Open AccessIntersectins as Novel Protein for Viral Endocytosis- A Mini Review
Author(s) -
Dluya Samuel Thagriki
Publication year - 2022
Publication title -
saudi journal of biomedical research
Language(s) - English
Resource type - Journals
eISSN - 2518-3222
pISSN - 2518-3214
DOI - 10.36348/sjbr.2022.v07i01.003
Subject(s) - endocytic cycle , endocytosis , biology , viral protein , microbiology and biotechnology , viral entry , virology , signal transducing adaptor protein , virus , signal transduction , viral replication , genetics , receptor
Intersectins (INSTNs) have been defined as scaffold proteins that have several biochemical functions. Initially INSTNs are described as endocytic regulators and function in different signalling pathways including Ras and Ras-like GTPases, PI3Ks and RTKs in several diseases. Recently, INSTNs have been reported in viral endocytosis. INSTNs was found to be upregulated in transcriptomic analysis of differentially expressed protein from Dengue virus serotype four from our recent data. Hence, this review summarises the role of INSTNs in viral endocytosis by interaction with signalling pathways. INSTN-2 interact with K15 protein of Kaposi’s Sarcoma-Associated Herpesvirus by selective SH3 domain, INSTN-1 interaction with Epstein-Barr virus Latent Membrane Protein 2 (LMP2A), while direct interaction of NPF motifs at C-terminus of A36 with INSTN-1 and Epsin15 homology domains recruiting AP-2 and clathrin mediate viral release was reported in Vaccinia virus. Most recent, INSTN-2 was shown to regulate adaptive immune response during viral infectivity. This was discovered when mice deficient in INSTN-2 exhibited high mortality rate, impaired antibody responses to vaccination and reduced germinal centre formation in Influenza A virus. This review revealed INSTNs as essential viral endocytic proteins. The review also highlights INSTNs role in other diseases and the regulation of signalling pathways. Targeting INSTNs could be important for the development of pharmaceuticals against viruses and diseases. More study is required to establish the mechanistic role of INSTNs for viral endocytosis.