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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Loricrin

LOR, Loricrin, NLRR-1
This gene encodes loricrin, a major protein component of the cornified cell envelope found in terminally differentiated epidermal cells. Mutations in this gene are associated with Vohwinkel's syndrome and progressive symmetric erythrokeratoderma, both inherited skin diseases. [provided by RefSeq, Jul 2008] (from NCBI)
Papers on LOR
Evidence for the absence of mutations at GJB3, GJB4 and LOR in progressive symmetrical erythrokeratodermia.
GeneRIF
Deng et al., Guangzhou, China. In Clin Exp Dermatol, 2011
There were no mutations found in the LOR gene and the true pathogenesis of progressive symmetrical erythrokeratodermia remains unknown.
mRNA-based skin identification for forensic applications.
GeneRIF
Kayser et al., Rotterdam, Netherlands. In Int J Legal Med, 2011
identified mRNA transcripts from three genes CDSN, LOR and KRT9, showing strong over-expression in skin samples relative to samples from forensic body fluids, making them suitable markers for skin identification
Activation of vascular endothelial growth factor receptor 2 in a cellular model of loricrin keratoderma.
GeneRIF
Kubota et al., Japan. In J Biol Chem, 2010
VEGF release and the subsequent activation of VEGF receptor 2 link loricrin gene mutations to rapid cell proliferation in a cellular model of loricrin keratoderma.
Protein kinase C delta and eta differently regulate the expression of loricrin and Jun family proteins in human keratinocytes.
GeneRIF
Ohba et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2010
These findings suggest that inverse effects of PKCdelta and PKCeta on loricrin expression attributes to the expression of c-Jun and JunD.
Locus 1q21 Gene expression changes in atopic dermatitis skin lesions: deregulation of small proline-rich region 1A.
GeneRIF
Jarzab et al., Zabrze, Poland. In Int Arch Allergy Immunol, 2009
the deregulated increase in SPRR1A expression in chronic atopic skin lesions reflects an insufficient rise in SPRR transcripts, unable to compensate for the lack of LOR and thus contributing to the persistence of chronic atopic dermatitis skin lesions.
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