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83 results about "Leucine-rich repeat" patented technology

A leucine-rich repeat (LRR) is a protein structural motif that forms an α/β horseshoe fold. It is composed of repeating 20–30 amino acid stretches that are unusually rich in the hydrophobic amino acid leucine. These tandem repeats commonly fold together to form a solenoid protein domain, termed leucine-rich repeat domain. Typically, each repeat unit has beta strand-turn-alpha helix structure, and the assembled domain, composed of many such repeats, has a horseshoe shape with an interior parallel beta sheet and an exterior array of helices. One face of the beta sheet and one side of the helix array are exposed to solvent and are therefore dominated by hydrophilic residues. The region between the helices and sheets is the protein's hydrophobic core and is tightly sterically packed with leucine residues.

Leucine-rich repeat kinase (LRRK2) drosophila model for parkinson's disease: wildtype1 (WT1) and G2019S mutant flies

Mutations in the leucine-rich repeat kinase (LRRK2) gene cause late-onset autosomal dominant Parkinson's disease (PD) with pleiomorphic pathology. Previously, we and others found that expression of mutant LRRK2 causes neuronal degeneration in cell culture. Here we used the GAL4/UAS system to generate transgenic Drosophila expressing either wild-type (WT1) human LRRK2 or LRRK2-G2019S, the most common mutation associated with PD. Expression of either WT1 human LRRK2 or LRRK2-G2019S in the photoreceptor cells caused retinal degeneration. Expression of WT1 LRRK2 or LRRK2-G2019S in neurons produced adult-onset selective loss of dopaminergic neurons, locomotor dysfunction, and early mortality. Expression of mutant G2019S-LRRK2 caused a more severe parkinsonism-like phenotype than expression of equivalent levels of WT1 LRRK2. Treatment with L-DOPA improved mutant LRRK2-induced locomotor impairment but did not prevent the loss of tyrosine hydroxylase (TH)-positive neurons. To our knowledge, this is the first in vivo “gain-of-function” model which recapitulates several key features of LRRK2-linked human parkinsonism. These flies may provide a useful model for studying LRRK2-linked pathogenesis and for future therapeutic screens for PD intervention.
Owner:THE JOHN HOPKINS UNIV SCHOOL OF MEDICINE

Nucleic acid ligands capable of binding to internalin B or internalin A

The present disclosure relates to the isolation of a novel reagent selected for its binding characteristics to the proteins internalin B or internalin A. InIB is a surface-localized protein of Listeria monocytogenes that binds and activates the receptor tyrosine kinase Met. InIB promotes invasion of a number of cells including hepatocytes, endothelial and epithelial cell lines and causes activation of the actin-mediated internalization of the bacterium. InIA belongs to a large group of surface-localized leucine-rich repeat (LRR) proteins identified in the Listeria genome. InIA enables Listeria monocytogenes to invade non-phagocytic cells such as those of the human intestinal epithelium and is sufficient for adhesion to and inducing uptake into epithelial cells. The disclosed nucleic acid ligands to internalin B and internalin A may be useful for determining the presence or absence of internalin B, internalin A, or Listeria in food, clinical or environmental samples; they may also be useful as an agent for combating Listeria infection by binding to and inactivating the infection-promoting inlB or inlA proteins. One object is to incorporate these nucleic acid ligands into an in vitro diagnostic or biosensor platform designed to detect the presence or absence of internalin B, internalin A, or Listeria in food, clinical or environmental samples. Another object is to employ these nucleic acid ligands in methods for treating or preventing Listeria infection.
Owner:RESONAC CORPORATION +1

Application of NtRLK2 gene to resistance of tobacco to bacterial wilt

The invention relates to a sequence and functional application of an LRR (Leucine-Rich Repeat) acceptor protein kinase gene NtRLK2 related to the resistance of tobacco to bacterial wilt, and belongs to the technical field of molecular biology. According to the sequence and the functional application, through the analysis of a gene chip, a partial segment of one LRR acceptor protein kinase gene NtRLK2 of which the expression is up-regulated by 2 times when being induced by ralstonia solanacearum is obtained; a full-length cDNA (complementary Deoxyribonucleic Acid) sequence of the LRR acceptor protein kinase gene NtRLK2 is obtained through an RACE (Rapid Amplification of cDNA end) technique; the gene is cloned from a high-bacterial-wilt-resistance variety line 3 of the tobacco, is used for constructing over-expression and RNAi (Ribonucleic Acid interference) expression vectors, and is transferred into a bacterial wilt infected variety Cuibi 1# in the tobacco; indicated by inoculation identification, the RANi of the gene obviously enhances the disease resistance of a tobacco plant to the bacterial wilt; preliminarily predicted, the gene is possibly an interacting gene of an endogenous disease-resistant gene; the expression of the disease-resistant gene is inhibited. According to the application, a foundation is about to be laid for the bacterial-wilt disease-resistant genetic breeding of the tobacco.
Owner:FUJIAN AGRI & FORESTRY UNIV

Application of chlamydomonas reinhardtii LRR (Leucine Rich Repeat) gene in regulating and controlling cadmium resistance of chlamydomonas reinhardtii

The invention discloses application of a chlamydomonas reinhardtii LRR (Leucine Rich Repeat) gene in regulating and controlling cadmium resistance of chlamydomonas reinhardtii, and belongs to the technical field of biologics and the field of environmental pollution improvement. According to the application, an aphVIII fragment with a paromomycin resistance gene is randomly inserted into chlamydomonas, then a chlamydomonas reinhardtii mutant alga strain which is remarkable in cadmium chloride resistance is cultured, and further identification shows that the cadmium sensitivity of the mutant alga strain is caused since the aphVIII (SEQ ID NO:3) fragment is inserted into an LRR gene (a CDS (Cadmium Sulfide) sequence is shown in SEQ ID NO:1 in the specification). By reducing expression of thechlamydomonas reinhardtii LRR gene, deactivating the LRR gene or by deleting the LRR gene, the cadmium resistance of the chlamydomonas reinhardtii can be improved; a cadmium resistance improved chlamydomonas reinhardtii strain obtained by means of genetic engineering can be applied to monitoring and improvement of cadmium polluted water areas, cadmium polluted water environments can be treated with the cadmium resistance improved chlamydomonas reinhardtii strain, the operation is simple and feasible, and the cost is low.
Owner:JIANGHAN UNIVERSITY
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