SDHB antibody Polyclonal Antibodies Primary antibodies
- Known as:
- SDHB (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100165
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- SDHB antibody Polyclonal Antibodies Primary antibodies
Related genes to: SDHB antibody Polyclonal Antibodies Primary antibodies
- Gene:
- SDHB NIH gene
- Name:
- succinate dehydrogenase complex iron sulfur subunit B
- Previous symbol:
- SDH1, SDH
- Synonyms:
- -
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: SDHB antibody Polyclonal Antibodies Primary antibodies
Related articles to: SDHB antibody Polyclonal Antibodies Primary antibodies
- Nasopharyngeal carcinoma (NPC) remains a therapeutically challenging malignancy due to its late diagnosis and limited treatment efficacy. Although metabolic reprogramming is a hallmark of cancer, the ubiquitin-mediated mechanisms underlying NPC progression are incompletely understood. Here, we demonstrate that tripartite motif-containing protein 47 (TRIM47) is significantly upregulated in NPC tissues and drives tumor aggressiveness. Through integrated in vitro and in vivo approaches, we found that TRIM47 promotes proliferation, migration, epithelial-mesenchymal transition (EMT), and tumor growth. Mechanistically, TRIM47 directly interacts with succinate dehydrogenase subunit B (SDHB)-a key component of mitochondrial complex II-via its B30.2/SPRY domain and catalyzes K48-linked polyubiquitination, leading to SDHB proteasomal degradation. This degradation induces metabolic reprogramming characterized by enhanced aerobic glycolysis, as evidenced by increased glucose consumption and lactate production. Critically, the oncogenic effects of TRIM47 were reversed by SDHB reconstitution. Moreover, supplementation with succinate, the enzymatic product of SDH, counteracted the tumor-suppressive effects of TRIM47 knockdown. Furthermore, exploiting the metabolic vulnerability induced by TRIM47, ascorbate treatment effectively suppressed TRIM47-driven tumor growth. Our results identify TRIM47 as a novel E3 ligase responsible for SDHB ubiquitination and degradation, thereby promoting Warburg-like metabolism and NPC progression. These findings unveil the TRIM47-SDHB axis as a promising therapeutic target and support metabolic intervention with ascorbate as a potential precision strategy for NPC treatment. - Source: PubMed
Publication date: 2026/06/06
Yu JieqingDing LeYang YongXie TaoPeng JunboLuo QingHuang XuanLi YongYe Jing - Pheochromocytoma and paraganglioma with a succinate dehydrogenase B subunit (SDHB) pathogenic variant are associated with a significant chance for metastasis. Polyamine pathway inhibitor N1,N11-diethylnorspermine (DENSPM) was previously shown to inhibit cell growth in progenitor cells derived from a human pheochromocytoma (hPheo1). Here, we hypothesized cell death associated with DENSPM treatment due to altered lipid metabolism affects protein kinase C (PKC). From targeted lipidomics analysis, baseline bioactive lipids that are distinct between the hPheo1 WT and SDHB KD cells are PE(P-18:1/16:0), PI(18:1/20:3), LPE(18:0), and LPE(22:4). With DENSPM treatment, the concentrations of multiple plasmanyl phosphatidylethanolamines (PE-O), sphingomyelins (SM), and hexosylceramides (HCER) increased, while the concentrations of several plasmenyl phosphatidylethanolamines (PE-P) were decreased in hPheo1 WT and SDHB KD cells. The differences in PE-Ps, PE-Os, and SMs after DENSPM treatment compared to the vehicle treatment were greater in the SDHB KD cells compared to the hPheo1 WT cells. Basal PKC alpha protein expression was increased in SDHB KD cells compared to hPheo1 WT cells. The protein expression of both PKC alpha and delta was significantly decreased with DENSPM treatment in both cell lines. DENSPM changed pro-caspase-3 and cleaved caspase-3. These data suggest ether phospholipids are biomarkers of DENSPM mediated cell apoptosis through a PKC dependent mechanism. - Source: PubMed
Alli Abdel ABala NiharikaXu YilingDenslow Nancy DGhayee Hans K - Pheochromocytomas and paragangliomas (PPGLs), rare neuroendocrine tumors, have been generally considered, since the 2017 WHO classification, as malignant neoplasms with various metastatic potential. Approximately 10-25% of PPGLs will develop metastases, with a varying 5-year-overall-survial of 40%-77%. Previous studies have extensively elucidated the mechanisms by which SDHB mutations promote tumor metastasis through inducing the pseudohypoxic and hypermethylation phenotype. Recent multi-omics studies further profiled the additional landscape of metastatic PPGLs, involving ATRX/TERT alterations, higher tumor mutational burden, microsatellite instability score, and somatic copy-number alteration, distinct microRNA (miRNA) profiling, aberrant kynurenine metabolic pathway, and immunosuppressive microenvironment, advancing our understanding of metastatic mechanisms. Consequently, beyond