Ask about this productRelated genes to: SDHB antibody
- 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
Related articles to: SDHB antibody
- Hereditary neuroendocrine neoplasms (NENs) are the basis of over 10% of all neuroendocrine tumors. They result from germline mutations in tumor suppressor genes or proto-oncogenes.Compared to sporadic forms, hereditary NENs usually manifest at a younger age. Characteristic features include multifocal tumor development within a single organ or the synchronous occurrence of tumors in different endocrine tissues. Histologically, specific precursor lesions, such as endocrine hyperplasia or microtumors, can provide diagnostic clues. Furthermore, immunohistochemical analyses can directly detect the loss of gene products (e.g., SDHB, menin), serving as a guide for the mandatory molecular genetic germline analysis.This overview explains the clinical and histological signs that may indicate a familial background. - Source: PubMed
Publication date: 2026/05/28
Chouchane AzizMarinoni IlariaPerren Aurel - Neopestalotiopsis species (spp.) have recently emerged as major pathogens worldwide, causing leaf spot, fruit rot, and crown rot of strawberry, resulting in increased disease outbreaks and economic losses. Despite their increasing impact, there is a limited genomic resource for this pathogen group, constraining insights into pathogenic mechanisms and fungicide resistance. We conducted whole-genome sequencing of 50 Neopestalotiopsis strains from major strawberry production regions in North Carolina using the Illumina NovaSeq platform. The generated genome assemblies enabled comprehensive analyses of fungicide-resistance-associated mutations and the prediction of effector repertoires using signal-peptide screening, secretion filtering, and machine-learning-based approaches. Eight key fungicide target genes (β-tubulin, cytb, cyp51A, cyp51B, Bos1, and SDHI subunits (sdhB/C/D) were examined for putative resistance mutations. Phylogenomic analysis based on single orthologs from protein-coding regions and average nucleotide identity (ANI) matrices grouped the strains into two major lineages (Clades A and B) of Neopestalotiopsis rosae and a third distinct lineage (Clade C) comprising other Neopestalotiopsis spp. Between 879 and 895, CAZymes were predicted per genome, with glycoside hydrolases and auxiliary activity enzymes predominating in plant cell wall degradation. Effector prediction revealed between 87 and 95 putative secreted effectors, including many cysteine-rich proteins and species-specific candidates. Variation in target gene sequence analysis revealed benzimidazole resistance mediated by β-tubulin E198A/K and widespread QoI resistance associated with cytb G143A. The cyp51 gene exhibited extensive polymorphism, particularly H147Y and N284H, while the L98H variant was rare. No resistance-associated mutations were detected in any SDHI- or Os-1-target genes. This study represents the first comprehensive genomic assessment of Neopestalotiopsis strains infecting strawberry in North Carolina, revealing substantial genomic diversity, various enzymes and effectors involved in host colonization, and mutations linked to resistance to benzimidazole, QoI, and DMI, but not SDHI fungicides. These findings provide a foundation for developing improved, sustainable fungicide-use and disease-management strategies. - Source: PubMed
Publication date: 2026/05/27
Adhikari Tika BMuzhinji NormanGaire SusmitaMagar Prem BPandey AnjuMoparthi SwarnalathaLouws Frank J - The aim of this preliminary study was to determine the effect of taurine on the expression of genes involved in glycolysis, oxidative phosphorylation, inflammation, autophagy, and regenerative activity in cultured peripheral blood mononuclear cells (PBMCs) and articular cartilage explants from patients with end-stage rheumatoid arthritis (RA). PBMCs and knee articular cartilage were obtained from 20 patients with RA (3 men and 17 women) aged 62.2 ± 10.9 years, with a mean disease duration of 17.5 years (range: 2-43), prior to arthroplasty. PBMCs and cartilage explants were cultured in the presence of 50 µM taurine. Gene expression was