SMG5, a component of nonsense-mediated mRNA decay, is essential for the mouse spermatogonial differentiation and maintenance.

Mammalian spermatogenesis is a tightly controlled cellular process including spermatogonial development and differentiation, meiosis of spermatocyte, and the morphological specification of haploid spermatozoa, during which the post-transcriptional gene regulations are vital but poorly understood. Nonsense-mediated mRNA decay (NMD), a highly conserved post-transcriptional regulatory mechanism of gene expression in eukaryotes, recently emerges as a licensing mechanism in cell fate transition, including stem cell differentiation and organogenesis. The function of NMD in spermatogonial development remains elusive.

Mohawk protects against tendon damage via suppressing Wnt/β-catenin pathway.

Degenerative tendon injuries are common clinical problems associated with overuse or aging, and understanding the mechanisms of tendon injury and regeneration can contribute to the study of tendon healing and repair. As a transcription factor, Mohawk (Mkx) is responsible for tendons development, yet, the roles of which in tendon damage remain mostly elusive. In this study, using Mkx overexpressed mice on long treadmill as an in vivo model and Mkx Achilles tenocytes stimulated by equiaxial stretch as an in vitro model, we anaylsed the effects of Mkx overexpression on the tendon.

CSNK1D is associated with stemness and invasiveness in glioblastoma.

Background: Glioblastoma (GBM) is the most common primary malignant brain tumor. It has a poor 5-year survival rate, a high recurrence rate, and few therapeutic options. Exploring the molecular processes underlying the formation and progression of GBM, as well as identifying novel therapeutic targets, is critical for improving GBM therapy and prognosis.

Essential role of MALAT1 in reducing traumatic brain injury.

As a highly evolutionary conserved long non-coding RNA, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was first demonstrated to be related to lung tumor metastasis by promoting angiogenesis. To investigate the role of MALAT1 in traumatic brain injury, we established mouse models of controlled cortical impact and cell models of oxygen-glucose deprivation to mimic traumatic brain injury in vitro and in vivo. The results revealed that MALAT1 silencing in vitro inhibited endothelial cell viability and tube formation but increased migration.

MALAT1 improves functional recovery after traumatic brain injury through promoting angiogenesis in experimental mice.

As a highly evolutionary conserved lncRNA, MALAT1 was first demonstrated to associate with metastasis of lung tumor by promoting angiogenesis. Activated vasculature was recently indicated to assist neurogenesis by secreting neurotrophic factor Ang1 (Angiopoietin-1). The purpose of this study is to investigate the potential role of MALAT1 in angiogenesis following traumatic brain injury (TBI).

Endothelial Regulation by Exogenous Annexin A1 in Inflammatory Response and BBB Integrity Following Traumatic Brain Injury.

Background And Target: Following brain trauma, blood-brain barrier (BBB) disruption and inflammatory response are critical pathological steps contributing to secondary injury, leading to high mortality and morbidity. Both pathologies are closely associated with endothelial remodeling. In the present study, we concentrated on annexin A1 (ANXA1) as a novel regulator of endothelial function after traumatic brain injury.

Polymyxins Bind to the Cell Surface of Unculturable and Cause Unique Dependent Resistance.

Multidrug-resistant is a top-priority pathogen globally and polymyxins are a last-line therapy. Polymyxin dependence in (i.e.

miR-24 Reduces Serum Lipid Levels and Inhibits Brain Tissue Cells Apoptosis of Rats with Cerebral Infarction.

Aim: To study miR-24 effects on cerebral infarction in rats.

Material And Methods: A rat middle cerebral artery occlusion model (MCAO) was constructed. Intracerebroventricular stereotactic injection of miR-24 agomir/antagomir was performed in the rat MCAO model.

Molecular docking and biological evaluation of novel urea-tailed mannich base against Pseudomonas aeruginosa.

Emergence of multi-drug resistant bacterial pathogens is escalating and it is essential to develop novel strategies to combat these super bugs. LasR is a regulator switch that plays a vital role in quorum sensing (QS) and pathogenesis of Pseudomonas aeruginosa. The present study reports two novel Mannich base (1-(phenyl (o-tolylamino) methyl) urea and 3-((1H-Imidazole-1-yl) methylnaphthalene-2-ol with enhanced anti-QS and antibiofilm activities.

Mannich base limits Candida albicans virulence by inactivating Ras-cAMP-PKA pathway.

Mannich bases and its derivatives are regarded as supreme pharmacophores in therapeutics. The study investigates the antimycotic potential of Mannich bases, 1-((1H-benzimidazol-1-yl) methyl) urea (C1) and 1-((3-hydroxynapthalen-2-yl) methyl) thiourea (C2), against Candida albicans. Biofilm and hyphal inhibitory activities of the Mannich bases were tested by crystal violet quantification, fluorescence imaging cAMP rescue, qRT PCR, and by molecular docking analysis.