1279 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 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.

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 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.

An MHCl binding peptide design method based on evolutionary information and a Transform neural network algorithm relates to the field of protein design, and comprises the following steps: S1, extracting evolutionary information features of alleles of MHCII molecules and binding core sequences of binding peptides corresponding to the alleles, S2, establishing a neural network model based on fusion of a convolution module and a Transform module, and S3, establishing a neural network model based on fusion of the convolution module and the Transform module, the method comprises the following steps: S1, extracting two frequency characteristic tensors from S11 and S12, taking the two frequency characteristic tensors extracted in S11 and S12 as double inputs, and finally obtaining probability distribution of 20 amino acids at each position of each sequence, and S3, according to an output result of a neural network model, carrying out random sampling according to the probability, and generating a binding core sequence of MHCII-peptide meeting target distribution. According to the method, evolutionary information such as sequence position amino acid frequency (first-order conservative analysis) and combined frequency (second-order conservative analysis) of amino acid pairs is introduced to design a new short peptide sequence, the problem that short peptides cannot be designed based on structures is solved, and the reliability of short peptide sequence design based on evolutionary information is provided.

The invention provides a method for deducing the abundance of each family in a group based on mixed pool simplified genome sequencing, which comprises the following steps of: (1) establishing a parent 2b-rad library, and extracting SNP (Single Nucleotide Polymorphism) genotypes and sites by using a 2b-rad standard process; combining the SNP genotypes of the 2n parents into genotypes of n parent pairs according to a male parent and female parent relationship; comparing the genotypes of the parent pairs, and determining family specific tags; (2) extracting offspring individual tissues, mixing, and carrying out DNA extraction and 2b-rad library building sequencing on the mixed sample tissues; counting the sequencing depth of all the specific tag sites and calculating the secondary allele frequency of the specific tag of the mixed sample filial generation; and (3) calculating the proportion of each family in the offspring according to the sequencing depth of the specific tag site and the secondary allele frequency of the specific tag of the mixed offspring. According to the method, the overall feature distribution of the family can be accurately evaluated without sequencing each individual, so that the cost is greatly reduced.

The invention discloses a molecular marker related to a soybean hundred-grain weight character as well as a primer composition and application of the molecular marker. The invention relates to the technical field of biology, in particular to a molecular marker related to the soybean hundred-grain weight character and a primer composition and application of the molecular marker. By detecting the polymorphism or genotype (allele) of an SNP site in a soybean genome to be detected, the soybean hundred-grain weight character is identified or identified in an auxiliary mode according to the genotype, the SNP site is a site on a soybean chromosome 19, the nucleotide type of the SNP site is A or C, and the SNP site is the 20th nucleotide of a sequence 1 in a sequence table. The hundred-grain weight of the soybean with the genotype of AA at the site is higher than that of the soybean with the genotype of CC. The substance for detecting SNP site polymorphism and genotype can be combined with other substances (such as substances for detecting single nucleotide polymorphism or genotype of other molecular markers with soybean hundred-grain weight character) to prepare products for identifying soybean hundred-grain weight character.

The invention discloses an anti-TP53 mutation T cell receptor and application thereof, the T cell receptor comprises specific alpha chain and beta chain variable domains, and the complementary determining region (CDR) sequence is shown as SEQ ID NO: 9-14. The TCR has the core advantage that the TCR has excellent broad-spectrum recognition capability, can target six different amino acid substitutions (A, G, I, N, S and T) at the R249 site, and effectively deals with tumor heterogeneity and mutation difference between patients. Aiming at high-frequency HLA-B * 07: 02 alleles in people, the TCR lays a foundation for developing TCR-T cell therapy covering a wide range of people, and has great clinical application value and market potential in treatment of various solid tumors carrying TP53 R249 hotspot mutation, such as liver cancer.

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 belongs to the technical field of pig molecular marker-assisted selection, and particularly relates to application of an SNP molecular marker related to the character of the number of live piglets born by pigs. The SNP molecular marker is a basic group of a 32663785th site of a ninth chromosome in a pig genome Sscrofa11.1. 109, the SNP site of the molecular marker has C / T polymorphism, and T is a favorable allelic variation of the character of the number of live piglets born by a pig. The dominant alleles of the SNP are preferably selected, the frequency of the dominant alleles can be increased generation by generation, the number of live piglets of pigs is increased, and the genetic improvement progress of the pigs is accelerated, so that the breeding and production benefits of the pigs are effectively improved.

The invention relates to a gene for regulating and controlling the grain number of crops and application thereof. Specifically, the invention provides an application of GNR1 (Grain Number in Rice1) or an allele of the GNR1 in Rice1 in the aspect of improving the yield of rice by regulating and controlling the change of the grain number per spike of the rice. Also disclosed are methods of growing plants with increased grain number per ear, increased stem number and / or increased yield. The GNR1 gene has a wide application prospect in plant breeding.

