For example, nanoparticles can induce different cellular responses by binding to proteins in the blood [28, 29].
For example, auxins can induce ethylene formation and in turn ethylene can trigger an auxin increase.
For example, miR-373 can induce the expression of E-Cadherin or CSDC2 when binding to these genes' promoters [ 11].
For example, Twist1 can induce Snail (Smit et al., 2009), and Slug can upregulate Twist2 and ZEB1 expression (Wels et al., 2011; Guo et al., 2012).
For example, STAT5 can induce expression of heat shock protein 90-A (HSP90A), a protein that can promote cancer cell survival.
For example, tamoxifen can induce autophagic cell death in MCF-7 cells [ 19], and arsenic trioxide can stimulate autophagy in lymphocytic leukaemia and multiple myeloma cells [ 20].
For example, it can induce collagen type 1, α5 integrin, and fibronectin much more potently than TGF β in fibroblasts [ 31].
For example, tamoxifen can induce endometrial cancer [ 13]; oophorectomy is associated with early menopause symptoms [ 14]; and prophylactic mastectomy is associated with morbidity and psychosocial effects [ 15].
For example, tamoxifen can induce FAK-mediated cytoskeletal remodelling [ 9] and the expression of matrix metalloproteinases [ 28] by non-genomic mechanisms.
For example, IL-8 can induce EGFR phosphorylation in epithelial cells via its receptors C-X-C chemokine receptor1 (CXCR1) and CXCR2 (28, 37), while binding of α1-antitrypsin to IL-8 has been reported to prevent activation of CXCR1 (4).
For example, IFI16 can induce the inflammasome in response to Kaposi's sarcoma-associated herpesvirus infection and act as a mediator of the anti-inflammatory actions of type I IFNs [ 73- 76].
