Proteomic revelations
- PMID: 25120144
- PMCID: PMC4133747
- DOI: 10.1038/jid.2014.242
Proteomic revelations
Abstract
The power of proteomics in cultured skin fibroblasts from individuals with either systemic sclerosis or recessive dystrophic epidermolysis bullosa has led to the common finding of senescence and deficiencies in autophagy. Both of these disorders exert high demand on fibroblast activity, and without the protective action of autophagy cellular stress could have many adverse effects that are further amplified by the senescent phenotype.
Comment on
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Altered MCM protein levels and autophagic flux in aged and systemic sclerosis dermal fibroblasts.J Invest Dermatol. 2014 Sep;134(9):2321-2330. doi: 10.1038/jid.2014.69. Epub 2014 Feb 4. J Invest Dermatol. 2014. PMID: 24496236 Free PMC article.
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Loss of collagen VII is associated with reduced transglutaminase 2 abundance and activity.J Invest Dermatol. 2014 Sep;134(9):2381-2389. doi: 10.1038/jid.2014.185. Epub 2014 Apr 14. J Invest Dermatol. 2014. PMID: 24732400
References
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- Kuttner V, Mack C, Gretzmeier C, et al. Loss of Collagen VII is Associated with Reduced Transglutaminase 2 Abundance and Activity. J Invest Dermatol. 2014 - PubMed
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- Fine JD, Bruckner-Tuderman L, Eady RA, et al. Inherited epidermolysis bullosa: Updated recommendations on diagnosis and classification. J Am Acad Dermatol. 2014 - PubMed
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- Itahana K, Campisi J, Dimri GP. Methods to detect biomarkers of cellular senescence: the senescence-associated beta-galactosidase assay. Methods Mol Biol. 2007;371:21–31. - PubMed
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- Cipriani P, Di Benedetto P, Liakouli V, et al. Mesenchymal stem cells (MSCs) from scleroderma patients (SSc) preserve their immunomodulatory properties although senescent and normally induce T regulatory cells (Tregs) with a functional phenotype: implications for cellular-based therapy. Clin Exp Immunol. 2013;173:195–206. - PMC - PubMed
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