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Potential role of triacontanol applied as a foliar treatment to ameliorate the adverse effects of salinity on hot pepper plants was evaluated. In this pot experiment, hot pepper plants under 75 mM NaCl stress environment were subjected to foliar application of 25, 50, and 75 µM triacontanol treatments; whereas, untreated plants were taken as control. Salt stress had a significant impact on morphological characteristics, photosynthetic pigments, gas exchange attributes, MDA content, antioxidants activities, electrolytes leakage, vitamin C, soluble protein, and proline contents. All triacontanol treatments significantly mitigated the adversative effects of salinity on hot pepper plants; however, foliar application triacontanol at 75 µM had considerably improved the growth of hot pepper plants in terms of plant height, shoot length, leaf area, plant fresh/dry biomasses by modulating above mentioned physio-biochemical traits. While, improvement in gas exchange properties, chlorophyll, carotenoid contents, increased proline contents coupled with higher SOD and CAT activities were observed in response to 75 µM triacontanol followed by 50 µM triacontanol treatment. MDA and H 2 O 2  contents were decreased significantly in hot pepper plants sprayed with 75 µM triacontanol followed by 50 µM triacontanol foliar treatment. Meanwhile, root and shoot lengths were maximum in 50 µM triacontanol sprayed hot pepper plants along with enhanced APX activity on exposure to salt stress. In crux, exogenous application triacontanol treatments improved hot pepper performance under salinity, however,75 µM triacontanol treatment evidently was more effective in mitigating the lethal impact of saline stress via controlling the ROS generation and increment in antioxidant enzyme activities., (© 2022. The Author(s).)

Identifying effective drug targets, with little or no side effects, remains an ever challenging task. A potential pitfall of failing to uncover the correct drug targets, due to side effect of pleiotropic genes, might lead the potential drugs to be illicit and withdrawn. Simplifying disease complexity, for the investigation of the mechanistic aspects and identification of effective drug targets, have been done through several approaches of protein interactome analysis. Of these, centrality measures have always gained importance in identifying candidate drug targets. Here, we put forward an integrated method of analysing a complex network of cancer and depict the importance of k-core, functional connectivity and centrality (KFC) for identifying effective drug targets. Essentially, we have extracted the proteins involved in the pathways leading to cancer from the pathway databases which enlist real experimental datasets. The interactions between these proteins were mapped to build an interactome. Integrative analyses of the interactome enabled us to unearth plausible reasons for drugs being rendered withdrawn, thereby giving future scope to pharmaceutical industries to potentially avoid them (e.g. ESR1, HDAC2, F2, PLG, PPARA, RXRA, etc). Based upon our KFC criteria, we have shortlisted ten proteins (GRB2, FYN, PIK3R1, CBL, JAK2, LCK, LYN, SYK, JAK1 and SOCS3) as effective candidates for drug development.

p66Shc-dependent ROS production contributes to many pathologies including ischemia/reperfusion injury (IRI) during solid organ transplantation. Inhibiting p66Shc activation may provide a novel therapeutic approach to prevent damage, which is poorly managed by antioxidants in vivo. Previous work suggested that pro-oxidant and a pro-apoptotic function of p66Shc required mitochondrial import, which depended on serine 36 phosphorylation. PKCß has been proposed as S36 kinase but cJun N-terminal kinases (JNKs) may also phosphorylate this residue. To simulate the early stages of ischemia/reperfusion (IR) we either used H2O2 treatment or hypoxia/reoxygenation (HR). As during reperfusion in vivo, we observed increased JNK and p38 activity in mouse embryonic fibroblasts (MEFs) and HL-1 cardiomyocytes along with significantly increased p66ShcS36 phosphorylation, ROS production and cell damage. Application of specific inhibitors caused a pronounced decrease in p66ShcS36 phosphorylation only in the case of JNK1/2. Moreover, S36 phosphorylation of recombinant p66Shc by JNK1 but not PKCß was demonstrated. We further confirmed JNK1/2-dependent regulation of p66ShcS36 phosphorylation, ROS production and cell death using JNK1/2 deficient MEFs. Finally, the low ROS phenotype of JNK1/2 knockout MEFs was reversed by the phosphomimetic p66ShcS36E mutant. Inhibiting JNK1/2-regulated p66Shc activation may thus provide a therapeutic approach for the prevention of oxidative damage.