SDHC Mouse Monoclonal Antibody
- Known as:
- SDHC Mouse Monoclonal Antibody
- Catalog number:
- ENZ-006391-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- SDHC Mouse Monoclonal Antibody
Related genes to: SDHC Mouse Monoclonal Antibody
- Gene:
- SDHC NIH gene
- Name:
- succinate dehydrogenase complex subunit C
- Previous symbol:
- PGL3
- Synonyms:
- CYB560, cybL
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-21
- Date modifiied:
- 2019-04-23
Related products to: SDHC Mouse Monoclonal Antibody
Related articles to: SDHC Mouse Monoclonal Antibody
- Phoma stem canker (PSC) of oilseed rape (Brassica napus) is a disease caused by a complex of two related fungal pathogens: Plenodomus lingam (Leptosphaeria maculans) and P. biglobosus (L. biglobosa). While P. biglobosus is increasingly recognised as an important PSC pathogen, its sensitivity to succinate dehydrogenase inhibitor (SDHI; FRAC group 7) fungicides remains poorly understood. - Source: PubMed
Publication date: 2026/09/22
King Kevin MWest Jonathan S - , the causal agent of Botrytis fruit rot (BFR), is one of the most destructive pathogens of strawberry. In Florida, BFR management relies heavily on succinate dehydrogenase inhibitor (SDHI) fungicides; however, resistance associated with mutations in the SdhB subunit has increasingly been reported. This study developed and validated a high-resolution melting (HRM) assay for rapid detection of SdhB mutations directly from spores, and evaluated resistance frequencies to fluopyram, isofetamid, and pydiflumetofen across Florida strawberry fields. Two HRM primer sets successfully differentiated SdhB mutations H272R or Y, N230I, and P225F based on distinct melting profiles. The assay detected mutations from spore concentrations as low as 10⁵ spores/ml, without requiring DNA extraction or post-PCR processing. Sanger sequencing subsequently confirmed complete agreement with HRM genotyping results. Among 133 field isolates collected from 2017 to 2022, N230I and P225F were the most frequent mutations, correlating with moderate to high resistance to fluopyram and isofetamid. Resistance monitoring of 1,496 isolates over eight strawberry seasons revealed increasing resistance to fluopyram (44.9-99%) and isofetamid (≤57%), whereas pydiflumetofen resistance remained below 15%. Sequencing of SdhC and SdhD subunits revealed minimal variability and no new target-site mutations. Detached fruit assays confirmed reduced efficacy of isofetamid against isolates harboring N230I. The HRM assay developed here provides a rapid, accurate, and cost-effective tool for detecting and monitoring SDHI resistance in populations in strawberry production systems. - Source: PubMed
Publication date: 2026/09/22
Zuniga Adrian IsraelWang Nan-YiSuguinoshita Rebello CarolinaBolognesi MayaraForcelini Bruna BalenPeres Natalia A - The succinate dehydrogenase (SDH) enzyme composed of four subunits (A-D) has a key role in the Krebs cycle and oxidative phosphorylation. Germline pathogenic variants (GPV) in the genes encoding the four subunits of the succinate dehydrogenase (SDH) enzyme (SDHA/SDHB/SDHC/SDHD), collectively known as SDHx are recognized as a paradigm for the role of disordered metabolism in oncogenesis as GPVs in SDHx lead to a truncated citric acid cycle due to reduced or absent function of the SDH enzyme and accumulation of the oncometabolite succinate. GPVs in SDHx are the most common cause of hereditary PPGL and are associated with a higher risk of malignant PPGL and predispose to other tumors including renal cell carcinoma, gastrointestinal stromal tumors (GIST) and pituitary adenomas. Utilizing the linkage of SDHx to metabolic dysfunction, we performed prospective plasma metabolomics and identified succinate as a biomarker for early diagnosis of an underlying SDHx variant. Succinate reflected SDHx deficiency, in individuals with germline predisposition and a small number of patients with somatic SDHx deficiency, and succinate levels correlated with tumor burden. Longitudinal sampling of patients illustrated that serial succinate measurements might be used as a biomarker for disease surveillance. These findings were validated by tissue analysis in a mouse model of Sdhb deficiency, where elevated succinate was observed in adrenal glands. While circulating plasma levels did not mirror the human cohort, this discrepancy suggests specific cellular thresholds for succinate or SDHx deficiency in adrenal gland tissue and highlights species-specific metabolic regulation. - Source: PubMed
