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Nuclear receptor binding SET domain protein 1

This gene encodes a protein containing a SET domain, 2 LXXLL motifs, 3 nuclear translocation signals (NLSs), 4 plant homeodomain (PHD) finger regions, and a proline-rich region. The encoded protein enhances androgen receptor (AR) transactivation, and this enhancement can be increased further in the presence of other androgen receptor associated coregulators. This protein may act as a nucleus-localized, basic transcriptional factor and also as a bifunctional transcriptional regulator. Mutations of this gene have been associated with Sotos syndrome and Weaver syndrome. One version of childhood acute myeloid leukemia is the result of a cryptic translocation with the breakpoints occurring within nuclear receptor-binding Su-var, enhancer of zeste, and trithorax domain protein 1 on chromosome 5 and nucleoporin, 98-kd on chromosome 11. Two transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, AMPK, SET, HAD, calcium/calmodulin-dependent protein kinase
Papers using STO antibodies
AMP-activated protein kinase: also regulated by ADP?
Zang Mengwei, In PLoS ONE, 2010
... STO-609 was purchased from Tocris Bioscience ...
Expression of Tie-2 by human monocytes and their responses to angiopoietin-2.
Harrison Jeffrey K., In PLoS ONE, 2006
... Anti-Flag bead antibody (M2-beads), anti-Flag antibody, STO-609 and other chemicals were obtained from Sigma Aldrich.
Dimethylbiguanide inhibits cell respiration via an indirect effect targeted on the respiratory chain complex I
Hardie D. Grahame et al., In Biochemical Journal, 1999
... STO-609 was from Tocris Bioscience and calmodulin was ...
Papers on STO
Two-dimensional electron gas at the LaAlO3/SrTiO3 inteface with a potential barrier.
Barnaś et al., Opole, Poland. In Phys Chem Chem Phys, Feb 2016
We present a tight binding description of electronic properties of the interface between LaAlO3 (LAO) and SrTiO3 (STO).
Betulinic Acid Increases eNOS Phosphorylation and NO Synthesis via the Calcium-Signaling Pathway.
Jeong et al., In J Agric Food Chem, Feb 2016
Treatment with W7 (a CaM antagonist), KN-93 (a selective inhibitor of CaMKII), and STO 609 (a selective inhibitor of CaMKK) suppressed eNOS phosphorylation and NO production.
Sotos syndrome: An unusual presentation with intrauterine growth restriction, generalized lymphedema, and intention tremor.
Goel et al., Newcastle, Australia. In Am J Med Genet A, Feb 2016
UNASSIGNED: Sotos syndrome is a childhood overgrowth syndrome characterized clinically by a distinctive facial gestalt, advanced bone age, childhood overgrowth, and non-progressive developmental delay; and genetically by haploinsufficiency of the Nuclear receptor binding SET Domain 1 (NSD1) gene.
Concurrent detection of targeted copy number variants and mutations using a myeloid malignancy next generation sequencing panel allows comprehensive genetic analysis using a single testing strategy.
Kelley et al., Salt Lake City, United States. In Br J Haematol, Feb 2016
The most frequent CNVs were 7q deletion including LUC7L2 and EZH2, TP53 deletion, ETV6 deletion, gain of RAD21 on 8q, and 5q deletion, including NSD1 and NPM1.
[Sotos syndrome diagnosed by comparative genomic hybridisation].
Ramírez-Cheyne et al., Cali, Colombia. In Rev Chil Pediatr, Jan 2016
UNASSIGNED: Sotos Syndrome (SS) is a genetic disease with an autosomal dominant pattern caused by haplo-insufficiency of NSD1 gene secondary to point mutations or microdeletion of the 5q35 locus where the gene is located.
Acute Myeloid Leukemia With Myelodysplasia-Related Changes.
