ArticleJournal of clinical immunology2007
Carboxypeptidase D: a novel TGF-beta target gene dysregulated in patients with lupus erythematosus.
Article in Journal of clinical immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Low-frequency and rare genetic variants associated with rheumatoid arthritis risk.Nature reviews. Rheumatology · 2024Review
- Combined Transcriptomic and Proteomic ofAnimals : an open access journal from MDPI · 2022Article
- Substrate specificity of human metallocarboxypeptidase D: Comparison of the two active carboxypeptidase domains.PloS one · 2017Article
- Prolactin/Stat5 and androgen R1881 coactivate carboxypeptidase-D gene in breast cancer cells.Molecular endocrinology (Baltimore, Md.) · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that mainly acts as an inhibitor of immune functions. A lack of functional TGF-beta leads to autoimmune disease in animal models and dysregulated TGF-beta signaling is implicated in human autoimmune diseases. To define target genes that play a part in the inhibitory role of TGF-beta in the immune system, we have identified genes stimulated by TGF-beta in macrophages by gene-chip analysis. One of the TGF-beta regulated genes is carboxypeptidase D (CpD), a 180-kDa type I membrane protein. We have demonstrated that CpD is regulated by TGF-beta in various cell types of both, murine and human origin and, interestingly, is significantly downregulated in CD14 positive cells isolated from patients with lupus erythematosus (LE). Moreover, we show that downregulation of CpD leads to downmodulation of TGF-beta itself, suggesting a role for CpD in a positive feedback loop, providing further evidence for a role of this enzyme in LE. To our knowledge, this is the first report that demonstrates carboxypeptidase D as a TGF-beta target gene that is implicated in the pathogenesis of LE.
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Registered trials
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