1726 results about "Allelic gene" patented technology

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

The invention relates to the technical field of molecular biology and molecular markers, in particular to an SNP (Single Nucleotide Polymorphism) molecular marker located on a porcine chromosome 14 and related to porcine reproductive traits and application. The SNP site of the SNP molecular marker located on the No.14 chromosome of the pig and related to the reproductive traits of the pig corresponds to the Cgt at the 105043272th site on the No.14 chromosome of the international pig reference genome version 11.1; t mutation is carried out, and the polymorphism of the basic group at the site affects the porcine reproductive traits; wherein the reproductive performance of pigs with CC and TC genotypes is superior to that of pigs with TT genotypes. By optimizing the dominant alleles of the SNP molecular marker, the frequency of the dominant alleles can be increased generation by generation, the reproductive performance of pigs is improved, and the genetic improvement progress of the pigs is accelerated, so that the economic benefit of pig breeding is effectively improved.

The invention belongs to the technical field of allele typing, and discloses a gene haplotype typing method and device based on sequencing data and a medium, and the method comprises the following steps: obtaining to-be-detected gene sequencing data from a to-be-detected sample; splitting the sequencing data into genes according to a reference sequence, and performing variation information detection and variation information filtering; after sequence splitting is carried out on the basis of the sequence obtained after variation information filtering, the haplotype sequence obtained after sequence splitting is corrected, and a to-be-detected gene haplotype typing result of the to-be-detected sample is obtained. According to the method, complex calculation is simplified by adopting a mode of firstly splitting sequences into genes, the method does not completely depend on sequence comparison results, and similar typing is finally evaluated by adopting a mode of combining comparison with backtracking variation information scoring, so that typing difference information can be effectively refined, and interference of sequencing data noise on the results is reduced; and a haplotype result is verified for multiple times by adopting a primary typing and correction mode, so that the result accuracy is higher.

The invention belongs to the technical field of molecular biotechnology and molecular markers, and particularly relates to an SNP (Single Nucleotide Polymorphism) molecular marker located on a chromosome 2 and related to abnormal delivery traits of sows and application of the SNP molecular marker. An SNP site of the SNP molecular marker corresponds to Cgt at the 23330829bp position on a chromosome 2 of an international pig reference genome version 11.1; and the polymorphism of the basic group at the site affects the abnormal delivery character of the sow. The method solves the problem of genetic improvement of abnormal delivery of sows by means of molecular breeding, and can increase the frequency of dominant alleles generation by generation, reduce the occurrence rate of abnormal delivery of sows and improve the reproductive performance of sows by optimizing the dominant alleles of variation sites. The pig genetic improvement progress is accelerated, so that the economic benefit of breeding pig breeding is effectively improved.

The invention discloses a rubber tree whole genome SNP molecular marker combination, a gene chip and application, and belongs to the field of molecular marker development. The rubber tree whole genome SNP molecular marker combination comprises 28923 SNP molecular markers, the 28923 SNP molecular markers comprise 28923 SNP sites, each SNP site comprises two different base variation sites and is used for detecting allelic change of the site, and the physical positions of the 28923 SNP sites are determined based on comparison of genome sequences of rubber tree wild germplasm MT / VB / 25A 57 / 8. The 28923 SNP loci adopted by the invention uniformly cover the whole genome of the rubber tree, so that the real level of genetic diversity of the rubber tree can be comprehensively revealed, and the SNP loci can be applied to genetic diversity analysis, population structure analysis, whole-genome association analysis, molecular marker-assisted breeding and whole-genome selective breeding research work of the rubber tree. The whole genome SNP site combination and the gene chip thereof are used for detection, have the advantages of simplicity, rapidness and low cost, and can realize large-scale application in hevea brasiliensis genetic breeding research.

The invention relates to the technical field of fish genetic breeding, in particular to a method for improving carassius auratus gibelio resistance to carassius auratus gibelio herpesvirus. A CRISPR (clustered regularly interspaced short palindromic repeats) / Cas9 (CRISPR associated protein 9) gene editing technology is utilized to specifically knock out the carassius auratus gibelio irf10-B gene to obtain a mutant genotype individual of which three irf10-B alleles are terminated in advance, namely the required carassius auratus gibelio with high resistance The invention also discloses two specific knockout targets of the irf10-B gene and an allele sequence corresponding to a mutant genotype individual in which three alleles of the irf10-B are terminated in advance. According to the invention, the function of the irf10-B in the prussian carp is verified for the first time, a new germplasm of which the capability of resisting the herpesvirus of the prussian carp is improved by 30% is rapidly obtained by knocking out the single gene of the irf10-B, and the new germplasm has important industrial value.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload inhibits expression or activity of a DMPK allele comprising a disease-associated-repeat. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide or RNAi oligonucleotide.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

The invention discloses an ultrahigh-sensitivity sample component evaluation and traceability method and device. The method comprises the following steps: acquiring a sample, and carrying out nucleic acid extraction, library construction, capture enrichment and sequencing to generate sequencing data; preprocessing the sequencing data to obtain high-quality sequencing data; identifying SNP loci and genotypes thereof in the high-quality sequencing data, and constructing an SNP combination database; carrying out quantitative statistics on the double allelic genotypes of the SNP sites, and calculating the variation abundance of secondary alleles; constructing an SNP site variation abundance background distribution model according to the genotype information and allele variation abundance of the SNP sites; and performing cross contamination assessment on the sample by using the constructed SNP combination database and the variation abundance background distribution model. According to the method, qualitative evaluation of multi-source components in the sample, quantitative calculation of the cross contamination proportion and traceability analysis of non-self sources are achieved.

