The present disclosure relates to use of a lectin receptor-like kinase LecRK-IX.1 as a protein for regulating insect resistance of Arabidopsis thaliana. A. thaliana with high resistance to Bemisia tabaci can be cultivated by reducing the expression of, or knocking out, an encoding gene of the protein. Therefore, Arabidopsis thaliana with the high-level resistance to Bemisia tabaci can be cultivated. The gene and its encoded protein can be applied to plant genetic improvement.

Methods of producing human stem cells are disclosed for parthenogenetically activating human oocytes by manipulation of O.sub.2 tension, including manipulation of Ca.sup.2+ under high O.sub.2 tension and contacting oocytes with serine threonine kinase inhibitors under low O.sub.2 tension, isolating inner cell masses (ICMs) from the activated oocytes, and culturing the cells of the isolated ICMs under high O.sub.2 tension. Moreover, methods are described for the production of stems cells from activated oocytes in the absence of non-human animal products, including the use of human feeder cells/products for culturing ICM/stem cells. Stem cells produced by the disclosed methods are also described.

The present invention relates to enzyme inhibitors. More specifically, the present invention relates to ligand-directed covalent modification of proteins; method of designing same; pharmaceutical formulation of same; and method of use.

The present invention relates to a mutant NNK1 allele, especially a mutant carrying a mutation at position of amino acid 807 of the wild type sequence. The invention relates further to the use of said mutant allele to increase the fermentation rate in yeast, preferably in Saccharomyces. The mutant allele is especially useful to increase the xylose to ethanol fermentation rate.

Provided is an acid-resistant yeast cell that is genetically engineered to enhance activity of a radiation sensitivity complementing kinase, and a method of producing lactate by using the yeast cell.

The invention discloses a method for determining the repair activity of NHEJ. In this method, HPRT gene is mutated by using a site-directed gene mutation technology, and plasmid transfection, and 6-TG treatment are performed. By means of the method of the invention, the NHEJ repair activity level of cells can be observed by measuring the cell viability. The method can be used for screening the effects of different drugs and different genes on the NHEJ repair activity.

Polynucleotides comprising the following base sequences: (a) a base sequence encoding a fusion protein of a nuclease-deficient CRISPR effector protein and a transcriptional repressor, and (b) a base sequence encoding a guide RNA targeting a continuous region of 18 to 24 nucleotides in length in a region set forth in SEQ ID NO: 127, SEQ ID NO: 46, SEQ ID NO: 128, SEQ ID NO: 129, SEQ ID NO: 130, SEQ ID NO: 131, SEQ ID NO: 132, SEQ ID NO: 88, SEQ ID NO: 91, SEQ ID NO: 133, SEQ ID NO: 137, SEQ ID NO: 117, or SEQ ID NO: 119 in an expression regulatory region of a human DMPK gene, are expected to be useful for treating muscular dystrophy.

Provided herein are methods, compounds, and compositions for reducing expression of a DMPK mRNA and protein in an animal. Also provided herein are methods, compounds, and compositions for preferentially reducing CUGexp DMPK RNA, reducing myotonia or reducing spliceopathy in an animal. Such methods, compounds, and compositions are useful to treat, prevent, delay, or ameliorate type 1 myotonic dystrophy, or a symptom thereof.

Provided are a polypeptide and nucleic acid for encoding the polypeptide, a nucleic-acid construct, an expression vector, and a host cell containing the nucleic acid, an antigen-presenting cell presenting the polypeptide on the surface of the cell, and immune effector cell thereof, a pharmaceutical composition containing the polypeptide, a vaccine containing the nucleic acid, the nucleic acid construct, the expression vector, the host cell, the antigen-presenting cell, and the immune effector cell, and an antibody recognizing the polypeptide. Also provided is a therapeutic method using the polypeptide, the nucleic acid, the pharmaceutical composition, the vaccine, and the antibody. Also provided are a diagnosis method and diagnosis apparatus for detecting the described polypeptide. Also provided is an application of the polypeptide in preparing a vaccine, a tumor diagnosis kit, or a pharmaceutical composition, and an application of the polypeptide or the nucleic acid as a test target in tumor diagnosis.

Compositions and methods for treating melanoma are provided. Compositions include BRAF.sub.V600E-based peptides, alone or admixed with T helper peptides. Other compositions include nucleic acid sequences encoding the BRAF.sub.V600E-based peptides, alone or admixed with nucleic acid sequences T helper peptides. Dendritic cells pretreated with the BRAF.sub.V600E-based peptides, alone or admixed with T helper peptides, are also provided. These compositions are useful to treat melanoma, optionally co-administered with antibodies to checkpoint inhibitors or molecules that mimic the action of such antibodies.