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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Iduronate 2-sulfatase

IDS, iduronate-2-sulfatase
Iduronate-2-sulfatase is required for the lysosomal degradation of heparan sulfate and dermatan sulfate. Mutations in this X-chromosome gene that result in enzymatic deficiency lead to the sex-linked Mucopolysaccharidosis Type II, also known as Hunter Syndrome. Iduronate-2-sulfatase has a strong sequence similarity with human arylsulfatases A, B, and C, and human glucosamine-6-sulfatase. Multiple alternatively spliced transcript variants that encode different protein isoforms have been described. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: sulfatase, CAN, HAD, AGE, ACID
Papers on IDS
Identification of high-grade serous ovarian cancer miRNA species associated with survival and drug response in patients receiving neo-adjuvant chemotherapy: a retrospective longitudinal analysis using matched tumor biopsies.
Marchini et al., Milano, Italy. In Ann Oncol, Feb 2016
PATIENTS AND METHODS: 164 matched tumor biopsies taken at initial laparoscopic evaluation and at interval-debulking surgery (IDS) after 4 courses of platinum based therapy were selected from 82 Stage IIIC-IV high-grade serous-EOC patients that were judged unsuitable for complete primary debulking and subjected the NACT protocol.
Wide allelic heterogeneity with predominance of large IDS gene complex rearrangements in a sample of Mexican patients with Hunter syndrome.
Rius-Domínguez et al., Villa Cuauhtémoc, Mexico. In Clin Genet, Feb 2016
UNASSIGNED: Hunter syndrome or mucopolysaccharidosis type II (MPSII) is caused by pathogenic variants in the IDS gene.
OEFinder: A user interface to identify and visualize ordering effects in single-cell RNA-seq data.
Stewart et al., Madison, United States. In Bioinformatics, Feb 2016
Specifically, Leng* et al. showed significantly increased gene expression in cells captured from sites with small or large plate output IDs.
Myozap Deficiency Promotes Adverse Cardiac Remodeling via Differential Regulation of MAPK/SRF- and β-Catenin/GSK-3β-Signaling.
Frey et al., Kiel, Germany. In J Biol Chem, Jan 2016
Expression of other ID proteins like N-Cadherin, Desmoplakin, Connexin-43, and ZO-1 was significantly perturbed upon pressure overload, underscored by disorganization of the IDs in Mzp-/- mice.
Data in support of a functional analysis of splicing mutations in the IDS gene and the use of antisense oligonucleotides to exploit an alternative therapy for MPS II.
Alves et al., Porto, Portugal. In Data Brief, Dec 2015
This data article contains insights into the methodology used for the analysis of three exonic mutations altering the splicing of the IDS gene: c.241C>T, c.257C>T and c.1122C>T.
Adsorption capacity of poly(ether imide) microparticles to uremic toxins.
Jankowski et al., Hyderābād, India. In Clin Hemorheol Microcirc, Dec 2015
Hydrophobic uremic toxins, such as hydroxy hipuric acid (OH-HPA), phenylacetic acid (PAA), indoxyl sulfate (IDS) and p-cresylsulfate (pCRS), contribute substantially to the progression of chronic kidney disease (CKD) and cardiovascular disease.
Congenital imprinting disorders: Application of multilocus and high throughput methods to decipher new pathomechanisms and improve their management.
Eggermann et al., Aachen, Germany. In Mol Cell Probes, Oct 2015
Imprinting disorders (IDs) are a group of congenital diseases affecting growth, development and metabolism.
Tumor necrosis factor-α confers cardioprotection through ectopic expression of keratins K8 and K18.
Capetanaki et al., Athens, Greece. In Nat Med, Sep 2015
In cardiomyocytes, K8 and K18 (K8/K18) formed an alternative cytoskeletal network that localized mainly at intercalated discs (IDs) and conferred cardioprotection by maintaining normal ID structure and mitochondrial integrity and function.
