ArticlePloS one2012
Activation of Fms-like tyrosine kinase 3 signaling enhances survivin expression in a mouse model of rheumatoid arthritis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 36 citations in OpenAlex.
- Get Spliced: Uniting Alternative Splicing and Arthritis.International journal of molecular sciences · 2024Review
- Toward Overcoming Treatment Failure in Rheumatoid Arthritis.Frontiers in immunology · 2021Review
- Survivin Measurement improves Clinical Prediction of Transition From Arthralgia to RA-Biomarkers to Improve Clinical Sensitivity of Transition From Arthralgia to RA.Frontiers in medicine · 2018Article
- Protective effect of ginkgo proanthocyanidins against cerebral ischemia/reperfusion injury associated with its antioxidant effects.Neural regeneration research · 2016Article
- Impact and mechanism of non-steroidal anti-inflammatory drugs combined with chemotherapeutic drugs on human lung cancer-nude mouse transplanted tumors.Oncology letters · 2016Article
- Murine germinal center B cells require functional Fms-like tyrosine kinase 3 signaling for IgG1 class-switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Serum survivin predicts responses to treatment in active rheumatoid arthritis: a post hoc analysis from the SWEFOT trial.BMC medicine · 2015Article
- Survivin co-ordinates formation of follicular T-cells acting in synergy with Bcl-6.Oncotarget · 2015Article
- Suppressed diversity of survivin splicing in active rheumatoid arthritis.Arthritis research & therapy · 2015Article
- Pathogenic Transdifferentiation of Th17 Cells Contribute to Perpetuation of Rheumatoid Arthritis during Anti-TNF Treatment.Molecular medicine (Cambridge, Mass.) · 2015Article
- Recognizing rheumatoid arthritis: oncoprotein survivin opens new possibilities: a population-based case-control study.Medicine · 2015Article
- Differences in growth promotion, drug response and intracellular protein trafficking of FLT3 mutants.Iranian journal of basic medical sciences · 2014Article
- Survivin but not Fms-like tyrosine kinase 3 ligand is up-regulated before the onset of rheumatoid arthritis: a pilot study.Arthritis research & therapy · 2014Article
- Novel insights into the regulatory architecture of CD4+ T cells in rheumatoid arthritis.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Survivin is known as an inhibitor of apoptosis and a positive regulator of cell division. We have recently identified survivin as a predictor of joint destruction in patients with rheumatoid arthritis (RA). Flt3 ligand (Flt3L) is expressed in the inflamed joints and has adjuvant properties in arthritis. Studies on 90 RA patients (median age 60.5 years [range, 24-87], disease duration 10.5 years [range, 0-35]) show a strong positive association between the levels of survivin and Flt3L in blood. Here, we present experimental evidence connecting survivin and Flt3L signaling. Treatment of BALB/c mice with Flt3L led to an increase of survivin in the bone marrow and in splenic dendritic cells. Flt3L changed the profile of survivin splice variants, increasing transcription of the short survivin40 in the bone marrow. Treatment with an Flt3 inhibitor reduced total survivin expression in bone marrow and in the dendritic cell population in spleen. Inhibition of survivin transcription in mice, by shRNA lentiviral constructs, reduced the gene expression of Flt3L. We conclude that expression of survivin is a downstream event of Flt3 signaling, which serves as an essential mechanism supporting survival of leukocytes during their differentiation, and maturation of dendritic cells, in RA.
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