Molecular promiscuity indicates the ability of a molecule to bind to interact with one or more other classes and subtypes of molecules, in synergistic or antagonistic ways. These interactions may involve multiple paracrine, endocrine and autocrine features.[1][2][3]
References
edit- ^ Clark, Adrian JL; Chan, Li F (April 2017). "Promiscuity among the MRAPs". Journal of Molecular Endocrinology. 58 (3): F1 – F4. doi:10.1530/JME-17-0002. PMID 28213370.F1 - F4&rft.date=2017-04&rft_id=info:doi/10.1530/JME-17-0002&rft_id=info:pmid/28213370&rft.aulast=Clark&rft.aufirst=Adrian JL&rft.au=Chan, Li F&rft_id=https://doi.org/10.1530%2FJME-17-0002&rfr_id=info:sid/en.wikipedia.org:Molecular promiscuity" class="Z3988">
- ^ Barth, Kenneth; Attardo Genco, Caroline (2016). "Microbial Degradation of Cellular Kinases Impairs Innate Immune Signaling and Paracrine TNFα Responses". Scientific Reports. 6: 34656. Bibcode:2016NatSR...634656B. doi:10.1038/srep34656. PMC 5048168. PMID 27698456.
- ^ Xiaofeng, Dai; Zhifu, Mao; Songping, Xie; Hao, Zhang; Jie, Huang (January 2013). "The CXCL12/CXCR4 autocrine loop increases the metastatic potential of non-small cell lung cancer in vitro". Oncology Letters. 5 (1): 277–282. doi:10.3892/ol.2012.960. PMC 3525341. PMID 23255935.277-282&rft.date=2013-01&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525341#id-name=PMC&rft_id=info:pmid/23255935&rft_id=info:doi/10.3892/ol.2012.960&rft.aulast=Xiaofeng&rft.aufirst=Dai&rft.au=Zhifu, Mao&rft.au=Songping, Xie&rft.au=Hao, Zhang&rft.au=Jie, Huang&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525341&rfr_id=info:sid/en.wikipedia.org:Molecular promiscuity" class="Z3988">