Ask about this productRelated genes to: NR5A1 Blocking Peptide
- Gene:
- NR5A1 NIH gene
- Name:
- nuclear receptor subfamily 5 group A member 1
- Previous symbol:
- FTZF1
- Synonyms:
- FTZ1, SF-1, ELP, AD4BP, hSF-1, SF1
- Chromosome:
- 9q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-06-07
- Date modifiied:
- 2018-02-14
Related products to: NR5A1 Blocking Peptide
Related articles to: NR5A1 Blocking Peptide
- Complete Androgen Insensitivity Syndrome (CAIS) is a rare X-linked disorder caused by pathogenic variants in the androgen receptor (AR) gene, leading to resistance to androgens in individuals with a 46, XY karyotype. - Source: PubMed
Publication date: 2026/08/03
Misgar Raiz AhmadUl Isam Mir SajadMasoodi Shariq RashidQadir AjazBhat Imtiyaz AhmadShah Zafar AminBashir Mir IftikharWani Arshad Iqbal - Differences of sex development (DSD) arise from disruptions in chromosomal, gonadal, or anatomical sex. Over the past 2 years, advances in sequencing technologies, enhancer biology, mitochondrial steroidogenesis, and sex-chromosome dosage effects have reshaped diagnostic and mechanistic understanding. This review synthesizes key discoveries and highlights their implications for clinical practice, including diagnostic pathways, endocrine surveillance, fertility counseling, and tumor-risk stratification. - Source: PubMed
Publication date: 2026/07/17
de Lapiscina Idoia MartinezKouri ChrysanthiFlück Christa E - The parabrachial nucleus (PBN) is an important hub located in the pons that relays sensory signals from peripheral regions. It is genetically diverse and contains many populations that modulate feeding and responses to threatening situations. A small -expressing population of neurons was identified that projects selectively to the ventromedial hypothalamus (VMH). The neurons are scattered throughout the lateral PBN with a cluster of cells along the border to the nucleus of the lateral lemniscus that overlap with and expression. Chemogenetic activation of PBN neurons results in induction in (SF1) and neurons in the VMH. Activation of PBN neurons or their terminals in the VMH reduces food intake after fasting and increases anxiety-like behaviors. In anxiogenic feeding assays, activation of PBN neurons increases latency to feed as well as reducing food intake. Photometry showed that PBN -neuronal activity increases during anxiogenic situations but is suppressed during food consumption, suggesting a role in threat-induced suppression of feeding. Silencing PBN neurons with tetanus toxin light-chain increased food intake and reduced anxiety. These findings reveal a genetically defined PBN to VMH circuit that responds to threats and suppresses feeding behavior. - Source: PubMed
Publication date: 2026/07/22
Pauli Jordan LPark SekunFelix Rachel RPalmiter Richard D - Is exome sequencing (ES) an efficient approach for simultaneous analysis of causative single gene defects and copy number variants (CNV) in unexplained premature ovarian insufficiency (POI)? - Source: PubMed
Publication date: 2026/06/17
Valkna AnuKikas TriinJakovlev ÜlleMõttus OliverDutta AvirupErlang KülliPunab MargusRull KristiinaLaan Maris - Lipopolysaccharide (LPS) impairs the function of ovine follicular granulosa cells (GCs), representing a primary cause of follicular atresia. Selenium (Se), an essential trace element, possesses anti-inflammatory and cytoprotective properties; however, its effects on GC ultrastructure remain largely unknown. In this study, primary ovine GCs were exposed to LPS (10 µg/mL) and treated with sodium selenite (25 nM). Transmission electron microscopy (TEM), JC-1 staining, enzyme-linked immunosorbent assay (ELISA), reactive oxygen species (ROS) detection, flow cytometry, and quantitative real-time PCR (qRT-PCR) were employed to evaluate cellular ultrastructure, mitochondrial membrane potential (ΔΨm), and downstream physiological processes. LPS induced severe mitochondrial pyknosis, cristae loss, and reduced ΔΨm, accompanied by inflammation, oxidative stress, apoptosis, and impaired steroidogenesis. Se intervention markedly ameliorated these ultrastructural injuries, preserving mitochondrial morphology and ΔΨm. Functionally, Se suppressed the release of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β); enhanced the activities of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) while attenuating ROS accumulation; inhibited apoptosis by upregulating and downregulating and ; and restored E and P secretion via upregulation of and . This study provides direct morphological evidence that Se protects ovine GCs from LPS-induced damage by repairing mitochondrial ultrastructure. This structural restoration is central to its integrated anti-inflammatory, antioxidant, anti-apoptotic, and steroidogenic effects. These in vitro findings suggest that Se may serve as a promising nutritional strategy for mitigating inflammation-driven follicular atresia, pending further in vivo validation. - Source: PubMed
Publication date: 2026/07/06
Guo ZeyuanLi JunFan XinyuLiu YufeiLi LinzhenLyu LihuaYang ChunheRen Youshen