Challenges in the Management of Mucopolysaccharidosis Type II (Hunter's Syndrome) in a Developing Country: a Case Report.
Gbadebo et al., Ilorin, Nigeria. In Ethiop J Health Sci, Jul 2015
BACKGROUND: Mucopolysaccharidosis type II (Hunter's syndrome) is an X-linked chromosomal storage disorder due to deficiency of the lysosomal enzyme iduronate-2-sulfatase with patients rarely living till adulthood.
Gap junctions - guards of excitability.
Nielsen et al., Copenhagen, Denmark. In Biochem Soc Trans, Jun 2015
Cardiomyocytes are connected by mechanical and electrical junctions located at the intercalated discs (IDs).
Id proteins in the vasculature: from molecular biology to cardiopulmonary medicine.
Morrell et al., Beijing, China. In Cardiovasc Res, 2015
In addition, current progress in identification of the interactors of Id proteins will further the understanding of the function of Ids in vascular cells and enable the identification of novel targets for therapy in PAH and other cardiovascular diseases.
Congenital imprinting disorders: - a network to decipher their aetiology and to improve the diagnostic and clinical care.
Maher et al., Aachen, Germany. In Clin Epigenetics, 2014
Imprinting disorders (IDs) are a group of eight rare but probably underdiagnosed congenital diseases affecting growth, development and metabolism.
Imprinting disorders: a group of congenital disorders with overlapping patterns of molecular changes affecting imprinted loci.
Netchine et al., Aachen, Germany. In Clin Epigenetics, 2014
Congenital imprinting disorders (IDs) are characterised by molecular changes affecting imprinted chromosomal regions and genes, i.e. genes that are expressed in a parent-of-origin specific manner.
Complete genome sequence of and proposal of Thermofilum uzonense sp. nov. a novel hyperthermophilic crenarchaeon and emended description of the genus Thermofilum.
Kublanov et al., Kaliningrad, Russia. In Stand Genomic Sci, 2014
Project information and genome sequence was deposited in Genbank under IDs PRJNA262459 and CP009961, respectively.
Severe phenotype in MPS II patients associated with a large deletion including contiguous genes.
Leistner-Segal et al., Porto Alegre, Brazil. In Am J Med Genet A, 2012
genetically analyze patients with severe Hunter syndrome that showed a total deletion of the iduronate-2-sulphatase (IDS) gene
Female Hunter syndrome caused by a single mutation and familial XCI skewing: implications for other X-linked disorders.
Węgrzyn et al., Gdańsk, Poland. In Clin Genet, 2011
Family members with 3 generations of X-inactivation with Hunter syndrome have 1568A>G missence mutation in the IDS gene
USP1 deubiquitinates ID proteins to preserve a mesenchymal stem cell program in osteosarcoma.
Dixit et al., San Francisco, United States. In Cell, 2011
Inhibitors of DNA binding (IDs) antagonize basic-helix-loop-helix (bHLH) transcription factors to inhibit differentiation and maintain stem cell fate.
LCR-initiated rearrangements at the IDS locus, completed with Alu-mediated recombination or non-homologous end joining.
Del Gaudio et al., Houston, United States. In J Hum Genet, 2011
LCR-initiated rearrangements at the IDS locus, completed with Alu-mediated recombination or non-homologous end joining
A mother and daughter with the p.R443X mutation of mucopolysaccharidosis type II: Genotype and phenotype analysis.
Jin et al., Seoul, South Korea. In Am J Med Genet A, 2010
study describes a woman with mild manifestations of Hunter syndrome who gave birth to a daughter; both the mother and daughter carried the p.R443X mutation in exon 9 of the ID2S gene
Enigmatic in vivo iduronate-2-sulfatase (IDS) mutant transcript correction to wild-type in Hunter syndrome.
Filocamo et al., Genova, Italy. In Hum Mutat, 2010
The in vivo correction of heritable gene lesions at the RNA level operating via a correction mechanism akin to RNA-editing, was observed for IDS mutant transcript.
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