Synthesis, crystal structure and Hirshfeld surface analysis of diacetatobis[4-(2-aminoethyl)morpholine]cadmium tetrahydrate

The title coordination compound, [Cd(C2H3O2)2(C6H14N2O)2]·4H2O, was synthesized by mixing 2 moles of 4-(2-aminoethyl)morpholine and 1 mole of cadmium acetate in double-distilled water. The Cd atom is octahedrally coordinated by two N,N′-bidentate ligands [4-(2-aminoethyl)morpholine] and two trans-located acetate molecules. The Cd atom is located on a center of inversion, whereas the 4-(2-aminoethyl)morpholine and four water molecules are adjacent to the acetate molecules. The chair conformation of the morpholine molecules is confirmed. In the crystal, adjacent metal complexes and uncoordinated water molecules are linked via N—H...O and O—H...O hydrogen-bonding interactions, generating R22(6), R66(16), R66(20) and S11(6) motifs and forming a three-dimensional network. A Hirshfeld surface analysis indicated the contributions of various contacts: H...H (71.8%), O...H/H...O (27.1%), and C...H/H...C (1.0%)

The multifaceted oncogene SND1 in cancer: focus on hepatocellular carcinoma

Staphylococcal nuclease and tudor domain containing 1 (SND1) is a protein that regulates a complex array of functions. It controls gene expression through transcriptional activation, mRNA degradation, mRNA stabilization, ubiquitination and alternative splicing. More than two decades of research has accumulated evidence of the role of SND1 as an oncogene in various cancers. It is a promoter of cancer hallmarks like proliferation, invasion, migration, angiogenesis and metastasis. In addition to these functions, it has a role in lipid metabolism, inflammation and stress response. The participation of SND1 in such varied functions makes it distinct from most oncogenes that are relatively more focused in their role. This becomes important in the case of hepatocellular carcinoma (HCC) since in addition to typical cancer drivers, factors like lipid metabolism deregulation and chronic inflammation can predispose hepatocytes to HCC. The objective of this review is to provide a summary of the current knowledge available on SND1, specifically in relation to HCC and to shed light on its prospect as a therapeutic target

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Not AvailablePlant-microbe interactions can be either beneficial or harmful depending on the nature of the interaction. Multifaceted benefits of plant-associated microbes in crops are well documented. Specifically, the management of plant diseases using beneficial microbes is considered to be eco-friendly and the best alternative for sustainable agriculture. Diseases caused by various phytopathogens are responsible for a significant reduction in crop yield and cause substantial economic losses globally. In an ecosystem, there is always an equally daunting challenge for the establishment of disease and development of resistance by pathogens and plants, respectively. In particular, comprehending the complete view of the complex biological systems of plant-pathogen interactions, co-evolution and plant growth promotions (PGP) at both genetic and molecular levels requires novel approaches to decipher the function of genes involved in their interaction. The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)/Cas9 (CRISPR-associated protein 9) is a fast, emerging, precise, ecofriendly and efficient tool to address the challenges in agriculture and decipher plant-microbe interaction in crops. Nowadays, the CRISPR/Cas9 approach is receiving major attention in the field of functional genomics and crop improvement. Consequently, the present review updates the prevailing knowledge in the deployment of CRISPR/Cas9 techniques to understand plant-microbe interactions, genes edited for the development of fungal, bacterial and viral disease resistance, to elucidate the nodulation processes, plant growth promotion, and future implications in agriculture. Further, CRISPR/Cas9 would be a new tool for the management of plant diseases and increasing productivity for climate resilience farming.Not Availabl

Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophy

Duchenne muscular dystrophy (DMD) is characterized by muscle degeneration and progressive weakness. There is considerable inter-patient variability in disease onset and progression, which can confound the results of clinical trials. Here we show that a common null polymorphism (R577X) in ACTN3 results in significantly reduced muscle strength and a longer 10 m walk test time in young, ambulant patients with DMD; both of which are primary outcome measures in clinical trials. We have developed a double knockout mouse model, which also shows reduced muscle strength, but is protected from stretch-induced eccentric damage with age. This suggests that α-actinin-3 deficiency reduces muscle performance at baseline, but ameliorates the progression of dystrophic pathology. Mechanistically, we show that α-actinin-3 deficiency triggers an increase in oxidative muscle metabolism through activation of calcineurin, which likely confers the protective effect. Our studies suggest that ACTN3 R577X genotype is a modifier of clinical phenotype in DMD patients