STAR (Steroidogenic Acute Regulatory Protein)

Conversely, co-overexpression of FOS and JUN suppressed key steroidogenic genes (StAR, CYP11B1, CYP11B2), reduced aldosterone and cortisol secretion, and increased reactive oxygen species accumulation. Together, this work demonstrates that FOS and JUN may function in coordinating the redox-steroidogenesis axis, linking molecular changes in the adjacent cortex to tumor function and microenvironmental remodeling.

GBD ameliorates ovarian injury in HLD, and its mechanism of action is associated with the suppression of the AGE/RAGE/NF-κB signaling pathway.

Keywords co-occurrence analysis showed four clusters of KRAS, including the role and molecular mechanism of KRAS in the process of cancer development, especially pancreatic cancer, studies on the characteristics and clinical value of KRAS in colorectal cancer, the role characteristics of KRAS in the occurrence of lung cancer and its clinical applications and research progress of clinical trials targeted KRAS. This study systematically elucidates emerging insights into the critical gene KRAS, providing a contemporary perspective on KRAS-driven oncogenesis.

By providing a classification framework rooted in biochemical features, ShortStop offers a practical solution for targeting smORFs in functional studies, benchmarking new discovery tools, and advancing microprotein research. The online version contains supplementary material available at 10.1186/s44330-025-00037-4.

This distinction highlights that Star expression alone is not a reliable marker of de novo neurosteroidogenic capacity in the brain, as its functional significance depends on the broader enzymatic context in which it occurs. The resulting single-cell map of de novo neurosteroid biosynthetic capacity across brain regions, including modest sex-associated differences, provides a foundational framework for understanding neurosteroid signaling in distinct cell types and its relevance to brain physiology and pathophysiology.

Moreover, age-associated progressive suppression of StAR-governed sex neurosteroids influences the most prevalent neurological disorder, Alzheimer's disease, in both women and men. This review summarizes significant findings and the current understanding of the regulation of StAR in a variety of steroid-coupled events, ranging from organogenesis to carcinogenesis to neurodegeneration, and helps unravel the mechanistic insights into relevant physiological and pathophysiological implications.

Besides, follicle number and AMH levels decreased in the BLM group, but remarkably increased in the BLM + ALA group. We established that ALA may have ameliorative effects on the harmful effects of BLM on ovary.

By modulating key metabolic pathways and potentially suppressing WNT signaling, STAR + cells could contribute to improved treatment responses. These findings position STAR + cells as a promising biomarker for predicting chemotherapy efficacy in SOC, which warrants further investigation.

Hormonal cluster #1 or #3 is an independent prognostic factor regarding poor progression-free survival. Hormonal cluster assignment also affects the predicted drug response with cluster-dependent susceptibility to specific novel therapeutic compounds.

LSP modulated the expression of Nrf2/Keap1/HO-1 and PPARγ signaling. Therefore, our data presents LSP as a promising candidate for enhancing reproductive health in patients undergoing CDDP treatment.

The mitochondrial dysfunction and abnormal steroidogenesis induced by HWL during lactation in ovarian cells harm the follicular development of weaning sows, which could be alleviated by butyrate.

Using a small molecule of AKT activator and SP1 overexpression approaches, we show that the suppressive effect of APAP on StAR expression is mediated through the inhibition of AKT-mediated upregulation of SP1 expression. This study contributes to a deeper understanding of the pharmacological actions of APAP and its impacts on female reproductive health.