Amino acid transporters (AATs) are essential membrane proteins that transfer amino acids across cells. They are necessary for plant growth and development. The lysine histidine transporter (LHT) gene family in maize (Zea mays) has not yet been characterized. According to sequence composition and phylogenetic placement, this study found 15 LHT genes in the maize genome. The ZmLHT genes are scattered across the plasma membrane. The study also analyzed the evolutionary relationships, gene structures, conserved motifs, 3D protein structure, a transmembrane domain, and gene expression of the 15 LHT genes in maize. Comprehensive analyses of ZmLHT gene expression profiles revealed distinct expression patterns in maize LHT genes in various tissues. This studys extensive data will serve as a foundation for future ZmLHT gene family research. This study might make easier to understand how LHT genes work in maize and other crops.

Type 2 diabetes (T2D) and hypertension are global public health concerns and major metabolic disorders in humans. Experimental evidence indicates considerable hereditary influences on the etiology of T2D and hypertension, but the molecular basis of these diseases is still limited. Thus, the current study analyzed 185 (132 T2D and 53 hypertension) GWAS catalog datasets and identified 83 common genes linked to T2D and hypertension pathogenesis. These genes were further examined using various bioinformatics approaches to elucidate their molecular mechanisms underlying the pathophysiology of T2D and hypertension. Gene ontology (GO) analysis revealed the biological, cellular, and molecular functions of these genes, which were also linked to different T2D and hypertension pathways. Specifically, seven genes were found to be crucial for T2D, and nine were directly associated with hypertension. Protein-protein interaction (PPI) analysis identified 28 candidate genes and seven hub genes through 11 topological methods. Among 231 miRNAs, seven were significant in interacting with the hub genes, and nine transcription factors (TFs) out of 36 were linked to these hub genes. Additionally, two of the seven hub genes were downregulated by 43 FDA-approved drugs. These findings elucidate the molecular processes underlying T2D and hypertension, suggesting that targeting these genes could lead to future drug development and therapeutic strategies to treat T2D and hypertension.

This study explores the impact of nonsynonymous single‐nucleotide polymorphisms (nsSNPs) on type 2 diabetes (T2D). The nsSNPs are genetic variations that alter amino acids within proteins, affecting protein structure and function. This study investigated seven candidate genes associated with T2D pathogenesis from genome‐wide association studies (GWASs) catalog datasets. Subsequently, six mutation‐prediction tools were employed to identify the most harmful nsSNPs within these candidate genes. Further analysis involved evaluating protein evolutionary conservation using the ConSurf server and assessing protein stability with I‐Mutant and MUpro. Functional and structural effects were predicted using MutPred2, Project HOPE, and FoldAmyloid tools. We obtained 42 of the most deleterious nsSNPs from identified candidate genes. Among these, 38 are located in highly conserved residues with a conservative score of 7–9. Furthermore, 20 of these conserved nsSNPs are found to decrease protein stability, with 18 of them classified as pathogenic mutations. These mutations can either reduce or increase protein size and can alter the charge and hydrophobic characteristics of the affected proteins. In addition, eight mutants from four genes were identified in amyloidogenic regions, suggesting a potential link to protein aggregation. These findings provide valuable insights into the physicochemical properties and structural changes associated with these deleterious nsSNPs. The study concludes that the distinctive physicochemical properties and significant structural changes of the identified nsSNPs suggest valuable insights for future research. Understanding these variants through large‐scale studies may pave the way for developing therapeutic interventions targeting genetic variations, ultimately improving our understanding of T2D pathogenesis and treatment.