The invention discloses a method for detecting a diallele editing cell based on a CRISPR / Cas12a technology. The invention provides crRNA, and the nucleotide sequence of a binding target of the crRNA is SEQ ID NO.6. The crRNA is obtained by in-vitro transcription of a transcription template; the transcription template is a product obtained by annealing a single-stranded DNA (Deoxyribose Nucleic Acid) molecule as shown in SEQ ID NO.10 and a single-stranded DNA molecule as shown in SEQ ID NO.13. The invention provides crRNA of the CD71 gene, a CRISPR / Cas12a system is constructed by using the crRNA, CRISPR / Cas12a detection is performed, screening of CRISPR / Cas9 induced CD71 gene diallele editing cells is realized, and the method is simple, convenient, quick and convenient for economically and effectively screening a large number of mutant cells.

The invention belongs to the technical field of plant molecular biology, and relates to application of VDAC1 / 3a allele in regulation of tomato cold resistance. According to the invention, the expression quantity of the SlVDAC1 / 3a gene in the VDAC1 / 3a allele is reduced by means of knockout or mutation and the like, so that the cold resistance of the tomato can be enhanced, the yield of the tomato and the content of soluble solids are not negatively influenced, and a theoretical basis and gene resources are provided for cultivating and screening cold-resistant tomato varieties.

The invention relates to the technical field of gene editing, and particularly provides a method for creating herbicide-resistant rice through gene editing of an OsEPSPS gene promoter region, and the method is characterized in that WT / 29bp single allelic deletion mutation is introduced into the OsEPSPS gene promoter region, i.e., A in an OsEPSPS gene initiation codon ATG is 0 site, A in the OsEPSPS gene initiation codon ATG is 0 site, A in the OsEPSPS gene initiation codon ATG is 0 site, and A in the OsEPSPS gene initiation codon ATG is 0 site; 29bp is deleted from the 112nd site to the 1150th site at the upstream of the initiation codon ATG on one allele, and the other allele is kept unchanged. By introducing the single allelic deletion mutation, the rice can obtain resistance to EPSPS inhibitor herbicides, the resistance is identified in T0-generation plants carrying the mutation and can be stably inherited to offspring plants, and the application value is high for guaranteeing agricultural production safety and improving the use efficiency of the herbicides.

The invention belongs to the technical field of animal breeding, and particularly relates to application of a detection reagent of an SNP (Single Nucleotide Polymorphism) molecular marker related to pork tenderness. An SNP site exists at the 232bp position from the 5'end of the sequence, the polymorphism is G / A, three genotypes of GG, GA and AA are shown, G allele is dominant allele, and the meat tenderness of a GG type individual is obviously higher than that of an AA type individual. The invention further develops a reagent for detecting the SNP molecular marker, the reagent can be used for pig assisted breeding, pig breeding or pork tenderness identification, and a method for identifying the pork tenderness is developed, which is beneficial to accelerating genetic breeding and early-stage seed selection of boars with high-quality meat traits.

The invention discloses a mixed DNA sample donor proportion analysis method based on STR typing and residual matrix analysis, which comprises the following steps: firstly, calculating the minimum donor number in a sample through a maximum allele counting method, further fitting the genotype distribution of the sample through an optimization algorithm, comparing the difference between the predicted peak height and the actually measured peak height, and determining the donor proportion of the sample according to the difference between the predicted peak height and the actually measured peak height. Therefore, the proportion of each donor in the mixed DNA sample is accurately estimated. Experimental results show that when the method is used for processing a multi-allele mixed DNA sample, estimation errors existing in a traditional method can be effectively reduced, and particularly, high accuracy is shown in complex sample analysis. By establishing a linear model and combining an optimization algorithm, the method not only provides high-precision technical support for DNA analysis in forensic science, but also provides a feasible solution for quantitative analysis of mixed DNA samples in other fields.

Methods, systems, and software for estimating circulating tumor fraction are provided. A first plurality of nucleic acid sequences for a plurality of loci in genomic DNA from a solid tumor sample is obtained. A second plurality of nucleic acid sequences for a plurality of cell-free DNA fragments obtained from a liquid biopsy sample from the same subject is obtained. One or more somatic mutations is identified in the first plurality of nucleic acid sequences. A variant allele frequency (VAF) is determined for each somatic mutation based on a frequency of the respective somatic mutation in the liquid biopsy sample and a frequency of the corresponding wild type allele in the liquid biopsy sample, thereby determining a set of VAFs. An estimate of the circulating tumor fraction for the test subject is determined based on the set of VAFs for the one or more somatic mutations.