TLDR Mouse and human keratin 16 can both form filaments, with differences likely due to the tail domain, not the helical domain.
The study successfully cloned and sequenced mouse keratin 16 (K16), revealing differences from human K16, particularly the absence of a proline residue in the 1B subdomain of the helical domain, which was previously thought to affect filament assembly. Contrary to earlier beliefs, both mouse and human K16 could integrate into the K8/K18 network and form filaments in vitro, suggesting that the unique functions of K16 are not due to the helical domain's sequence but likely related to the tail domain. This research provided insights into the assembly characteristics and potential functional domains of K16 in mice compared to humans.
63 citations
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July 2006 in “British Journal of Dermatology” Psoriasis causes changes in certain keratins and shrinks sebaceous glands in the scalp.
141 citations
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February 1988 in “Molecular and Cellular Biology” The study characterized type I keratin genes K16 and K14 on human chromosome 17, finding two genes for K16 and three for K14 in distinct clusters. These genes showed high homology, particularly the K16 genes, which shared similarities in coding sequences and surrounding regions. However, only one K16 gene produced a functional protein capable of forming keratin filaments, likely due to a stronger promoter. The functional K16 gene was confirmed to be responsible for K16 expression in human tissues using a specific polyclonal antiserum.
135 citations
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November 1987 in “Differentiation” 57 citations
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January 1987 in “Journal of Biological Chemistry” Different keratins have unique expression patterns in mouse skin cells.
686 citations
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February 2002 in “Current Opinion in Cell Biology” This review explored the structure, function, and regulation of keratin intermediate filaments (IFs), highlighting both established ('hard') and emerging ('soft') principles. It discussed the discovery of novel keratin genes, the mechanics of keratin filaments, and the functional redundancy revealed by gene knockouts. The study also examined the role of keratin mutations in various diseases and the regulation of keratin through interactions with other proteins. The field was noted to be rapidly advancing, driven by transgenic models and new insights into keratin's protective roles in cellular stress responses.