Publication date: 2026/09/18
Cole YaseminAbramovich IfatFernandez-Garcia JonatanDocquier FranceMacFarlane JamesXu XiaAndresson ThorkellIndig IrisWang HeruiKrishnan AnaghaChen ShuranChallis BenGottlieb EyalZhuang ZhengpingMaher Eamonn RCasey Ruth T - Brown rot, caused by , is the most destructive pre- and postharvest fruit rot of peach worldwide. In 2024, a disease outbreak occurred in a South Carolina orchard despite a rigorous chemical management program consisting of preharvest applications of SDHI, QoI, and DMI fungicides. Isolates from affected orchards carried the element upstream of the gene, associated with reduced DMI fungicide sensitivity in the southeastern region. They displayed low, moderate, or high levels of resistance to boscalid, isofetamid, fluopyram, and fluxapyroxad based on EC values ranging from 0.33 to >300, 0.22 to 1.95, 0.28 to 7.41 and 0.30 to 115.11 µg/ml, respectively. In contrast, EC values obtained for historic isolates were ≤ 0.05 µg/ml for all SDHI fungicides. Whole-genome sequencing identified five SDH genotypes: wild type (WT; no aa substitutions); G1 (N226H in SDHB); G2 (P80H in SDHC); G3 (N226H in SDHB + V26I in SDHD); and G4 (N226H in SDHB, P80H in SDHC, and T24A in SDHD). Isolates harboring aa changes in multiple SDH subunits had the highest EC values and were resistant to all SDHIs tested. Detached fruit assays confirmed that label rates of SDHI fungicides failed to control isolates carrying multiple aa changes. To the best of our knowledge, this study provides the first report worldwide of SDHI resistance in species field isolates linked to aa changes in the SDH subunits and combined SDHI and DMI resistance in peach orchards, highlighting the need for resistance monitoring and management. - Source: PubMed
Publication date: 2026/08/26
Gelain JhuliaWesche JohannaTrotter Emma KatherineBeger MatheusOrtiz MaximilianoSchnabel Guido - Genetic testing of patients with pituitary adenomas enables delivery of genotype-based precision care. Germline testing might identify variants predisposing to formation of pituitary adenomas and, potentially, other neoplasms. These include loss-of-function variants in AIP, MEN1, CDKN1B, PRKAR1A, SDHA, SDHB, SDHC, SDHD and MAX; GPR101-containing Xq26.3 microduplications; and postzygotic gain-of-function GNAS variants. Somatic testing might help identify and manage aggressive pituitary adenoma types and very rarely encountered pituitary carcinomas. This Pituitary Society Consensus Statement provides evidence-based guidance on the clinical application of these genetic tests, focusing on germline genetic testing, with recommendations regarding genes for inclusion in panel testing, test indications, pre-test counselling, test methodologies, and the interpretation and follow-up of results. As somatic genetic testing is gradually becoming available in clinical practice, recommendations are provided regarding clinical scenarios in which somatic testing might be considered and which genes to test. The consensus group concluded that genetic testing is an increasingly valuable adjunct in the assessment and management of people with pituitary adenomas. When indicated, genetic testing should ideally be undertaken within a multidisciplinary team comprising endocrine, genetic and laboratory expertise to ensure high-quality testing and safe and effective result interpretation and follow-up. - Source: PubMed
Publication date: 2026/08/25
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