Molecular promiscuity

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

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.
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. 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. PMID 23255935.

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[1] 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.

[2] 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. PMID 27698456.

[3] 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. PMID 23255935.