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Heparan sulfate 6-O-sulfotransferase 1

HS6ST, heparan sulfate 6-O-sulfotransferase, HS6ST-1, Heparan-sulfate 6-sulfotransferase, 6-OST1
The protein encoded by this gene is a member of the heparan sulfate biosynthetic enzyme family. Heparan sulfate biosynthetic enzymes are key components in generating a myriad of distinct heparan sulfate fine structures that carry out multiple biological activities. This enzyme is a type II integral membrane protein and is responsible for 6-O-sulfation of heparan sulfate. This enzyme does not share significant sequence similarity with other known sulfotransferases. A pseudogene located on chromosome 1 has been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: 2-O-sulfotransferase, ACID, CAN, HAD, FGFR1
Papers on HS6ST
Proteoglycan expression correlates with the phenotype of malignant and non-malignant EBV-positive B-cell lines.
Grigorieva et al., Novosibirsk, Russia. In Oncotarget, Jan 2016
In this study, expression of major proteoglycans (syndecan-1, glypican-1, perlecan, versican, brevican, aggrecan, NG2, serglycin, decorin, biglycan, lumican, CD44), heparan sulphate (HS) metabolic system (EXT1/2, NDST1/2, GLCE, HS2ST1, HS3ST1/2, HS6ST1/2, SULF1/2, HPSE) and extracellular matrix (ECM) components (collagen 1A1, fibronectin, elastin) in primary B cells and EBV carrying cell lines with different phenotypes, patterns of EBV-host cell interaction and viral latency stages (type I-III) was investigated.
Genome-wide Association Studies Identify Genetic Loci Associated with Albuminuria in Diabetes.
Köttgen et al., Greifswald, Germany. In Diabetes, Jan 2016
Gene-by-diabetes interactions were detected and confirmed for variants in HS6ST1 and near RAB38/CTSC.
Kallmann syndrome patient with gender dysphoria, multiple sclerosis, and thrombophilia.
Korbonits et al., London, United Kingdom. In Endocrine, Nov 2015
The genetic basis of Kallmann syndrome remains unknown: his screening tests were negative for mutations in CHD7, FGF8, FGFR1, GNRH1, GNRHR, HS6ST1, KAL1, KISS1R, KISS1, NELF, PROK2, PROKR2, TAC3, and TACR3.
Expanding the Spectrum of Founder Mutations Causing Isolated Gonadotropin-Releasing Hormone Deficiency.
Crowley et al., Caen, France. In J Clin Endocrinol Metab, Oct 2015
RESULTS: A total of eight founder mutations in five genes, GNRHR (Q106R, R262Q, R139H), TACR3 (W275X), PROKR2 (R85H), FGFR1 (R250Q, G687R), and HS6ST1 (R382W) were identified.
Overexpression of heparan sulfate 6-O-sulfotransferase-2 enhances fibroblast growth factor-mediated chondrocyte growth and differentiation.
Zhang et al., Xi'an, China. In Int J Mol Med, Sep 2015
In our previous study, we reported that heparan sulfate 6-O-sulfotransferase‑2 (HS6ST2) plays an important role in the cartilage of patients with osteoarthritis and Kashin-Beck disease and that it regulates aggrecan (Acan) metabolism and the viability of chondrocytes.
Heparan sulfate 6-O-sulfotransferase 3 is involved in bone marrow mesenchymal stromal cell osteogenic differentiation‍.
Chen et al., Wuxi, China. In Biochemistry (mosc), Mar 2015
Among all the sulfotransferases examined, heparan sulfate 6-O-sulfotransferase 3 (HS6ST3) mRNA and protein were upregulated in these calcified cell spheroids.
Heparan sulfate proteoglycans undergo differential expression alterations in right sided colorectal cancer, depending on their metastatic character.
Quirós et al., Spain. In Bmc Cancer, 2014
Regarding the enzymes responsible for the modificaton of the HS chains, alterations were only found in non-metastatic tumors, affecting N-sulfation and the isoforms HS6ST1, HS3ST3B and HS3ST5.
Comparison of microarray expression profiles between follicular variant of papillary thyroid carcinomas and follicular adenomas of the thyroid.
Al-Maghrabi et al., In Bmc Genomics, 2014
Amongst the most significantly upregulated genes in FVPTCs were GABA B receptor, 2 (GABBR2), neuronal cell adhesion molecule (NRCAM), extracellular matrix protein 1 (ECM1), heparan sulfate 6-O-sulfotransferase 2 (HS6ST2), and retinoid X receptor, gamma (RXRG).
[Congenital hypogonadotropic hypogonadism and Kallmann syndrome in males].
