The possible antimicrobial mechanism of nanomaterials.

The survival of wetland plant species largely relies on physiological adaptations essential for submergence and desiccation. Intertidal seaweeds, unlike terrestrial plants, have unique adaptations to submergence and can also sustain desiccation arising from tidal rhythms. This study determined the differential metabolic regulations in the inter-tidal seaweed species Ulva lactuca against the submergence and desiccation. During desiccation, the relative water content of the algal thalli declined with concomitant increase in reactive oxygen species (ROS) and lipid peroxidation. Nevertheless, the trends reversed during recovery on re-submergence and attained homeostasis. Metabolite profiling of U. lactuca revealed desiccation induced balance in energy reserve utilization by adjusting carbohydrate metabolism and switch over to ammonia metabolism. Upon re-submergence, thalli showed an increase in fermentative metabolites, pyruvate-alanine conversion, and the GABA shunt. Prolonged submergence induced substrate level phosphorylation mediated sugar biosynthesis while continuing the alternative carbon flux through fermentative metabolism, an increase in osmoprotectants glycine and betaine, sulfur bearing compounds cysteine and hypotaurine, and phenolic compound coniferaldehyde. The determined metabolic regulations in U. lactuca for submergence tolerance provide insights into potential evolutionarily conserved protective mechanisms across the green lineage and also highlights the possible role of sulfur oxoforms as strong free radical scavengers.

Background: Tumorous imaginal disc 1 (hTid-1) or DnaJ homolog subfamily A member 3 (DNAJA3), is a part of the heat shock protein (Hsp) 40 family and is predominantly found to reside in the mitochondria. hTid-1 has two mRNA splicing variants, hTid-1S and hTid-1L of 40 and 43 kDa respectively in the cytosol which are later processed upon import into the mitochondrial matrix. hTid-1 protein is a part of the DnaJ family of proteins which are co-chaperones and specificity factors for DnaK proteins of the Hsp70 family, and bind to Hsp70, thereby activating its ATPase activity. hTid-1 has been found to be critical for a lot of important cellular processes such as proliferation, differentiation, growth, survival, senescence, apoptosis, and movement and plays key roles in the embryo and skeletal muscle development. Main body: hTid-1 participates in several protein–protein interactions in the cell, which mediate different processes such as proteasomal degradation and autophagy of the interacting protein partners. hTid-1 also functions as a co-chaperone and participates in interactions with several different viral oncoproteins. hTid-1 also plays a critical role in different human diseases such as different cancers, cardiomyopathies, and neurodegenerative disorders. Conclusion: This review article is the first of its kind presenting consolidated information on the research findings of hTid-1 to date. This review suggests that the current knowledge of the role of hTid-1 in disorders like cancers, cardiomyopathies, and neurodegenerative diseases can be correlated with the findings of its protein–protein interactions that can provide a deep insight into the pathways by which hTid-1 affects disease pathogenesis and it can be stated that hTid-1 may serve as an important therapeutic target for these disorders. Graphical

Psoriasis is a chronic skin disease characterized by keratinocyte hyperproliferation, involving T cells as the major players in the manifestation of lesional and systemic inflammation. With the extensive exploration of keratinocyte dysfunctionality, T cell centric deregulation has gained much focus with limited molecular understanding in the context of disease etiology. miRNAs, the molecular switches known to drive disease manifestation via altering keratinocyte biology, have not been much studied in the context of T cell alterations. This study aims to explore T cell-associated miRNAs and their target signaling networks to understand their role in modulating psoriasis specific T cell changes. miRNAs with altered expression in psoriatic T cells were identified through a comprehensive analysis of the available literature and datasets. The relevant miRNAs were used for prediction and enrichment of cognate targets and mapping of associated pathways involved in different modalities of T cell functionality. The study identified 14 miRNAs dysregulated in psoriatic T cells along with 256 downstream targets involved in 15 distinct T cell associated signaling pathways. 5/14 miRNAs identified were further validated with a significant increase in their expression in enriched CD3+T cells from blood of psoriatic patients versus healthy subjects. The psoriatic T cell specific miRNA driven signaling cascades identified were modelled to propose yet unexplored molecular basis of dysregulated T cell activation, proliferation, survival, and subset differentiation associated with the disease. The new findings delineate candidate miRNA target signaling components that need to be validated in T cell disease etiology. Importantly, the key miRNAs/targets can be employed towards psoriasis-specific diagnostics and therapeutic interventions.