Although βHB did not induce expression of four specific heat shock proteins monitored (Supplementary Fig. 3), it did activate the DAF-16 and SKN-1 signaling pathways, which are both likely responsible for the increased thermotolerance observed following βHB treatment.
Comparable to an SH3 domain-containing actin nucleation mixture lacking N-WASP (Figure 5B), also full-length Abp1 - although used in a concentration of 150 nM corresponding to full activation of N-WASP by the Abp1 SH3 domain (Figure 5B) - did not influence Arp2/3 complex-mediated actin dynamics (Figure 5C), while it did activate N-WASP in a manner similar to the SH3 domain (data not shown).
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Although LG100754 activates the PPARα/RXR heterodimer [15], it does not activate TR/RXR, VDR/RXR or LXR/RXR [14].
Note that MSP can activate Brk in HaCaT cells, but it does not activate ERK5, nor do these cells migrate in response to this ligand.
TNF-α binding to its receptor activates a cascade of intracellular signals but in contrast to RANKL it does not activate TRAF6 which is required for the initial induction of NFATc1 expression [12].
The major transforming activity of BPV-1 E5 is due to its ability to specifically bind and activate PDGF βR in a ligand independent manner, and, importantly, it does not activate other related receptors [ 15– 15].
Interestingly, while being a potent activator, capsaicin also exhibits high selectivity for TRPV1 as it does not activate other homologous channels within the TRPV family (Yang et al., 2016).
While it is evident that cFR activates expression of many carotenoid and chlorophyll biosynthesis genes, and can induce de-etiolation (repress hypocotyl elongation) via a PHYA-dependent mechanism [ 67], it does not activate chlorophyll biosynthesis or chloroplast development which is dependent on light-induced activation of POR that catalyzes the conversion of Pchlide to chlorophyllide [ 22].
