MMP-13 regulation in osteoarthritis.European cells & materials · 2011Article
- Gadd45 stress sensors in malignancy and leukemia.Critical reviews in oncogenesis · 2011Review
- MYBBP1A: a new Ipr1's binding protein in mice.Molecular biology reports · 2010Article
- Gadd45β expression in chondrosarcoma: a pilot study for diagnostic and biological implications in histological grading.Diagnostic pathology · 2010Article
- Gadd45 proteins as critical signal transducers linking NF-kappaB to MAPK cascades.Current cancer drug targets · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cell numbers are regulated by a balance among proliferation, growth arrest, and programmed cell death. A profound example of cell homeostasis, controlled throughout life, is the complex process of blood cell development, yet little is understood about the intracellular mechanisms that regulate blood cell growth arrest and programmed cell death. In this work, using transforming growth factor beta 1 (TGF beta 1)-treated M1 myeloid leukemia cells and genetically engineered M1 cell variants, the regulation of growth arrest and apoptosis was dissected. Blocking of early expression of MyD118, a novel differentiation primary response gene also shown to be a primary response gene induced by TGF beta 1, delayed TGF beta 1-induced apoptosis, demonstrating that MyD118 is a positive modulator of TGF beta 1-mediated cell death. Elevated expression of bcl-2 blocked the TGF beta 1-induced apoptotic pathway but not growth arrest induced by TGF beta 1. Deregulated expression of either c-myc or c-myb inhibited growth arrest and accelerated apoptosis, demonstrating for the first time that c-myb plays a role in regulating apoptosis. In all cases, the apoptotic response was correlated with the level of MyD118 expression. Taken together, these findings demonstrate that the primary response gene MyD118 and the c-myc, c-myb, and bcl-2 proto-oncogenes interact to modulate growth arrest and apoptosis of myeloid cells.
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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.