ArticleMolecular and cellular biology1990
Evi-2, a common integration site involved in murine myeloid leukemogenesis.
Article in Molecular and cellular biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 93 citations in OpenAlex.
- Methodological landscape in the field of integration site identification of retroviruses and retroviral vectors.Frontiers in bioengineering and biotechnology · 2025Review
- Exploring potential causal genetic variants and genes for endometrial cancer: Open Targets Genetics, Mendelian randomization, and multi-tissue transcriptome-wide association analysis.Translational cancer research · 2024Article
- Analysis of scRNA-seq and bulk RNA-seq demonstrates the effects of EVI2B or CD361 on CD8Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Bioinformatics analysis of the key genes in osteosarcoma metastasis and immune invasion.Translational pediatrics · 2022Article
- Article
- Review
- EVI2B is a C/EBPα target gene required for granulocytic differentiation and functionality of hematopoietic progenitors.Cell death and differentiation · 2017Article
- A Combined Omics Approach to Generate the Surface Atlas of Human Naive CD4+ T Cells during Early T-Cell Receptor Activation.Molecular & cellular proteomics : MCP · 2015Article
- APOBEC3A cytidine deaminase induces RNA editing in monocytes and macrophages.Nature communications · 2015Article
- New insights into the DT40 B cell receptor cluster using a proteomic proximity labeling assay.The Journal of biological chemistry · 2014Article
- Dr.VIS: a database of human disease-related viral integration sites.Nucleic acids research · 2012Article
- Identifying viral integration sites using SeqMap 2.0.Bioinformatics (Oxford, England) · 2011Article
- Article
- Animal models of acute myelogenous leukaemia - development, application and future perspectives.Leukemia · 2005Review
- Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative disease.The EMBO journal · 2005Article
- Large-scale identification of disease genes involved in acute myeloid leukemia.Journal of virology · 2004Article
- Inhibition of p53-induced apoptosis without affecting expression of p53-regulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- A Moloney murine leukemia virus-based retrovirus with 4070A long terminal repeat sequences induces a high incidence of myeloid as well as lymphoid neoplasms.Journal of virology · 2003Article
- Article
- Article
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 1 institution in 1 country.
Funding
Abstract
BXH-2 mice have the highest incidence of spontaneous retrovirally induced myeloid leukemia of any known inbred strain and, as such, represent a valuable model system for identifying cellular proto-oncogenes involved in myeloid disease. Chronic murine leukemia viruses often induce disease by insertional activation or mutation of cellular proto-oncogenes. These loci are identified as common viral integration sites in tumor DNAs. Here we report on the characterization of a novel common viral integration site in BXH-2 myeloid leukemias, designated Evi-2. Within the cluster of viral integration sites that define Evi-2, we identified a gene that has the potential for encoding a novel protein of 223 amino acids. This putative proto-oncogene possesses all of the structural features of a transmembrane protein. Within the transmembrane domain is a "leucine zipper," suggesting that Evi-2 is involved in either homopolymer or heteropolymer formation, which may play an important role in the normal functioning of Evi-2. Interestingly, the human homolog of Evi-2 has recently been shown to be tightly linked to the von Recklinghausen neurofibromatosis locus, suggesting a role for Evi-2 in human disease as well.
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.