ArticleThe Journal of clinical investigation1997
MxA overexpression reveals a common genetic link in four Fanconi anemia complementation groups.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 52 citations in OpenAlex.
- Expression of MxA in esophageal cancer cell lines can influence sensitivity to chemotherapeutic agents but this does not require apoptosis.Cancer medicine · 2024Article
- Influence of MX1 promoter rs2071430 G/T polymorphism on susceptibility to systemic lupus erythematosus.Clinical rheumatology · 2016Article
- Host genetics of severe influenza: from mouse Mx1 to human IRF7.Current opinion in immunology · 2016Review
- Review
- Landscape features and helminth co-infection shape bank vole immunoheterogeneity, with consequences for Puumala virus epidemiology.Heredity · 2014Article
- The Curious Case of Type I IFN and MxA: Tipping the Immune Balance in AIDS.Frontiers in immunology · 2014Review
- TNF-α signaling in Fanconi anemia.Blood cells, molecules & diseases · 2014Review
- Elevated levels of STAT1 in Fanconi anemia group A lymphoblasts correlate with the cells' sensitivity to DNA interstrand crosslinking drugs.Haematologica · 2013Article
- Fanconi anemia complementation group A (FANCA) protein has intrinsic affinity for nucleic acids with preference for single-stranded forms.The Journal of biological chemistry · 2012Article
- Article
- Article
- Oxidative stress in Fanconi anemia hematopoiesis and disease progression.Antioxidants & redox signaling · 2008Review
- Induction of MxA gene expression by influenza A virus requires type I or type III interferon signaling.Journal of virology · 2007Article
- Article
- Inhibition of infectious pancreatic necrosis virus replication by atlantic salmon Mx1 protein.Journal of virology · 2004Article
- Fanconi anemia C gene product regulates expression of genes involved in differentiation and inflammation.Oncogene · 2004Article
- Analysis of baseline and cisplatin-inducible gene expression in Fanconi anemia cells using oligonucleotide-based microarrays.BMC blood disorders · 2002Article
- The Fanconi anemia protein FANCC binds to and facilitates the activation of STAT1 by gamma interferon and hematopoietic growth factors.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) consists of a group of at least five autosomal recessive disorders that share both clinical (e.g., birth defects and hematopoietic failure) and cellular (e.g., sensitivity to cross-linking agents and predisposition to apoptosis) features with each other. However, a common pathogenetic link among these groups has not been established. To identify genetic pathways that are altered in FA and characterize shared molecular defects, we used mRNA differential display to isolate genes that have altered expression patterns in FA cells. Here, we report that the expression of an interferon-inducible gene, MxA, is highly upregulated in cells of FA complementation groups A, B, C, and D, but it is suppressed in FA group C cells complemented with wild-type FAC cDNA as well as in non-FA cells. A posttranscriptional mechanism rather than transcriptional induction appears to account for MxA overexpression. Forced expression of MxA in Hep3B cells enhances their sensitivity to mitomycin C and induces apoptosis, similar to the FA phenotype. Thus, MxA is a downstream target of FAC and is the first genetic marker to be identified among multiple FA complementation groups. These data suggest that FA subtypes converge onto a final common pathway, which is intimately related to the interferon signaling mechanism. Constitutive activity of this pathway may explain a number of the phenotypic features of FA, particularly the pathogenesis of bone marrow failure.
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