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Human Polyclonal SMC3 Primary Antibody for ICC, IF - ABIN151536
Revenkova, Eijpe, Heyting, Hodges, Hunt, Liebe, Scherthan, Jessberger: Cohesin SMC1 beta is required for meiotic chromosome dynamics, sister chromatid cohesion and DNA recombination. in Nature cell biology 2004
Show all 8 Pubmed References
H2 inhibited lung cancer progression through down-regulating SMC3.
Both the SMC1A and SMC3 gene mutation tests were negative in all Chinese patients with Cornelia de Lange syndrome.
We identified a large number of mutations in the CC region of both Smc1 and Smc3... we introduced them to the yeast Smc1 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) 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 and the coiled-coil region of Smc3.
Cross-sectional deep-sequencing analysis for clonal hierarchy demonstrated STAG2, SMC3, and RAD21 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.
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 down-regulation caused by cohesin mutations in SMC1A and SMC3 genes may be an early/primary event in the pathogenesis of Cornelia de Lange syndrome.
NIPBL, SMC1A, and SMC3 mutation-positive patients were equally likely to have congenital heart diseases in Cornelia de lange syndrome.
SMC3 and separase are upregulated and securin is downregulated in malignant transformation of BEAS-2B cells induced by coal tar pitch smoke extracts.
these studies clearly suggest that bamacan interacts with the vaccinia virus-N1L and such interactions seem to play a positive role in promoting the viral growth and perhaps contribute to the virulence of VV in neural cells.
The identification of 14 additional mutations of the cohesin complex genes NIPBL and SMC1A in a cohort of 30 unrelated patients with Cornelia de Lange syndrome, is reported.
identification as target for beta-catenin/T-cell factor 4 transactivation pathway
Hinderin is a novel binding partner of SMC3. Based on its ability to modulate SMC1/SMC3 interaction we postulate that Hinderin affects the availability of SMC3 to engage in the formation of multimeric protein complexes
RPGR-ORF15, which is mutated in retinitis pigmentosa, associates with SMC3.
RhoB and cAMP cis-acting response elements -BPa two known oncogenic mediators whose expression is significantly increased following SMC3 overexpression play a significant role in mediating SMC3 tumorigenesis
SMC3 deficiency affects chromosomal stability leading to the activation of p53-dependent mitotic checkpoint.
antecedent mutations may be required to optimize the leukemogenic potential of Smc3 mutations.
A positively charged channel within the Smc1/Smc3 hinge required for sister chromatid cohesion.
XEco2 is the cohesin acetyltransferase responsible for Smc3 acetylation.
Endogenous SMC3 and newly expressed hRAD21 co-localize on chromosomal axes, sites where sister chromatids are tightly paired. hRAD21 recruitment to lampbrush chromosomes is modulated by chromosomal SMC1 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