Young et al., Cluj-Napoca / Kolozsvár, Romania. In Presse Med, 2014
Mutations in KAL1, FGFR1/FGF8/FGF17, PROK2/PROKR2, NELF, CHD7, HS6ST1, WDR11, SEMA3A, SOX10, IL17RD2, DUSP6, SPRY4, and FLRT3 have been associated with KS but sometimes also with its milder hyposmic/normosmic CHH clinical variant.
Scleral gene expression during recovery from myopia compared with expression during myopia development in tree shrew.
Norton et al., Birmingham, United States. In Mol Vis, 2013
Eight of these genes (NPR3, CAPNS1, NGEF, TGFB1, CTGF, NOV, TIMP1, and HS6ST1) were bidirectionally regulated at both time points in the GO and STOP conditions.
Structural alteration of cell surface heparan sulfate through the stimulation of the signaling pathway for heparan sulfate 6-O-sulfotransferase-1 in mouse fibroblast cells.
Yabe et al., Gifu, Japan. In Biosci Biotechnol Biochem, 2013
Furthermore, adrenaline-induced up-regulation of HS 6-O-sulfotransferase-1 (6-OST-1) was controlled by Src-ERK1/2 signaling pathway.
Reproduction, smell, and neurodevelopmental disorders: genetic defects in different hypogonadotropic hypogonadal syndromes.
Beckers et al., Liège, Belgium. In Front Endocrinol (lausanne), 2013
KS is associated with mutations in KAL1, FGFR1/FGF8, FGF17, IL17RD, PROK2/PROKR2, NELF, CHD7, HS6ST1, FLRT3, SPRY4, DUSP6, SEMA3A, NELF, and WDR11 genes that are related to defects in neuronal migration.
[Clinical and molecular aspects of congenital isolated hypogonadotropic hypogonadism].
Latronico et al., São Paulo, Brazil. In Arq Bras Endocrinol Metabol, 2011
Mutations in KAL1, FGFR1/FGF8, PROK2/PROKR2, NELF, CHD7, HS6ST1 and WDR11 are associated with defects in neuronal migration, leading to Kallmann syndrome.
Heparan sulfate 6-O-sulfotransferase 1, a gene involved in extracellular sugar modifications, is mutated in patients with idiopathic hypogonadotrophic hypogonadism.
Bülow et al., United States. In Proc Natl Acad Sci U S A, 2011
idiopathic hypogonadotrophic hypogonadism--associated HS6ST1 mutations display reduced activity in vitro and in vivo, suggesting that HS6ST1 and the complex modifications of extracellular sugars are critical for normal development
Mice deficient in heparan sulfate 6-O-sulfotransferase-1.
Kimata et al., Japan. In Prog Mol Biol Transl Sci, 2009
HS6STs in mammals such as humans and mice comprise of three isoforms (HS6ST-1, -2, and -3) and one alternatively spliced form of HS6ST-2 (HS6ST-2S).
Tetra-amelia and lung hypo/aplasia syndrome: new case report and review.
Saraiva et al., Coimbra, Portugal. In Am J Med Genet A, 2008
No mutation was identified upon molecular analysis of WNT3, HS6ST1, and HS6ST3.
Systemic inactivation of Hs6st1 in mice is associated with late postnatal mortality without major defects in organogenesis.
Cardoso et al., Boston, United States. In Genesis, 2008
there is a critical role for HS 6-O sulfation by Hs6st1 in postnatal processes
Specific and flexible roles of heparan sulfate modifications in Drosophila FGF signaling.
Nakato et al., Minneapolis, United States. In J Cell Biol, 2006
We found that mutations in Hs2st or Hs6st had unexpectedly little effect on tracheal morphogenesis. Structural analysis of mutant HS revealed not only a loss of corresponding sulfation, but also a compensatory increase of sulfation at other positions.
Heparan sulphation patterns generated by specific heparan sulfotransferase enzymes direct distinct aspects of retinal axon guidance at the optic chiasm.
Mason et al., Edinburgh, United Kingdom. In J Neurosci, 2006
Hs2st and/or Hs6st1 expression coincides with Slit expression domains at locations where retinal ganglion cell(RGC) axons make navigation errors in Hs2st-/- and Hs6st1-/- mutants, and Hs6st1-/-RGC axons are less sensitive to Slit2 repulsion.
Overexpression of heparan sulfate 6-O-sulfotransferases in human embryonic kidney 293 cells results in increased N-acetylglucosaminyl 6-O-sulfation.
Kusche-Gullberg et al., Uppsala, Sweden. In J Biol Chem, 2006
Data show that high expression of 6-O-sulfotransferase (6-OST)-1, 2, or 3 resulted in increased 6-O-sulfation of N-sulfated and N-acetylated glucosamine units, and in altered heparan sulfate domain structure.
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