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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)
Top mentioned proteins: CAN, cytokeratin, ACID, Filaggrin, Involucrin
Papers on LOR
Gene Expression Profiles in Generalized Aggressive Periodontitis: A Gene Network-Based Microarray Analysis.
New
Savli et al., Kocaeli, Turkey. In J Periodontol, 02 Aug 2015
The most up-regulated genes were found as MZB1, TNFRSF17, PNOC, FCRL5, LAX1, BMS1P20, IGLL5, MMP7, SPAG4, MEI1; the most down-regulated genes were found as LOR, LAMB4, AADACL2, MAPT, ARG1, NPR3, AADAC, DSC1, LRRC4, CHP2.
AKT1-mediated Lamin A/C degradation is required for nuclear degradation and normal epidermal terminal differentiation.
New
O'Shaughnessy et al., London, United Kingdom. In Cell Death Differ, 05 Jul 2015
Using AKT-phosphorylation-dead Lamin A constructs we show that the retention of nuclear material is sufficient to cause profound changes in epidermal terminal differentiation, specifically a reduction in Loricrin, Keratin 1, Keratin 10, and filaggrin expression.
RNA/DNA co-analysis from human skin and contact traces--results of a sixth collaborative EDNAP exercise.
New
Ballantyne et al., Zürich, Switzerland. In Forensic Sci Int Genet, May 2015
Two sets of previously described skin-specific markers were used: skin1 pentaplex (LCE1C, LCE1D, LCE2D, IL1F7 and CCL27) and skin2 triplex (LOR, KRT9 and CDSN) in conjunction with a housekeeping gene, HKG, triplex (B2M, UBC and UCE).
Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner.
New
Furue et al., Fukuoka, Japan. In Clin Exp Dermatol, Apr 2015
AIM: To examine whether GFF upregulates the expression of the filaggrin and loricrin genes, FLG and LOR, in an AhR-dependent manner.
Characterization of the 5-HT2C receptor agonist lorcaserin on efficacy and safety measures in a rat model of diet-induced obesity.
New
Dobson et al., Toronto, Canada. In Pharmacol Res Perspect, Feb 2015
Lorcaserin (1-2 mg/kg SC b.i.d.) significantly reduced percentage body weight gain compared to vehicle-treated controls (VEH: 10.6 ± 0.4%; LOR 1: 7.6 ± 1.2%; LOR 2: 5.4 ± 0.6%).
Effects of ornithine decarboxylase antizyme 1 on the proliferation and differentiation of human oral cancer cells.
New
Jiang et al., Guangzhou, China. In Int J Mol Med, Dec 2014
Further results from quantitative reverse transcription‑polymerase chain reaction and western blot analysis proved the upregulation of several terminal differentiation marker genes (K10, FLG and LOR) in OAZ1‑expressed SCC15 cells.
A microfluidic method to synthesize transferrin-lipid nanoparticles loaded with siRNA LOR-1284 for therapy of acute myeloid leukemia.
New
Teng et al., Columbus, United States. In Nanoscale, Sep 2014
The siRNA LOR-1284 targets the R2 subunit of ribonucleotide reductase (RRM2) and has shown promise in cancer therapy.
Computational modeling predicts the ionic mechanism of late-onset responses in unipolar brush cells.
D'Angelo et al., Pavia, Italy. In Front Cell Neurosci, 2013
UBCs have recently been reported to generate, in addition to early-onset glutamate receptor-dependent synaptic responses, a late-onset response (LOR) composed of a slow depolarizing ramp followed by a spike burst (Locatelli et al., 2013).
Enhanced antisense oligonucleotide delivery using cationic liposomes incorporating fatty acid-modified polyethylenimine.
Xie et al., Changchun, China. In Curr Pharm Biotechnol, 2013
LOR-2501, an ASOs targeting ribonucleotide reductase R1 subunit (R1) was used as the therapeutic cargo.
Control of somatic tissue differentiation by the long non-coding RNA TINCR.
Impact
Khavari et al., Stanford, United States. In Nature, 2013
TINCR is required for high messenger RNA abundance of key differentiation genes, many of which are mutated in human skin diseases, including FLG, LOR, ALOXE3, ALOX12B, ABCA12, CASP14 and ELOVL3.
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.
Towards characterization of palmoplantar keratoderma caused by gain-of-function mutation in loricrin: analysis of a family and review of the literature.
Review
Hennies et al., Köln, Germany. In Br J Dermatol, 2006
We identified the previously reported mutation 730insG in LOR, which elongates loricrin by 22 amino acids because of delayed termination.
Subcellular localization of the product of the long open reading frame of human T-cell leukemia virus type I.
Impact
Haseltine et al., In Science, 1985
In addition to containing the gag, pol, and env genes of the chronic leukemia viruses, the genome of HTLV-I contains a long open reading frame (LOR) located between the 3' end of the envelope gene and the 3' long terminal repeat sequence (LTR).
Antigens encoded by the 3'-terminal region of human T-cell leukemia virus: evidence for a functional gene.
Impact
Essex et al., In Science, 1984
Radiolabel sequence analysis of cyanogen bromide fragments of p42 led to the conclusion that this antigen is encoded in part by LOR, a conserved portion of the "X" region that is flanked by the envelope gene and the 3' long terminal repeat of HTLV-I.
Bovine leukemia virus, a distinguished member of the human T-lymphotropic virus family.
Review
Marbaix et al., In Princess Takamatsu Symp, 1983
The most striking feature of these retroviruses is the existence of a long open reading frame (LOR) located at the 3' side of the provirus between the right end of the 3' side of env gene and the left end of the long terminal repeat (LTR).
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