determined using real-time reverse transcriptase polymerase chain reaction (RT-PCR). Protein expression of the examined genes in PBMCs was quantified using ELISA. In the presence of 50 µM taurine PBMCs from patients with RA demonstrated a significant increase in the expression of genes encoding pyruvate kinase (PKM2), succinate dehydrogenase (SDHB), uncoupler of oxidation and phosphorylation (UCP2), ATP synthase (ATP5B), and unc-51-like kinase 1 (ULK1). At the same time a significant decrease in tumor necrosis factor (TNF)α and interleukin (IL)-1β expression was noted. In cartilage explants, taurine upregulated SDHB, UCP2, ULK1, and type 2 collagen gene (COL2A1), and decreased TNFα expression. We concluded that, under in vitro conditions, taurine can influence the expression of genes involved in glycolysis, oxidative phosphorylation, inflammation, autophagy, and regenerative processes in PBMCs and articular chondrocytes from patients with end-stage RA. - Source: PubMed
Publication date: 2026/05/09
Tchetina ElenaKushnareva IrinaAnisimova EkaterinaVienozinskaite AngelePlastinina OksanaMakarov MaksimLila Aleksandr - DNA methylation is a key epigenetic modification with diagnostic and prognostic relevance across a wide range of diseases, particularly cancer. Modern array-based technologies enable high-throughput quantification of methylation states at hundreds of thousands of CpG sites, yielding high-dimensional datasets that pose significant challenges for exploratory analysis and feature prioritization. Existing visualization tools often lack interactivity, integration with machine learning methods, or flexible mechanisms for dynamic dimensionality reduction and biological interpretation. This work presents an interactive analytical framework that extends the Self-Organizing Map approach for epigenomic data exploration. Our method introduces meta sites-representative prototypes of CpG site clusters-enabling interpretable, real-time visualization and machine learning over reduced feature spaces. Through conditional sample projections (e.g., via PCA, t-SNE, or UMAP), user-driven region selection, and the integration of sparsity-controlled logistic regression, we generate metasite relevance maps that reveal discriminative epigenetic patterns and guide downstream analysis. The proposed approach supports iterative, visually driven discovery of co regulated modules and disease-associated methylation signatures, offering a powerful and intuitive interface for multidimensional exploration of complex methylation landscapes. Its utility is demonstrated through the analysis of DNA methylation in pheochromocytomas and paragangliomas, focusing on SDHB mutation status and the role of protocadherine gene clusters. - Source: PubMed
Publication date: 2026/05/25
Diaz IgnacioEnguita Jose MCuadrado Abel AGarcia DiegoRoos-Hoefgeest SaraCubiella TamaraValdes NuriaChiara Maria D - Succinate dehydrogenase (SDH)-deficient paraganglioma and pheochromocytoma (PPGL) are rare neuroendocrine neoplasms for which no effective targeted therapies currently exist. To uncover potential therapeutic targets, we performed an unbiased CRISPR-Cas9 genetic screen in immortalized mouse chromaffin cells (imCCs) with and without loss. Our screen identified genes that differentially affect cell proliferation in -deficient versus normal imCCs. Subunits of the transcriptional mediator complex emerged as potential tumor suppressors, as their loss selectively promoted growth of -deficient cells. The neddylation pathway, required for ubiquitin-mediated selective protein degradation, plays a critical role in -deficient imCC growth and survival: loss of the neddylation regulator Ube2m led to increased proliferation, while loss of Ube2f suppressed growth of -deficient imCCs. Neddylation inhibitors MLN4924 (Pevonedistat) and HA-9104 reduced UBE2F activity and selectively inhibited growth of -deficient imCCs. This unexpected result highlights the neddylation pathway as a promising druggable vulnerability to be studied in SDH-deficient PPGL. - Source: PubMed
Publication date: 2026/04/28
Al Khazal Fatimah JEmch Michael JCorreia CristinaFavier JudithHawse John RMaher L James