12 results about "Adenosine deaminase" patented technology

The present application provides an engineered circular RNA capable of recruiting adenosine deaminase acting on RNA (ADAR; arRNA) and its application in treating Duchenne muscular dystrophy (DMD).

The application provides an adenosine deaminase content detection method and application thereof. The adenosine deaminase content detection method comprises the following steps: using the intrinsic fluorescence of adenosine, using adenosine deaminase to hydrolyze adenosine, and detecting the content of adenosine deaminase by a fluorescence analysis method. Adenosine itself has strong fluorescence, and after being hydrolyzed by adenosine deaminase, the fluorescence of the obtained hydrolysis product is reduced, thereby causing the fluorescence intensity of the solution of the detection system to be reduced; the content of adenosine deaminase in the system is detected by the change of the fluorescence intensity before and after adenosine hydrolysis. The adenosine deaminase content detection method in the application is simple to operate, does not need large instruments and equipment, and is cheap and easy to obtain materials, can accurately and rapidly detect the content of adenosine deaminase in a sample to be detected, has good sensitivity and specificity, and has a relatively wide application prospect.

This application belongs to the field of biotechnology and relates to an efficient and specific editing system, method, and application for A-G base substitution. The fusion protein described in this application comprises, from the N-terminus to the C-terminus, a first SaCas9 nickase fragment, a chimeric deaminase fragment, and a second SaCas9 nickase fragment. The deaminase is selected from adenosine deaminase or a variant thereof, specifically ecTadA8e. The amino acid sequence of ecTadA8e is shown in SEQ ID NO. 20, or has more than 80% sequence identity with the amino acid sequence shown in SEQ ID NO. 20, and possesses the function or activity of ecTadA8e. The fusion protein provided in this application, combined with the corresponding guide RNA, can efficiently and specifically replace the base A with G at the target site, providing an effective tool for repairing pathogenic mutations, studying gene function, and improving cell function, and has promising application prospects.

The present invention features genetically modified immune cells comprising novel adenosine base editors (e.g., ABE8) having enhanced anti-neoplasia activity, resistance to immune suppression, and decreased risk of eliciting a graft-versus-host reaction or host-versus-graft reaction, or a combination thereof. The present invention also features methods for producing and using these modified immune effector cells.

This invention discloses the application of adenosine deaminase or its modified forms in the preparation of therapeutic drugs that improve pancreatic islet inflammation and protect pancreatic β-cell function in diabetic patients. This invention is the first to discover that exogenous ADA, through a systemic clearance-local decompression mechanism, enhances circulating ADO clearance, reduces tissue ADO load, restores compensatoryly elevated tissue ADA activity to normal, significantly reduces macrophage infiltration in the islets, inhibits inflammatory factor expression, promotes β-cell proliferation and functional recovery, and improves glucose and lipid metabolism. This invention provides a disease-modifying therapy for diabetes that can simultaneously regulate immunity and metabolism, possessing extremely high clinical application value.

The technology described herein is directed to compositions, kits, systems and methods related to an engineered, inducible adenosine deaminase (iAD) enzymes, including but not limited to, an engineered inducible adenosine deaminase acting on RNA (ADAR) enzyme, which can be activated in the presence of an inducer. Also described are synthetic RNA molecules, to which the iAD can be specifically recruited to edit at least one target codon, leading to decreased or increased translation of the RNA molecules depending on the specific construct. The technology described herein is also directed to systems comprising the iAD and synthetic RNA molecule, nucleic acids and vectors encoding the iAD and synthetic RNA molecule, and methods of using such systems, nucleic acids, and vectors.

The invention provides compositions comprising novel adenosine base editors (e.g., ABE8) that have increased efficiency and methods of using base editors comprising adenosine deaminase variants for altering mutations associated with Glycogen Storage Disease Type 1a (GSD1a).

The present disclosure relates to a chemically modified oligonucleotide for use in site-directed A-to-l editing of a target RNA inside a cell with endogenous adenosine deaminase acting on RNA (ADAR), the oligonucleotide comprising a sequence capable of binding to a target sequence in a target RNA and a central base triplet (CBT) of 3 nucleotides (5' - N+1 N0 N-1 - 3'), wherein N0 is the central nucleotide directly opposite to a target adenosine in the target RNA that is to be edited, and wherein the oligonucleotide comprises an asymmetry of 25-1-8 in a 5' to 3' direction; and comprises: (i) one or more phosphorothioate (PS) linkages at one or more of position +22, position +21, position +11, and position +4; and / or (ii) a 2'-O-methyl (2'-O-Me) modified nucleosides at position +13 and / or position +9.

The present disclosure relates to a chemically modified oligonucleotide for use in site-directed A-to-I editing of a target RNA inside a cell with endogenous adenosine deaminase acting on RNA (ADAR), the oligonucleotide comprising a sequence capable of binding to a target sequence in a target RNA and a central base triplet (CBT) of 3 nucleotides (5′-N+1 N0 N−1-3′), wherein N0 is the central nucleotide directly opposite to a target adenosine in the target RNA that is to be edited, and wherein the oligonucleotide comprises an asymmetry of 25-1-8 in a 5′ to 3′ direction; and comprises: (i) one or more phosphorothioate (PS) linkages at one or more of position +22, position +21, position +11, and position +4; and / or (ii) a 2′-O-methyl (2′-O-Me) modified nucleosides at position +13 and / or position +9.

This application relates to the technical field of *Lactobacillus plantarum*, specifically to a strain of *Lactobacillus plantarum* LP305 and its application in the degradation of nucleosides and uric acid. This strain is *Lactobacillus plantarum* with accession number CGMCC NO.33425. Lactiplantibacillus plantarum LP305. This strain possesses the ability to completely degrade nucleosides in vitro and inhibits metabolic enzymes involved in the uric acid synthesis pathway, particularly adenosine deaminase, xanthine oxidase, and phosphoribosyl pyrophosphate synthase. Furthermore, this strain can improve kidney damage and intestinal flora imbalance caused by hyperuricemia.

The present invention features genetically modified immune cells comprising novel adenosine base editors (e.g., ABE8) having enhanced anti-neoplasia activity, resistance to immune suppression, and decreased risk of eliciting a graft-versus-host reaction or host-versus-graft reaction, or a combination thereof. The present invention also features methods for producing and using these modified immune effector cells.

Adenosine deaminase base editors, compositions comprising the same, and methods for use thereof for altering a target nucleobase in a polynucleotide sequence. In embodiments of the disclosure, the base editors of the disclosure may be used to treat a disease or disorder, such as a hemoglobinopathy (e.g., sickle cell disease (SCD)).