http://rdf.ncbi.nlm.nih.gov/pubchem/patent/KR-20190029979-A

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filingDate 2017-09-13-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_62d292b63d3372abf6ed7dc72d708afa
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_df3dd10c32741a32be85a29cd7995e2d
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publicationDate 2019-03-21-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber KR-20190029979-A
titleOfInvention Therapeutic method of hepatocyte growth factor overexpressing adipose tissue derived mesenchymal stem cells for Amyotrophic Lateral Sclerosis
abstract The present invention relates to mammalian adipose derived mesenchymal stem cells comprising a person having the therapeutic effect of amyotrophic lateral sclerosis. In the present invention, the hepatocyte growth factor gene is introduced by the pMEX expression vector vector. Specifically, (a) the step of culturing the mesenchymal stem cells derived from the mammalian adipose, (b) the step of culturing the mesenchymal stem Introducing a hepatocyte growth factor gene into the cell, (c) selecting mesenchymal stem cells derived from the mammalian adipose tissue into which the hepatocyte growth factor gene has been introduced, (d) selecting the mesenchymal stem cells derived from the selected mammalian adipose tissue, And optionally culturing. As a result of analysis by reverse transcription polymerase chain reaction analysis in the present invention, it was confirmed that the expression of mesenchymal stem cells in mammalian adipose-derived mesenchymal stem cells including human with overexpression of hepatocyte growth factor was remarkably increased compared to the control group. In the enzyme immunoassay, And that overexpression of mesenchymal stem cells in mammalian adipose-derived mesenchymal stem cells, including those with overexpression of hepatocyte growth factor, was overexpressed. In addition, mesenchymal stem cells from mammalian adipose tissue, including those with overexpression of hepatocyte growth factor, promoted motor neuron function in SOD1 G93A mutant mice and contributed to delaying the onset of symptoms.
isCitedBy http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2021034162-A1
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