mProX™ Human RPS6KA5 Stable Cell Line

Malcher, Agnieszka. et al. "ESX1 gene as a potential candidate responsible for male infertility in nonobstructive azoospermia." Scientific reports, 2023.
The problem of infertility affects approximately 15% of couples, with male infertility being responsible for 40-50% of these cases. The causes of male infertility are still not well understood and effective treatment methods are lacking. One of the main causes of male infertility is disturbed spermatogenesis, leading to nonobstructive azoospermia (NOA). To better understand the role of the ESX1 gene in NOA, the study aimed to activate the gene using CRISPRa technology in human germ cells (testicular seminoma cells-TCam-2). Results showed successful activation of the ESX1 gene, with significantly increased expression levels in modified TCam-2 cells compared to wild-type cells or negative controls with nontargeted gRNA. Additionally, RNA-seq analysis identified a network of over 50 genes potentially regulated by ESX1. Verification through gene expression analysis in azoospermic patients with and without a mutation in ESX1 as well as those with normal spermatogenesis showed correlations between the levels of ESX1 and 6 genes related to cell proliferation and differentiation.
Malcher, Agnieszka. et al. "ESX1 gene as a potential candidate responsible for male infertility in nonobstructive azoospermia." Scientific reports, 2023.
Pubmed: 37783880   DOI: 10.1038/s41598-023-43854-9

J W Easton, Zachary. et al. "The impact of hyperglycemia upon BeWo trophoblast cell metabolic function: A multi-OMICS and functional metabolic analysis." PloS one, 2023.
Recent studies have linked pre-existing and gestationally-developed diabetes mellitus with impairments in placental villous trophoblast cell metabolic function, which may contribute to the development of metabolic diseases in exposed offspring. Using placental cell lines and ex vivo trophoblast preparations, previous research has identified hyperglycemia as a significant independent regulator of placental function. However, the direct effects of hyperglycemia on specific aspects of placental metabolism, such as nutrient storage and mitochondrial respiration, remain poorly understood. This study aimed to further characterize these effects by examining metabolic and mitochondrial function, as well as nutrient storage, in both undifferentiated cytotrophoblast and differentiated syncytiotrophoblast BeWo cells cultured under hyperglycemic conditions. Results showed increased glycogen and triglyceride nutrient stores in hyperglycemic-exposed BeWo trophoblasts, but no changes in real-time functional readouts of metabolic enzyme activity and mitochondrial respiratory activity. Further investigation into mitochondrial dynamics revealed increased expression of markers associated with mitochondrial fission, indicating a potential transition towards mitochondrial dysfunction in high-glucose exposed trophoblasts. A multi-omics approach was then used to evaluate the transcriptomic and metabolomic signatures of BeWo cytotrophoblasts exposed to hyperglycemia, which showed changes in the expression of genes related to glucose, glutathione, fatty acid, and glucocorticoid metabolism, as well as alterations in specific metabolite levels. These findings highlight the role of hyperglycemia as an independent regulator of various aspects of placental metabolism, nutrient storage, and mitochondrial function, providing further insights into the mechanisms behind placental dysfunction.
J W Easton, Zachary. et al. "The impact of hyperglycemia upon BeWo trophoblast cell metabolic function: A multi-OMICS and functional metabolic analysis." PloS one, 2023.
Pubmed: 36930661   DOI: 10.1371/journal.pone.0283118