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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Nov 2014.

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, ACID, cytokeratin, Involucrin, Filaggrin
Papers on LOR
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, 31 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.
Two novel mutations in the LOR gene in three families with loricrin keratoderma.
New
Fischer et al., Freiburg, Germany. In Br J Dermatol, 18 Oct 2014
UNLABELLED: Loricrin keratoderma (LK, MIM #604117) is an autosomal dominant disorder characterized by honeycomb palmoplantar keratoderma (PPK) and generalized mild ichthyosis, often associated with pseudoainhum.
No exonic mutations at GJB2, GJB3, GJB4, GJB6, ARS (Component B), and LOR genes responsible for a Chinese patient affected by progressive symmetric erythrokeratodermia with pseudoainhum.
New
Zhang et al., Hefei, China. In Int J Dermatol, Sep 2014
The GJB2, GJB3, GJB4, GJB6, ARS (Component B), and LOR gene mutation might contribute to PSEK manifestation.
Novel microdeletion in LOR causing autosomal dominant Loricrin keratoderma.
New
O'Shaughnessy et al., London, United Kingdom. In Br J Dermatol, Sep 2014
A novel heterozygous deletion inducing a frameshift was found in the Loricrin gene LOR c. 660_661delGC p.Gln222Alafs*113 het, predicted damaging in silico.
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.
Proteinase K-containing lipid nanoparticles for therapeutic delivery of siRNA LOR-1284.
New
Lee et al., Chinju, South Korea. In Anticancer Res, Jul 2014
BACKGROUND: The objective of the present study was to develop an efficient delivery vehicle for siRNA LOR-1284 through incorporation of proteinase K (PrK) as a means of preventing siRNA degradation by serum nucleases.
A novel alpha-thalassemia nonsense mutation in HBA2: C.382 A > T globin gene.
New
Shariati et al., Ahvāz, Iran. In Arch Iran Med, Jul 2014
DNA sequencing revealed this mutation in unrelated persons in Khuzestan province, Southwestern Iran of Lor ethnicity.
Are clinical measures influenced by various ethnic origins in Iranian patients with ankylosing spondylitis?A pilot study.
New
Qorbani et al., Tehrān, Iran. In Caspian J Intern Med, Dec 2013
The patients were classified into Fars, Turk, Kord, Lor and other ethnic origins.
Enhanced antisense oligonucleotide delivery using cationic liposomes incorporating Fatty Acid-modified polyethylenimine.
New
Xie et al., Changchun, China. In Curr Pharm Biotechnol, Dec 2013
LOR-2501, an ASOs targeting ribonucleotide reductase R1 subunit (R1) was used as the therapeutic cargo.
Computational modeling predicts the ionic mechanism of late-onset responses in unipolar brush cells.
New
D'Angelo et al., Pavia, Italy. In Front Cell Neurosci, Dec 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).
Control of somatic tissue differentiation by the long non-coding RNA TINCR.
New
Impact
Khavari et al., Stanford, United States. In Nature, Feb 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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