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Publikasi Scopus 926 artikel (Per 14 Maret 2022)
Publikasi Scopus 926 artikel (Per 14 Maret 2022)
Nidogen-1 (NID1) as specific ligand in natural killer (NK) cells stimulated from advanced ovarian cancer: Immunotherapy review
2021
AIP Conference Proceedings
2344
040009
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85103487578&doi=10.1063%2f5.0049157&partnerID=40&md5=c45066e93f8193a8972229dcd9d4bfb0
Biology Undergraduate Program, Faculty of Mathematics and Natural Science, Universitas Indonesia, Kampus UI Depok, West Java, 16424, Indonesia; Stem Cell and Tissue Engineering Research Cluster, Indonesian Medical Education and Research Institute (IMERI), Universitas Indonesia, Salemba Raya, Jakarta, West Java, 10430, Indonesia; Department of Biology, Faculty of Mathematics and Natural Science, Universitas Indonesia, Kampus UI Depok, West Java, 16424, Indonesia; Department of Histology, Faculty of Medicine, Universitas Indonesia, Salemba Raya, Jakarta, West Java, 10430, Indonesia
The pathway for the introduction of NK cell into abnormal cells is mediated by the receptor-ligand interaction on the cell surface. Among all the activation receptors, NKP44 has become a unique activation receptor because it has an ITIMs signaling pathway and actively plays an important role in several functions of stimulated NK cells. A potential ligand that can specifically regulate the activity of NKP44 receptors is NID1. NID1 is a novel ligand that can initiate two different regulations on NK cells activity. In addition, NID1 also provides predictions that are compatible with the electrophoretic glycoprotein mobility that has been detected by NKp44 through SDS-PAGE and ELISA tests compared to all proteins in the microenvironment of ovarian cancer. Curently, NID1 has been proven to be able to increase the cytotoxic reaction of non-cancerous NK cells. Further research is needed for the development of ovarian cancer immunotherapy based on the receptor-ligand interactions. © 2021 Author(s).
American Institute of Physics Inc.
0094243X
9780735440869
Conference Paper
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177
20880