The invention provides an SNP (Single Nucleotide Polymorphism) site of an ABO blood group variant, and a B subtype variant blood group identification kit and method, and relates to the technical field of biology. The SNP (Single Nucleotide Polymorphism) sites of the ABO blood group variant comprise the 842th c.842Cgt from an initiation codon of an ABO * B.01 allele coding region of an ABO gene; mutation of T. A substance for detecting the SNP site of the ABO blood group variant can be applied to preparation of a B subtype variant blood group identification method and product, so that the substance can be effectively applied to rapid detection of patients and blood donors, the B subtype variant blood group of an individual can be defined, and potential possible blood transfusion reaction can be prevented in time.

Aspects of the disclosure relate to complexes comprising a muscle-targeting agent covalently linked to a molecular payload. In some embodiments, the muscle-targeting agent specifically binds to an internalizing cell surface receptor on muscle cells. In some embodiments, the molecular payload promotes the expression or activity of a functional dystrophin protein. In some embodiments, the molecular payload is an oligonucleotide, such as an antisense oligonucleotide, e.g., an oligonucleotide that causes exon skipping in a mRNA expressed from a mutant DMD allele.

Among other things, the present disclosure pertains to methods and compositions related to phasing of allelic variants of genetic loci. Phasing of allelic variants of genetic loci on an individual patient's chromosomes is highly valuable for many purposes, including patient stratification for allele-specific therapeutics.

The invention discloses a corn kernel size regulation gene X1 as well as an SNP (Single Nucleotide Polymorphism) marker and application thereof. The invention discovers that the X1 gene has the function of regulating and controlling the grain shape and the grain weight for the first time. The invention provides a novel SNP (Single Nucleotide Polymorphism) marker related to the corn grain size, the SNP marker has two alleles AA and GG, and the allele AA is clear to be regarded as an excellent / synergistic allele. The X1 gene provided by the invention can lead to increase of grain types such as the length of a corn grain of a mutant strain compared with that of a control grain; the length and other grain types of the X1 gene overexpression strain are reduced compared with those of the control grain. Precious gene resources are provided for corn breeding, and the application prospect is wide.

The invention discloses a rice SDR1 gene as well as an encoding protein and application thereof. The invention relates to a gene SDR1 for regulating the plant height. One or more nucleotides are added, substituted, inserted or deleted in the nucleotide sequence shown in SEQ ID NO: 1 or SEQ ID NO: 2 of the SDR1 gene to generate a mutant, an allele or a derivative. Through phenotypic analysis, genetic analysis, gene cloning and expression analysis of the screened dwarf mutant, the gene participating in rice plant height development regulation of the dwarf mutant is determined, and a foundation is laid for further analysis of a molecular regulation network of rice stem development. The gene SDR1 disclosed by the invention has a remarkable effect on further adjustment of the plant height of the dwarf rice, so that the gene SDR1 has an important influence on optimization of the plant type of the dwarf rice.

The invention belongs to the technical field of molecular biotechnology and molecular markers, and particularly relates to an SNP (Single Nucleotide Polymorphism) site related to pig intramuscular fat content, a related molecular marker and application of the SNP site. The SNP site corresponds to the 151330919bp site of a No.6 chromosome of an international pig reference genome version 11.1, the polymorphism of a base of the site affects the intramuscular fat content of the pig, the related index of a TT genotype is greater than that of a pig individual with TG and GG genotypes, and the related index of the TG genotype is greater than that of a pig individual with GG genotype. According to the invention, a molecular breeding means is utilized to solve the problem of improving the character expression of the intramuscular fat content of the pig, and by optimizing the dominant alleles of the SNP, the frequency of the dominant alleles can be increased generation by generation, the intramuscular fat content of the pig can be improved, the pork quality can be improved, the genetic modification breeding of the pig can be accelerated, and the economic benefit of a pig farm can be improved.

The invention provides a fusion protein with a tribasic group editing function and application thereof, and relates to the technical field of basic group editing. The fusion protein comprises adenine deaminase, N-methylpurine DNA (deoxyribonucleic acid) glycosylase and nuclease. Aiming at the problem that an existing base editing tool cannot edit by taking three bases as substrates at the same time, the invention provides a novel three-function base editor which is named as A, Camp; and G-BE. A, Camp; the G-BE can be edited by independently using A, C and G as substrates to realize the editing activity of A-G / T / C, C-T / G / A and G-T / A / C, and can also be edited by simultaneously using A, C and G as substrates on alleles.