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We identified a large number of mutations in the CC region of both Smc1 (show SMC1A Proteins) and Smc3... we introduced them to the yeast Smc1 (show SMC1A Proteins) and Smc3 CC domains and characterized the effect of these mutant alleles on cohesin's function. We identified a missense mutation in the region of the kink domain of Smc3, which was previously identified in kidney carcinoma
Results show that SMC3 is upregulated in asthma patients and suggest that it may play an important role in atopic asthma development, especially in asthma epithelial-mesenchymal transition.
Data show that histone deacetylase 8 (HDAC8 (show HDAC8 Proteins)) inhibition led to accumulation of acetylated-SMC3 protein but had no influence on the transcription of estrogen-responsive genes.
De novo heterozygous mutations in SMC3 cause a range of Cornelia de Lange syndrome-overlapping phenotypes
cohesin's proposed DNA exit gate is formed by interactions between Scc1 (show PTPRJ Proteins) and the coiled-coil region of Smc3.
Cross-sectional deep-sequencing analysis for clonal hierarchy demonstrated STAG2 (show STAG2 Proteins), SMC3, and RAD21 (show RAD21 Proteins) mutations to be ancestral in 18%, 18%, and 47% of cases, respectively, and each expanded to clonal dominance concordant with disease transformation
Mutations in SMC3 is associated with acute myeloid leukemia (show BCL11A Proteins).
Upon knock-down of human SMC1, much of SMC3 remains stable, accumulates in the cytoplasm and does not associate with other cohesin proteins.
c-MYC (show MYC Proteins) down-regulation caused by cohesin mutations in SMC1A (show SMC1A Proteins) and SMC3 genes may be an early/primary event in the pathogenesis of Cornelia de Lange syndrome.
NIPBL (show NIPBL Proteins), SMC1A (show SMC1A Proteins), and SMC3 mutation-positive patients were equally likely to have congenital heart diseases in Cornelia de lange syndrome.
A positively charged channel within the Smc1 (show SMC1A Proteins)/Smc3 hinge required for sister chromatid cohesion.
XEco2 (show ESCO2 Proteins) is the cohesin acetyltransferase responsible for Smc3 acetylation.
Endogenous SMC3 and newly expressed hRAD21 (show RAD21 Proteins) co-localize on chromosomal axes, sites where sister chromatids are tightly paired. hRAD21 (show RAD21 Proteins) recruitment to lampbrush chromosomes is modulated by chromosomal SMC1 (show SMC1A Proteins) and SMC3.
This gene belongs to the SMC3 subfamily of SMC proteins. The encoded protein occurs in certain cell types as either an intracellular, nuclear protein or a secreted protein. The nuclear form, known as structural maintenance of chromosomes 3, is a component of the multimeric cohesin complex that holds together sister chromatids during mitosis, enabling proper chromosome segregation. Post-translational modification of the encoded protein by the addition of chondroitin sulfate chains gives rise to the secreted proteoglycan bamacan, an abundant basement membrane protein.
chondroitin sulfate proteoglycan 6 (bamacan)
, SMC protein 3
, basement membrane-associated chondroitin proteoglycan
, chromosome-associated polypeptide
, structural maintenance of chromosomes protein 3
, chondroitin sulfate proteoglycan 6
, chromosome segregation protein SmcD
, mad member-interacting protein 1
, structural maintenace of chromosomes 3
, cohesin complex subunit
, basement membrane chondroitin sulfate proteoglycan