ArticleOncogene2001
HoxB8 requires its Pbx-interaction motif to block differentiation of primary myeloid progenitors and of most cell line models of myeloid differentiation.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 63 citations in OpenAlex.
- Integrated proteogenomic and metabolomic profiling of acute myeloid leukemias to identify molecular subtypes and associated therapy targets.Nature cancer · 2026Article
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- CTG-Initiated Cryptic Peptide Translation Up- and Downstream of a Canonical ATG Start Codon Is Enhanced by TLR Stimulation and Induces Tumor Regression in Mice.Cancer immunology research · 2025Article
- NUPA10hd-immortalized and genetically engineered progenitors allow studying dendritic cell immune functions.Frontiers in immunology · 2025Article
- Downstream of the HOX genes: Explaining conflicting tumour suppressor and oncogenic functions in cancer.International journal of cancer · 2022Review
- Engraftment, Fate, and Function of HoxB8-Conditional Neutrophil Progenitors in the Unconditioned Murine Host.Frontiers in cell and developmental biology · 2022Article
- Roles of mitochondria in neutrophils.Frontiers in immunology · 2022Review
- A rapid CRISPR competitive assay forComputational and structural biotechnology journal · 2021Article
- Oncogenic HOXB8 is driven by MYC-regulated super-enhancer and potentiates colorectal cancer invasiveness via BACH1.Oncogene · 2020Article
- Cas9eLife · 2019Article
- Hoxb8 regulates expression of microRNAs to control cell death and differentiation.Cell death and differentiation · 2013Article
- Microglial dysregulation in psychiatric disease.Clinical & developmental immunology · 2013Review
- Homeobox genes in obsessive-compulsive disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012Article
- Disentangling the many layers of eukaryotic transcriptional regulation.Annual review of genetics · 2012Review
- Hox proteins display a common and ancestral ability to diversify their interaction mode with the PBC class cofactors.PLoS biology · 2012Article
- Pbx1 is a downstream target of Evi-1 in hematopoietic stem/progenitors and leukemic cells.Oncogene · 2009Article
- Methylation detection oligonucleotide microarray analysis: a high-resolution method for detection of CpG island methylation.Nucleic acids research · 2009Article
- High miR-196a levels promote the oncogenic phenotype of colorectal cancer cells.World journal of gastroenterology · 2009Article
- Identification of chromatin remodeling genes Arid4a and Arid4b as leukemia suppressor genes.Journal of the National Cancer Institute · 2008Article
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
HoxB8 was the first homeobox gene identified as a cause of leukemia. In murine WEHI3B acute myeloid leukemia (AML) cells, proviral integration leads to the expression of both HoxB8 and Interleukin (IL-3). Enforced expression of HoxB8 blocks differentiation of factor-dependent myeloid progenitors, while IL-3 co-expression induces autocrine proliferation and overt leukemogenicity. Previously, we demonstrated that HoxB8 binds DNA cooperatively with members of the Pbx family of transcription factors, and that HoxB8 makes contact with the Pbx homeodomain through a hexameric sequence designated the Pbx-interaction motif (PIM). E2a-Pbx1, an oncogenic derivative of Pbx1, both retains its ability to heterodimerize with Hox proteins and arrest myeloid differentiation. This observation prompts the question of whether E2a-Pbx1 and Hox oncoproteins use endogenous Hox and Pbx proteins, respectively, to target a common set of cellular genes. Here, we use four different models of neutrophil and macrophage differentiation to determine whether HoxB8 needs to bind DNA or Pbx cofactors in order to arrest myeloid differentiation. The ability of HoxB8 to bind DNA or to bind Pbx was essential (1) to block differentiation of factor-dependent myeloid progenitors from primary marrow; (2) to block IL-6-induced monocytic differentiation of M1-AML cells; and (3) to block granulocytic differentiation of GM-CSF-dependent ECoM-G cells. However, while DNA-binding was required, the HoxB8 Pbx-interaction motif was unnecessary for preventing macrophage differentiation of ECoM-M cells. We conclude that HoxB8 prevents differentiation by directly influencing cellular gene expression, and that the genetic context within a cell dictates whether the effect of HoxB8 is dependent on a physical interaction with Pbx proteins.
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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.