conventional predictors (e.g., SDHB mutation status, tumor size and location, levels of dopamine and methoxytyramine, Ki-67 labeling index, and loss of S100), emerging biomarkers for metastasis prediction were discovered and evaluated, including levels of circulating miR-483-5p, plasma succinate, tissue xanthurenic acid, and CDK1 expression, etc. Several scoring systems integrating tumor clinicopathological characteristics have been constructed to predict metastatic PPGLs; however, their clinical utility may be limited by high observer variation and low positive predictive value. Recent prediction models integrating multi-omics signatures of metastatic tumors have also been established, but without validation. This review comprehensively synthesizes current and emerging multi-omics signatures of metastatic PPGLs to elucidate underlying metastatic mechanisms. A systematic review of existing scoring systems and emerging predictive models for metastasis prediction was also conducted to highlight their advantages and limitations in the clinical application. - Source: PubMed
Publication date: 2026/06/02
Zhou YueCui YunyingLi TianyiTong Anli - Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by complex molecular alterations across multiple brain regions. In this study, we applied an integrative systems-level framework combining multi-region transcriptomic analysis, protein-protein interaction (PPI) network topology, machine learning-based validation, and in silico approaches to identify robust and pharmacologically relevant molecular targets in AD. Gene expression data from four AD-related brain regions (entorhinal cortex, frontal cortex, hippocampus, and temporal cortex) were obtained from the GSE5281 dataset, yielding 467 genes consistently dysregulated across all regions. Network analysis identified a subset of downregulated hub genes predominantly associated with mitochondrial bioenergetics and proteostasis pathways. Intersection with experimentally curated targets of genistein and resveratrol prioritized four elite genes, COX5B, ENO1, HSP90AB1, and SDHB as shared and biologically central nodes. To assess the collective discriminative capacity of the identified gene set, a random forest classifier was trained using shared differentially expressed genes. The model demonstrated strong classification performance with a low out-of-bag error rate, while feature importance analysis identified SDHB as the most influential contributor, followed by COX5B and ENO1, indicating synergistic multigene effects rather than isolated biomarker behavior. Machine learning was applied as an integrative validation layer to reinforce biological relevance, rather than as a standalone diagnostic tool. Finally, molecular docking analyses revealed favorable binding affinities of genistein and resveratrol toward all four elite targets. Overall, these findings highlight a convergent mitochondrial-proteostasis dysfunction axis in AD and suggest COX5B, ENO1, HSP90AB1, and SDHB as promising multi-target nodes for polyphenol-based therapeutic strategies. - Source: PubMed
Publication date: 2026/06/02
Isıyel MuratCeylan HamidDemir Yeliz - Male infertility has been increasing globally, raising concerns for reproductive health. Ornidazole (ORN) emerges as a novel environmental pollutant and compromises male fertility. However, the protective role and underlying mechanisms of docosahexaenoic acid (DHA) against ORN-induced testicular damage remain unexplored. Our clinical data showed that elevated serum ORN levels were negatively correlated with sperm quality. In vivo, ORN exposure led to impaired spermatogenesis, including meiotic disorders. Specifically, ORN impaired redox balance and reduced the expression of mitochondrial respiratory chain proteins (Ndufs1 and SdhB) in spermatocytes. Supplementation with docosahexaenoic acid significantly restored the quantity of DDX4-positive germ cells and SYCP3-positive spermatocytes and facilitated the progression from zygotene to pachytene stage. Mechanistically, DHA restored mitochondrial function and ROS levels by stimulating peroxisome proliferator-activated receptor gamma (PPARγ) signaling. Moreover, DHA reduced the expression of mitochondria-associated endoplasmic reticulum membranes (MAMs)-tethered voltage-dependent anion channel 1 (VDAC1), restoring MAMs balance and mitochondrial calcium homeostasis in a PPARγ-dependent manner. The DHA/PPARγ/VDAC1 axis in spermatocytes functions as a critical metabolic switch for regulating MAMs and ensuring mitochondrial homeostasis during meiosis. DHA is a promising therapeutic metabolite for oligoasthenozoospermia induced by environmental pollution. - Source: PubMed
Publication date: 2026/05/27
Li ChuweiZhao ShanmeiziShi ChongliSun ShanshanHe ZhaowanyueXu YaoZheng LuTang TingQiu ShengjieLiang KuanZhang HongZou ZhichuanFeng YumingZang MinDong JieMa JinzhaoMa RujunFu ChuanhaiGe XieWang YongJing JunYao Bing