Ask about this productRelated genes to: NSDHL antibody
- Gene:
- NSDHL NIH gene
- Name:
- NAD(P) dependent steroid dehydrogenase-like
- Previous symbol:
- -
- Synonyms:
- XAP104, H105e3, SDR31E1
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-30
- Date modifiied:
- 2015-08-25
Related products to: NSDHL antibody
Related articles to: NSDHL antibody
- Congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD) syndrome is a rare X-linked dominant disorder that primarily affects the skin and skeletal system but can also involve multiple organ systems. The disease usually presents with unilateral dermatological and skeletal abnormalities; however, rarely might bilateral involvement occur. This condition is associated with mutations in the NSDHL gene, which affects cholesterol biosynthesis. Herein, we report a 7-year-old female with bilateral involvement and a novel c.449 T>C (p.Phe150Ser) mutation in the NSDHL gene whose lesions cleared completely with topical cholesterol-lovastatin cream. - Source: PubMed
Publication date: 2026/05/05
Zeyrek MetinBalan KeremErsoy-Evans Sibel - Elevated expression of NAD(P)-dependent steroid dehydrogenase-like (NSDHL), a key enzyme in cholesterol biosynthesis, is associated with ovarian cancer progression and poor prognosis. However, the mechanisms underlying its tumor-promoting effects remain unclear. Here, we show that high NSDHL expression correlates with adverse clinical outcomes, particularly in aggressive subtypes such as high-grade serous ovarian cancer. NSDHL knockdown in cultured ovarian cancer cells reduced viability, triggered lipid peroxidation, and disrupted cholesterol and redox homeostasis, accompanied by elevated reactive oxygen species (ROS). Quantitative proteomic profiling revealed broad alterations in lipid metabolism, including suppression of fatty acid oxidation and PPARγ signaling, with upregulation of ACSL4 and downregulation of ACSL3. This shift toward polyunsaturated fatty acid (PUFA) enrichment enhanced susceptibility to oxidative stress but did not induce ferroptosis, owing to reduced intracellular iron levels. Notably, this paradoxical increase in lipid peroxidation despite iron deficiency contrasts with the classical ferroptosis model, in which iron is required to initiate and propagate lipid peroxidation, suggesting that NSDHL depletion uncouples oxidative membrane damage from canonical ferroptotic execution. Instead, apoptosis was mediated by lipid peroxidation–induced endoplasmic reticulum (ER) stress, as confirmed by upregulation of ER stress markers and activation of ER-specific caspases. Importantly, NSDHL depletion suppressed tumor growth and promoted ER stress–mediated apoptosis in ovarian cancer xenografts. These findings identify NSDHL as a key regulator of lipid metabolism and oxidative stress in ovarian cancer and highlight its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/04/08
Shanshan XuJinshi RanWanlin CaiYuwan LiuHanye JinShizhou YangWeidong FeiHuimei ZhengYongmei XiWeiguo Lu - Incontinentia pigmenti and CHILD syndrome are genodermatoses characterized by an X-linked dominant inheritance pattern, resulting from pathogenic variants in the and genes, respectively. - Source: PubMed
Publication date: 2025/12/19
Vergara AngelaMonge IvanGaroz Barbara FernandezRuiz SergioAlonso MatildeTorrelo AntonioOrtiz Cabrera Nelmar Valentina - Obesity is closely linked to dyslipidemia, hepatic injury, and chronic inflammation through disturbances in the gut-liver axis. Here, we evaluated the anti-obesity effects of () CU262 in a high-fat diet (HFD) mouse model and elucidated mechanisms using an integrated multi-omics strategy. Male C57BL/6 mice received CU262 during 12 weeks of HFD feeding. Phenotypes, serum/liver biochemistry, gut microbiota (16S rRNA sequencing), fecal short-chain fatty acids (SCFAs), and hepatic transcriptomes (RNA-seq) were assessed. CU262 significantly attenuated weight gain and adiposity; improved serum TC, TG, LDL-C and HDL-C; lowered ALT/AST and FFA; and mitigated oxidative stress and inflammatory imbalance (↓ IL-6/TNF-α, ↑ IL-10). CU262 restored alpha diversity, reduced the / ratio, enriched beneficial taxa (e.g., ), and increased acetate and butyrate. Liver transcriptomics showed CU262 reversed HFD-induced activation of cholesterol/steroid biosynthesis and endoplasmic reticulum stress, with downregulation of key genes (, , , , and ) and , yielding negative enrichment of steroid and terpenoid backbone pathways and enhancement of oxidative phosphorylation and glutathione metabolism. Correlation analyses linked and SCFAs with improved lipid/inflammatory indices and repression of cholesterol-synthetic and stress-response genes. These findings demonstrate that CU262 alleviates HFD-induced metabolic derangements via microbiota-SCFA-hepatic gene network reprogramming along the gut-liver axis, supporting its potential as a functional probiotic for obesity management. - Source: PubMed
Publication date: 2026/01/16
Guo HezixianPan LiyiWang LinhaoHuang ZongjianWu QiuyiWang JieLiao Zhenlin - Gemcitabine (GEM) is a standard treatment for bladder cancer (BLCA), but resistance to this chemotherapy often reduces its efficacy. Thus, to uncover the molecular mechanisms of this resistance is essential to reverse GEM resistance. - Source: PubMed
Publication date: 2025/12/23
Li MingxingLiu TianyunShi JiagengZhou FenfangDeng ZhaoLuo YongwenTu ShengJiang WenyuWang GangQian KaiyuZhang YiXiao YuWang XinghuanLiu TongzuJu Lingao