SREBF2 antibody - middle region (P100696_P050)
- Known as:
- SREBF2 (anti-) - middle region (P100696_P050)
- Catalog number:
- p100696_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SREBF2 antibody - middle region (P100696_P050)
Related genes to: SREBF2 antibody - middle region (P100696_P050)
- Gene:
- SREBF2 NIH gene
- Name:
- sterol regulatory element binding transcription factor 2
- Previous symbol:
- -
- Synonyms:
- SREBP2, bHLHd2
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-23
- Date modifiied:
- 2014-11-19
Related products to: SREBF2 antibody - middle region (P100696_P050)
Related articles to: SREBF2 antibody - middle region (P100696_P050)
- The objectives of this study were to develop a real-world-data (RWD) database for patients with epilepsy to provide further real-world-evidence (RWE) for monogenic genetic epilepsies; to assess the usefulness of a diagnostic algorithm in epilepsy; and to examine protein 3D structures using in silico tools to predict variant pathogenicity. - Source: PubMed
Publication date: 2026/06/01
Morris HaleyMathew ElizabethBahl ShaliniVilla-Lopez MartaMercimek-Andrews Saadet - Dysregulated cholesterol metabolism is a recognized metabolic hallmark of cancer. While the transcription factor SREBP2 is a master regulator of this pathway, how its activation converts metabolic stress into the development of carcinogenic signals in colorectal cancer (CRC) remains unclear. Through clinical and preclinical analyses, we first confirmed that hypercholesterolemia and elevated tumoral SREBP2 are hallmarks of CRC. Using multi-omics integration, we identified CNPY3 as a direct transcriptional target of SREBP2. Functionally, CNPY3 drives CRC cell proliferation, invasion, and tumor growth via a cholesterol synthesis-independent oncogenic program. Clinically, high CNPY3 expression robustly correlated with advanced disease and poor patient survival. Mechanistically, we discovered that CNPY3 undergoes liquid-liquid phase separation (LLPS), a property dependent on its intrinsically disordered C-terminal region. This LLPS capacity is essential for its oncogenic function, as it enables CNPY3 to enhance MDM2 phosphorylation at the activating Ser166 site and promote its nuclear translocation. Consequently, CNPY3 potentiates MDM2-mediated ubiquitination and degradation of the tumor suppressor p53. Genetic ablation of p53 completely abolished the pro-tumorigenic effects of CNPY3, confirming p53 as the critical downstream effector. Crucially, this axis specifically targets wild-type p53, having no effect on common p53 mutants. Pharmacological disruption of the MDM2-p53 interaction with Nutlin-3 effectively reversed CNPY3-driven malignancy both and . Our work unveils a SREBP2-CNPY3-MDM2-p53 signaling axis that links cholesterol metabolic dysregulation to p53 pathway inactivation in CRC. We further established that the oncogenic activity of CNPY3 is mediated through its biophysical property of LLPS. These findings nominate CNPY3 as a novel prognostic biomarker and a compelling therapeutic target for p53-wild-type CRC. - Source: PubMed
Publication date: 2026/05/15
Li XueYin Min-YueWei Yan-FeiXing JieZhang QianZong YeZhang Shu-TianXie Si-An - N6-methyladenosine (m6A) modification is a crucial epigenetic event in the development of head and neck squamous cell carcinoma (HNSCC). Here, we show that methyltransferase-like 16 (METTL16) expression is elevated in the tumor tissues of patients with HNSCC and is associated with poor prognosis. In addition, our data show that METTL16 promotes the proliferation of HNSCC cells in vitro and in vivo by enhancing cholesterol biosynthesis. Mechanistically, METTL16 catalyzes a key transcription factor in cholesterol biosynthesis-sterol regulatory element-binding transcription factor 2 (SREBP2) m6A modification and then stabilizes SREBP2 mRNA and ultimately elevates SREBP2 mRNA expression in HNSCC cells. Moreover, we validate that METTL16 promotes HNSCC progression dependent on SREBP2 mRNA expression. Overall, our results reveal a novel function of METTL16 in regulating SREBP2 expression, revealing a previously unrecognized METTL16/SREBP2 pathway in HNSCC cells. - Source: PubMed
Ma XinruiDing XiaojunDeng JianhuaGao QianLiu HuitingYuan ShuoXiao ZhiJiang Rui - Fatty liver is a common metabolic disease in dairy cows during early postpartum period, which is characterized by excessive hepatic triacylglycerol (TAG) accumulation. However, the mechanisms of bile acid (BA) metabolism in dairy cows experiencing fatty liver remain poorly elucidated. The farnesoid X receptor () plays a critical role in the regulation of BA homeostasis. Consequently, the aim of this study was to investigate the effect of -mediated BA metabolism following stimulation with high concentrations of free fatty acids (FFA). - Source: PubMed
Publication date: 2026/04/30
Jia BinTian YanGao ChanghongChang YaqiZhang ZexinSong YuxiXia ChengQu YongliYang Wei - Bitter taste receptors (TAS2Rs) beyond the oral cavity have gained increasing attention in recent years due to their expression in tissues and organs not traditionally linked to chemosensation, although their role in metabolism remains poorly understood. While the expression of TAS2Rs has been studied, the presence and function of these receptors in the liver are still unclear. Therefore, the aim of the present study was to assess whether a Western style diet regulates the mRNA and protein content of TAS2Rs' in mouse liver. Using both untargeted and targeted approaches, we analyzed the mRNA and protein content of bitter taste receptors in the liver and examined the potential correlation between TAS2Rs and cholesterol levels in the liver. We identified the mRNA of seven Tas2rs (Tas2r108, Tas2r120, Tas2r123, Tas2r130, Tas2r138, Tas2r143, and Tas2r144) in the liver of which the Tas2r138 mRNA and protein content was lower after 8 weeks on western diet, compared to control diet. Notably, the hepatic Tas2r138 mRNA level correlated positively with Srebf2 mRNA content as well as hepatic cholesterol and triglyceride levels. These findings suggest a potential regulatory link between Tas2rs and cholesterol, provide new insights into the roles of extra-oral bitter taste receptors and their possible regulation. - Source: PubMed
Pych EwelinaGudiksen AndersPilegaard HenrietteRasmussen Martin Krøyer