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Establishment of cohesion 1 homolog 2

This gene encodes a protein that may have acetyltransferase activity and may be required for the establishment of sister chromatid cohesion during the S phase of mitosis. Mutations in this gene have been associated with Roberts syndrome. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, lacZ, V1a
Papers on RBS
Expanding the mutation and clinical spectrum of Roberts syndrome.
Gaber et al., Cairo, Egypt. In Congenit Anom (kyoto), Jan 2016
UNASSIGNED: Roberts syndrome and SC phocomelia syndrome are rare autosomal recessive genetic disorders representing the extremes of the spectrum of severity of the same condition, caused by mutations in ESCO2 gene.
Characterization of the full-length btuB riboswitch from Klebsiella pneumoniae.
Barceló-Oliver et al., Palma, Spain. In J Inorg Biochem, Jan 2016
Consequently, gene regulation is induced by un/masking of the ribosome binding site (RBS).
Structural analysis and insertion study reveal the ideal sites for surface displaying foreign peptides on a betanodavirus-like particle.
He et al., Guangzhou, China. In Vet Res, Dec 2015
Here, the three-dimensional structure of orange-spotted grouper nervous necrosis virus (OGNNV) VLP (RBS) at 3.9 Å reveals the organization of capsid proteins (CP).
Improved transcription and translation with L-leucine stimulation of mTORC1 in Roberts syndrome.
Gerton et al., Kansas City, United States. In Bmc Genomics, Dec 2015
BACKGROUND: Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2.
Construction of a novel twin-arginine translocation (Tat)-dependent type expression vector for secretory production of heterologous proteins in Corynebacterium glutamicum.
Xu et al., Baoding, China. In Plasmid, Nov 2015
In this study, we constructed a shuttle expression vector pAU3, which harbors the strong promoter tac-M for constitutive gene transcription, the consensus RBS sequence for protein translation, and the strong cgR_0949 signal sequence for protein secretion via the Tat pathway in C. glutamicum.
Viral receptor-binding site antibodies with diverse germline origins.
Harrison et al., Boston, United States. In Cell, Jun 2015
Vaccines for rapidly evolving pathogens will confer lasting immunity if they elicit antibodies recognizing conserved epitopes, such as a receptor-binding site (RBS).
A novel approach for metabolic pathway optimization: Oligo-linker mediated assembly (OLMA) method.
Lou et al., Beijing, China. In J Biol Eng, 2014
Several targets were intensively investigated to balance the gene expression, such as promoter, ribosome binding site (RBS), the order of genes, as well as the species of the enzymes.
Iron-sulfur clusters as biological sensors: the chemistry of reactions with molecular oxygen and nitric oxide.
Le Brun et al., Norwich, United Kingdom. In Acc Chem Res, 2014
The major iron nitrosyl product is EPR silent and has optical characteristics similar to Roussin's red ester, [Fe2(NO)4(RS)2] (RRE), although a species similar to Roussin's black salt, [Fe4(NO)7(S)3](-) (RBS) cannot be ruled out.
Temperature-driven differential gene expression by RNA thermosensors.
Narberhaus et al., Bochum, Germany. In Biochim Biophys Acta, 2014
Efficiency of translation initiation is primarily determined by the structural accessibility of the ribosome binding site (RBS).
Receptor binding and pH stability - how influenza A virus hemagglutinin affects host-specific virus infection.
Sieben et al., Berlin, Germany. In Biochim Biophys Acta, 2014
Human adapted influenza virus strains (H1N1, H3N2, H2N2) as well as recent avian influenza virus strains (H5, H7 and H9 subtypes) which gained the ability to infect humans mostly contained mutations in the receptor binding site (RBS) of HA enabling increased binding affinity of these viruses to human type (α-2,6 linked sialic acid) receptors.
Structural determinants for naturally evolving H5N1 hemagglutinin to switch its receptor specificity.
Sasisekharan et al., Cambridge, United States. In Cell, 2013
Here, we describe a structural framework that outlines a necessary set of H5 HA receptor-binding site (RBS) features required for the H5 HA to quantitatively switch its preference to human receptors.
Evaluation of oxidative stress in patients with acute ischemic stroke.
Ionescu et al., Bucureşti, Romania. In Rom J Intern Med, 2013
Malondialdehyde (MDA), plasma glutathione, plasma glutathione peroxidase (GPX), catalase (CAT), uric acid, bilirubin, plasma superoxide dismutase (SOD), red blood cells superoxide dismutase (RBS SOD) (spectrophotometric assay), total antioxidant capacity (TAC) (enhanced chemiluminescence), ceruloplasmin, C-reactive protein (CRP), albumin, transferrin (nephelometric assay) were performed in 57 patients (mean age 73.4 +/- 6.5 years) with acute ischemic stroke within 24 hours and at 7 days after stroke onset as compared to 51 age-and sex-matched controls.
Cohesinopathies of a feather flock together.
Tanzosh et al., Bethlehem, United States. In Plos Genet, 2012
Roberts Syndrome (RBS) and Cornelia de Lange Syndrome (CdLS) are severe developmental maladies that present with nearly an identical suite of multi-spectrum birth defects.
A child with Roberts syndrome.
Qureshi et al., Lahore, Pakistan. In J Coll Physicians Surg Pak, 2011
the ESCO2 gene mutation responsible for developmental abnormalities maps to chromosome 8p21.
Transcriptional regulation of the human establishment of cohesion 1 homolog 2 gene.
Yanagihara et al., Izumi, Japan. In Biochem Biophys Res Commun, 2010
These results demonstrated that the Staf binding site functioned as the basal transcriptional activator of the S phase-specific gene ESCO2, but other mechanisms are required for cell cycle-dependent expression.
Phenotypic variability in 49 cases of ESCO2 mutations, including novel missense and codon deletion in the acetyltransferase domain, correlates with ESCO2 expression and establishes the clinical criteria for Roberts syndrome.
Jabs et al., New York City, United States. In J Med Genet, 2010
In situ hybridisation on human embryos showed ESCO2 expression in the brain, face, limb, kidney and gonads, which corresponds to the structures affected in Roberts syndrome.
Cohesin acetylation speeds the replication fork.
Jallepalli et al., New York City, United States. In Nature, 2009
Unexpectedly, we discovered that cohesin acetylation itself is a central determinant of fork processivity, as slow-moving replication forks were found in cells lacking the Eco1-related acetyltransferases ESCO1 or ESCO2 (refs 8-10) (including those derived from Roberts' syndrome patients, in whom ESCO2 is biallelically mutated) and in cells expressing a form of SMC3 that cannot be acetylated.
The cellular phenotype of Roberts syndrome fibroblasts as revealed by ectopic expression of ESCO2.
de Winter et al., Amsterdam, Netherlands. In Plos One, 2008
ESCO2 has an S-phase specific role in the maintenance of genome stability
Esco2 is a novel corepressor that associates with various chromatin modifying enzymes.
Kim et al., Suwŏn, South Korea. In Biochem Biophys Res Commun, 2008
These results suggest a novel function of Esco2 in transcription repression through modulation of the chromatin structure.
Roberts syndrome is caused by mutations in ESCO2, a human homolog of yeast ECO1 that is essential for the establishment of sister chromatid cohesion.
Joenje et al., Bogotá, Colombia. In Nat Genet, 2005
required for the establishment of sister chromatid cohesion during S phase
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