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SDHB (show SDHB Antibodies) mutation is associated with metastatic pheochromocytoma.
we found a higher estimated penetrance compared to several other studies, and a striking difference in age-related penetrance between male and female SDHB (show SDHB Antibodies) mutation carriers with no association between mutation and gender or tumor location
LASS5 (show LASS5 Antibodies) interacts with SDHB (show SDHB Antibodies) and synergistically represses p53 (show TP53 Antibodies) and p21 (show CDKN1A Antibodies) activity.
A novel SDHB (show SDHB Antibodies) germline mutation in a paraganglioma
SDHB (show SDHB Antibodies)-related tumours are picked up as early as 2 years after initial negative surveillance scan
miR (show MLXIP Antibodies)-183 cluster (miR (show MLXIP Antibodies)-96/182/183) are related to clinical parameters and SDHB (show SDHB Antibodies) expression in pheochromocytomas.
In SDHB (show SDHB Antibodies) mutation carriers, a lower rate of metastatic disease and a higher number of head and neck paragangliomas compared to previous reports was observed in a nationwide study in the Netherlands.
Loss of FH immunohistochemical (IHC) expression in cutaneous leiomyomas is a sensitive and specific marker for detection of hereditary leiomyomatosis and renal cell carcinoma (show MOK Antibodies) (HLRCC (show FH Antibodies)). FH expression by IHC was absent in 9 specimens and retained in 85 specimens and 2 cases were equivocal with minimal FH expression while succinate dehydrogenase B (show SDHB Antibodies) expression was retained in 95 specimens and equivocal in 1 specimen.
Identify small molecule binding to the succinate dehydrogenase subunit B (SDHB (show SDHB Antibodies)) protein of complex II of the mitochondrial electron transfer chain to block mitochondrial apoptotic pathway.
We have shown that ASO treatment diminished aberrant splicing and increased ISCU (show ISCU Antibodies) protein levels in both patient fibroblasts and patient myotubes in a concentration dependent fashion. Upon ASO treatment, levels of SDHB (show SDHB Antibodies) in patient myotubular cell lines increased to levels observed in control myotubular cell lines
Deficiency of the ribosome biogenesis gene Sbds (show SBDS Antibodies) in hematopoietic stem and progenitor cells causes neutropenia in mice by attenuating lineage progression in myelocytes
Sbds (show SBDS Antibodies) genotypes correlated with phenotypes in a mouse model of Shwachman-Diamond syndrome. Defects developed specifically in the pancreata of mice, reducing growth of mice and production of digestive enzymes.
Sbds (show SBDS Antibodies) is required for osteoclastogenesis by regulating monocyte migration via Rac2 (show RAC2 Antibodies) and osteoclast differentiation signaling downstream of RANK.
Sbds (show SBDS Antibodies) is an essential gene for early mammalian development, with an expression pattern consistent with a critical role in cell proliferation.
loss of Sbds (show SBDS Antibodies) is sufficient to induce abnormalities in hematopoiesis
The majority of Shwachman-Diamond syndrome cases are results of mutations in SBDS (show SBDS Antibodies) gene on chromosone 7q11.
Complex II of the respiratory chain, which is specifically involved in the oxidation of succinate, carries electrons from FADH to CoQ. The complex is composed of four nuclear-encoded subunits and is localized in the mitochondrial inner membrane. The iron-sulfur subunit is highly conserved and contains three cysteine-rich clusters which may comprise the iron-sulfur centers of the enzyme. Sporadic and familial mutations in this gene result in paragangliomas and pheochromocytoma, and support a link between mitochondrial dysfunction and tumorigenesis.
, L-serine dehydratase/L-threonine deaminase
, L-serine ammonia-lyase
, L-serine deaminase
, L-serine dehydratase
, L-threonine dehydratase
, protein 22A3
, ribosome maturation protein SBDS
, shwachman-Bodian-Diamond syndrome protein homolog
, iron-sulfur subunit of complex II
, succinate dehydrogenase [ubiquinone] iron-sulfur subunit, mitochondrial