ArticleOncotarget2015
The proteomic investigation reveals interaction of mdig protein with the machinery of DNA double-strand break repair.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Epigenetics and environment in breast cancer: New paradigms for anti-cancer therapies.Frontiers in oncology · 2022Review
- Cooperation between NRF2-mediated transcription and MDIG-dependent epigenetic modifications in arsenic-induced carcinogenesis and cancer stem cells.Seminars in cancer biology · 2021Review
- Mdig promotes oncogenic gene expression through antagonizing repressive histone methylation markers.Theranostics · 2020Article
- Expression of HDAC1 and RBBP4 correlate with clinicopathologic characteristics and prognosis in breast cancer.International journal of clinical and experimental pathology · 2020Article
- New discoveries of mdig in the epigenetic regulation of cancers.Seminars in cancer biology · 2019Review
- MINA53 deficiency leads to glioblastoma cell apoptosis via inducing DNA replication stress and diminishing DNA damage response.Cell death & disease · 2018Article
- Proteomic Characterization of the World Trade Center dust-activated mdig and c-myc signaling circuit linked to multiple myeloma.Scientific reports · 2016Article
- Oxidative stress, epigenetics, and cancer stem cells in arsenic carcinogenesis and prevention.Current pharmacology reports · 2016Article
- Current understanding of mdig/MINA in human cancers.Genes & cancer · 2015Review
- Loss of mdig expression enhances DNA and histone methylation and metastasis of aggressive breast cancer.Signal transduction and targeted therapyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
To investigate how mineral dust-induced gene (mdig, also named as mina53, MINA, or NO52) promotes carcinogenesis through inducing active chromatin, we performed proteomics analyses for the interacting proteins that were co-immunoprecipitated by anti-mdig antibody from either the lung cancer cell line A549 cells or the human bronchial epithelial cell line BEAS-2B cells. On SDS-PAGE gels, three to five unique protein bands were consistently observed in the complexes pulled-down by mdig antibody, but not the control IgG. In addition to the mdig protein, several DNA repair or chromatin binding proteins, including XRCC5, XRCC6, RBBP4, CBX8, PRMT5, and TDRD, were identified in the complexes by the proteomics analyses using both Orbitrap Fusion and Orbitrap XL nanoESI-MS/MS in four independent experiments. The interaction of mdig with some of these proteins was further validated by co-immunoprecipitation using antibodies against mdig and its partner proteins, respectively. These data, thus, provide evidence suggesting that mdig accomplishes its functions on chromatin, DNA repair and cell growth through interacting with the partner proteins.
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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.