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Loss of SDHAF2 gene is associated with paragangliomas.
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The SDHA, TMEM127, MAX, and SDHAF2 genes contribute to hereditary pheochromocytoma and paraganglioma.
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data show that SDHA flavination is independent of SDHAF2 in breast cancer cells, employing an alternative mechanism.
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FAD interacts noncovalently with SDHA in the absence of SDH5
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Autosomal dominant susceptibility for Paraganglioma is modified by imprinting and mutations in the SDHAF2 gene cause Paragangliomas only when the mutation is inherited from father.
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Loss of heterozygosity was found in more than 50 % of the von Hippel-Lindau-associated pheochromocytomas, and was correlated with a significant decrease (p < 0.05) in both SDHAF2 and SDHD mRNA expression, which may be suggestive of a pathogenic role.
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New mutation found in SDHAF2 gene in pheochromocytoma/paraganglioma patients.
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Data indicate that SDH5 is protected from mitochondrial LON (LONM)-mediated degradation in mitochondria by its stable interaction with SDHA, a state that is dysregulated in hereditary paraganglioma 2 (PGL2).
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Data indicate that succinate dehydrogenase 5 (SDH5) functions as a critical protein in regulating epithelial-mesenchymal transition (EMT) by modulating the glycogen synthase kinase (GSK)-3beta-beta-catenin signaling pathway.
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Studies indicate that mutations in the mitochondrial complex II structural subunit genes SDHB, SDHC and SDHD and the regulatory subunit gene SDHAF2 in many paraganglioma families.
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Studies indicate that an array of tumor syndromes caused by complex II-associated mutations in genes SDHA, SDHB, SDHC, SDHD, SDHAF1 and SDHAF2 have been identified over a decade.
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Studies indicate that the flavinylation factor Sdh5 (SDHAF2) provided insight into the possible mechanism associated with Sdh1 (SDHA) flavinylation.
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We established the SDHAF2 mutation status of PGL2 family members
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Somatic mutations of the SDHAF2 tumor suppressor gene are unlikely to frequently contribute to parathyroid tumor development in sporadic primary hyperparathyroidism.
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germline loss-of-function mutations in the SDH5 gene segregate with disease in a family with hereditary paraganglioma
