Lves the binding of ABA for the PYR/PYL/RCAR receptor, which in turn interacts with PP2Cs that act as adverse regulators of ABA signaling and thereby regulate the downstream components [76]. Mutation in ABI1 disrupts ABA signaling upstream of H2 O2 Coelenteramine 400a Biological Activity synthesis, whereas mutation in ABI2 impairs signaling downstream of H2 O2 production inside the guard cells [77]. Preceding study has shown that ABA-induced stomatal closure is regulated by GPX, an antioxidant enzyme that catalyzes the reduction of H2 O2 by utilizing GSH as a substrate. GPX3, which functions as redox transducer in H2 O2 signal transduction, interacts with ABI2 and thereby directly influences guard cell plasma membrane Ca2 channels in regulating ABA-induced stomatal closure [46]. Consistently, the gpx3 mutant of Arabidopsis is much less sensitive to ABA- and H2 O2 -induced stomatal closure [46]. Similarly, silencing of GPX3 in rice makes plants much less sensitive to ABA-induced stomatal closure [49]. Proteomic studies have also revealed that silencing of GPX3 induces S-glutathionylation and inhibits protein ubiquitination [49]. The involvement of protein ubiquitination in ABA signaling is nicely established, as an example, ABA signaling is activated by the degradationGenes 2021, 12,9 ofof ABI1, a adverse regulator of ABA signaling, through the UBC27-AIRP3 ubiquitination complicated [78]. Additionally, the protein components involved inside the ubiquitination and proteasome complicated are reported to be S-glutathionylated at cysteine residues below stress circumstances [79,80]. General, these reports indicate the