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)
- Cortico-striatal synaptic dysfunction is an early hallmark of Huntington's disease (HD), yet the mechanisms underlying synapse loss and its reversibility remain poorly understood. Brain cholesterol is essential for neuronal and synaptic function, and dysregulated cholesterol metabolism has emerged as a key feature of HD, with reduced cholesterol biosynthesis reported in rodent models and cholesterol replenishment shown to be beneficial. Consistent with these findings, GWAS identified HD modifier loci outside canonical DNA repair pathways, including MED15, which among its functions supports SREBF2-mediated transcription of cholesterol biosynthesis genes, and a chr22 locus encompassing SREBF2, the master regulator of cholesterol biosynthesis. These findings suggest that pathways regulating cholesterol homeostasis may contribute to modifying the course of HD. Here, we show that increasing cholesterol availability prevents synapse loss and restores cortico-striatal connectivity in HD models. Cholesterol supplementation restores excitatory synapse density in vivo and in vitro. In primary HD neurons, cholesterol stabilizes dendritic spines and promotes the enrichment of GluA1-containing AMPA receptors in mature mushroom spines during chemically induced long-term potentiation, consistent with improved synaptic plasticity. Using microfluidic devices to spatially resolve the cortico-striatal circuit, we identified a compartment-specific mechanism whereby cholesterol delivery to cortical neurons is necessary and sufficient to restore cortico-striatal connectivity, whereas cholesterol administration to the striatal compartment selectively restores intra-striatal inhibitory synapses. Mechanistically, NMDA receptor and BDNF/TrkB signalling mediate the cholesterol-dependent restoration of synaptic connectivity, establishing cholesterol as a critical regulator of cortico-striatal synaptic integrity in HD and supporting targeting cholesterol homeostasis as a therapeutic strategy to restore synaptic function. - Source: PubMed
Publication date: 2026/08/12
Lenci AllegraVilla MichelaScolz AndreaBirolini GiuliaConforti PaolaPepe GiuseppeCastagno Antonio NicolasCassarino ChristianColombo LauraFavagrossa MonicaPolimeno AntoninoOttoboni LindaCorti StefaniaPardo Alba DiSalmona MarioMaglione VittorioZuccato ChiaraCattaneo Elena - Tumour cells commonly exhibit aerobic glycolysis and produce lactate despite oxygen availability. Lactate dehydrogenase (LDH) catalyses pyruvate-lactate interconversion and regulates intracellular lactate levels. Endothelial cells also depend on glycolysis for ATP production, which prompted us to investigate LDH in canine hemangiosarcoma (HSA), a malignant endothelial tumour. We inhibited LDH with (R)-GNE-140 or sodium oxamate in two canine HSA cell lines (HU-HSA-2 and HU-HSA-3) and generated HU-HSA-3 clones with knockout of LDHA or LDHB to evaluate the effects of LDH perturbation. (R)-GNE-140 and sodium oxamate suppressed proliferation and reduced global histone lactylation levels in both cell lines. mRNA-sequencing (mRNA-seq) of (R)-GNE-140-treated HU-HSA-2 cells identified cholesterol/lipid metabolism-related gene sets among the top negatively enriched pathways. Representative cholesterol/lipid metabolism genes such as SREBF2, SQLE and LDLR responded differently depending on cell lines and inhibitors. (R)-GNE-140 decreased these genes in HU-HSA-2 but not HU-HSA-3, whereas sodium oxamate decreased them in HU-HSA-3 with limited effects in HU-HSA-2. In HU-HSA-3, LDHA and LDHB knockout clones decreased SREBP2 expression and reduced the number of lipid droplets. Fluvastatin, a cholesterol metabolism inhibitor, inhibited HSA cell growth in vitro but did not significantly suppress tumour growth in two HSA patient-derived xenograft (PDX) models. In contrast, combined fluvastatin and dipyridamole treatment inhibited proliferation in vitro and tumour growth in PDX models. Collectively, these results suggest a context-dependent association between LDH and cholesterol/lipid metabolism in canine HSA cell lines and provide a rationale for further evaluation of combined cholesterol pathway inhibition. - Source: PubMed
Publication date: 2026/08/10
Suzuki TamamiTanaka SuzuneKishimoto KeikaGoto TakumaYamazaki JumpeiKimura TakashiAoshima Keisuke - Alzheimer's disease (AD) is a progressive neurodegenerative disorder with limited diagnostic tools and therapeutic options. Dysregulated mitophagy in astrocytes plays a pivotal role in AD pathogenesis. This study aims to identify a mitophagy and astrocyte (MA)-associated molecular signature for AD diagnosis and therapeutic targeting. - Source: PubMed
Publication date: 2026/07/24
Liu JiachengChen Wei - Cancer recurrence and distant metastasis are major causes of cancer-related death, yet existing biomarkers and single-omics models have limited accuracy and interpretability across tumor types. - Source: PubMed
Publication date: 2026/07/15
Li JunxianXing YuchenGao XiminLiu Renhe - Iron overload is a recognized risk factor for female reproductive dysfunction, yet the underlying cellular and molecular mechanisms remain incompletely understood. In this study, the effects of iron overload on ovarian granulosa cells were investigated, and a protective role of the steroid biosynthesis pathway against ferroptosis was identified. A mouse model of ovarian iron overload was established by daily gavage of ferric citrate (FC, 120 mg/kg for 40 days). Iron-overloaded female mice exhibited disrupted estrous cycles, reduced serum estradiol levels, impaired antral follicle development, and decreased pregnancy rates and litter sizes. Metabolomic analysis of freshly isolated granulosa cells revealed significant depletion of unsaturated glycerophospholipids and fatty acids, along with reduced antioxidants such as glutathione, vitamin E, and coenzyme Q6, and enrichment of the ferroptosis pathway. Transcriptomic analysis showed marked upregulation of genes involved in steroid biosynthesis, including and , and their master transcription factor . In cultured KK1 granulosa cells, FC treatment increased intracellular Fe and reactive oxygen species, decreased glutathione content and NADPH/NADP ratio, elevated malondialdehyde levels, and induced lipid peroxidation and plasma membrane rupture, all of which were attenuated by the iron chelator deferoxamine. Knockdown of suppressed and expression, exacerbated lipid peroxidation, and increased membrane damage in iron-overloaded cells, confirming that SREBF2-driven steroid biosynthesis acts as an endogenous anti-ferroptotic mechanism. Collectively, these findings demonstrate that iron overload triggers ferroptosis in granulosa cells, leading to follicular arrest and reduced fertility, and that activation of the steroid biosynthesis pathway counteracts ferroptosis, likely through the production of protective intermediates. This study provides a mechanistic basis for iron overload-induced female infertility and identifies the steroid biosynthesis pathway as a potential therapeutic target. - Source: PubMed
Publication date: 2026/07/17
Gao FeiyanMao WeiranHe XiaoyingLiu YingLiu YangLiu ShujunLiu JiweiMa Libing