ArticleExperimental dermatology2011
Expression of the Abca-subfamily of genes in Abcc6-/- mice--upregulation of Abca4.
Article in Experimental dermatology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- The ABCC6 transporter: what lessons can be learnt from other ATP-binding cassette transporters?Frontiers in genetics · 2013Article
- Mouse Samd9l is not a functional paralogue of the human SAMD9, the gene mutated in normophosphataemic familial tumoral calcinosis.Experimental dermatology · 2012Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Pseudoxanthoma elasticum (PXE), a heritable multi-system disorder, is caused by mutations in the ABCC6 gene primarily expressed in the liver. Recent analysis of cultured fibroblasts from patients with PXE has suggested compensatory alterations in the expression of the ABCA-subfamily of genes. We have now determined by quantitative RT-PCR the level of expression of Abca-family of genes in a mouse model of PXE developed by targeted ablation of Abcc6. The results indicated variable levels of mRNA for different Abca genes in the liver; however, only one of them, Abca4, was significantly, ∼6.5-fold, upregulated in the Abcc6(-/-) mice in comparison with wild-type mice. In the same mice, Abca4 was not upregulated in the eyes or the kidney, suggesting that the upregulation of Abca4 in the liver is a tissue-specific compensatory consequence of the 'knock-out' of Abcc6.
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