http://rdf.ncbi.nlm.nih.gov/pubchem/patent/CN-112390873-B

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classificationCPCAdditional http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K38-00
classificationCPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P39-06
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/C07K14-47
classificationIPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K14-47
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-17
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P39-06
filingDate 2020-11-19-04:00^^<http://www.w3.org/2001/XMLSchema#date>
grantDate 2021-11-02-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationDate 2021-11-02-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber CN-112390873-B
titleOfInvention Autophagy key protein ATG 7-based mutant and application thereof
abstract The invention belongs to the field of biotechnology and anti-aging treatment, relates to a mutant based on an autophagy key protein ATG7 and application thereof in anti-aging treatment, and particularly relates to a protein modification state simulated by amino acid site mutation and application thereof in anti-aging treatment. The amino acid sequence of the mutant based on the autophagy key protein ATG7 is SEQ ID No1, wherein the 411 th and 413 th amino acids are lysine mutated into glutamine, and the 513 th, 514 th and 516 th amino acids are mutated into arginine, and the mutant based on the autophagy key protein ATG7 is applied to preparation of a medicament for targeting senescence delaying or preventing and treating senescence-related diseases. Experiments prove that the mutant based on the autophagy key protein ATG7 can play a pharmacological role in delaying senescence by improving the function of cell nucleus, improving the proliferation state of cells and improving the metabolic state of cells.
priorityDate 2020-11-19-04:00^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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Total number of triples: 413.