Reichard et al., Rochester, United States. In Am J Clin Pathol, Jul 2015
RESULTS: Session 3 of the workshop cases displayed heterogeneity as expected within AML-MRC, yet several cases suggested that recently recognized entities may exist within this category, such as familial MDS/AML predisposition syndromes and rare cases of high-risk AML associated with the cryptic t(5;11)(q35;p15);NUP98-NSD1 that may masquerade as a del(5q).
Malan syndrome: Sotos-like overgrowth with de novo NFIX sequence variants and deletions in six new patients and a review of the literature.
Scott et al., Maastricht, Netherlands. In Eur J Hum Genet, May 2015
There is overlap of the facial phenotype with NSD1-positive Sotos syndrome in some cases including a prominent forehead, high anterior hairline, downslanting palpebral fissures and prominent chin.
Comprehensive genomic characterization of head and neck squamous cell carcinomas.
Cancer Genome Atlas Network, In Nature, Mar 2015
Other distinct subgroups contained loss-of-function alterations of the chromatin modifier NSD1, WNT pathway genes AJUBA and FAT1, and activation of oxidative stress factor NFE2L2, mainly in laryngeal tumours.
AF10 regulates progressive H3K79 methylation and HOX gene expression in diverse AML subtypes.
Armstrong et al., Boston, United States. In Cancer Cell, 2015
AF10 inactivation reverses leukemia-associated epigenetic profiles, precludes abnormal HOXA gene expression, and impairs the transforming ability of MLL-AF9, MLL-AF6, and NUP98-NSD1 fusions-mechanistically distinct HOX-activating oncogenes.
Sotos syndrome 1 and 2.
Sotos, In Pediatr Endocrinol Rev, 2014
It is a genetic disorder due to haploinsufficiency of the NSD1 gene (Nuclear receptor-binding SET Domain protein 1) on chromosome 5q35.2-35.3 in 90% of the patients: Sotos syndrome 1.
Genetic syndromes associated with overgrowth in childhood.
Ko, Seoul, South Korea. In Ann Pediatr Endocrinol Metab, 2013
However, it is now understood that Sotos syndrome is caused by a variety of molecular genetic alterations resulting in haploinsufficiency of the NSD1 gene at chromosome 5q35 and that Beckwith-Wiedemann syndrome is caused by heterogeneous abnormalities in the imprinting of a number of growth regulatory genes within chromosome 11p15 in the majority of cases.
A peculiar mutation in the DNA-binding/dimerization domain of NFIX causes Sotos-like overgrowth syndrome: a new case.
Laganà et al., Reggio di Calabria, Italy. In Gene, 2013
The present report further confirms that mutations in DNA-binding/dimerization domain cause haploinsufficiency of the NFIX protein and strongly suggests that in individuals with Sotos-like features unrelated to NSD1 changes genetic testing of NFIX should be considered.
Arabidopsis STO/BBX24 negatively regulates UV-B signaling by interacting with COP1 and repressing HY5 transcriptional activity.
Li et al., Guangzhou, China. In Cell Res, 2012
STO/BBX24 functions as a negative regulator of photomorphogenic UV-B responses by interacting with both COP1 and HY5.
Understanding the language of Lys36 methylation at histone H3.
Carpenter et al., Houston, United States. In Nat Rev Mol Cell Biol, 2012
Several enzymes from yeast and humans, including the methyltransferases SET domain-containing 2 (Set2) and nuclear receptor SET domain-containing 1 (NSD1), respectively, alter the methylation status of H3K36, and significant progress has been made in understanding how they affect chromatin structure and function.
NUP98/NSD1 characterizes a novel poor prognostic group in acute myeloid leukemia with a distinct HOX gene expression pattern.
Zwaan et al., Rotterdam, Netherlands. In Blood, 2011
NUP98/NSD1 identifies a previously unrecognized group of young AML patients, with distinct characteristics and dismal prognosis, for whom new treatment strategies are urgently needed.
Structural insights into the regulation and the recognition of histone marks by the SET domain of NSD1.
di Luccio et al., Taegu, South Korea. In Biochem Biophys Res Commun, 2011
these finding exposes a key regulatory and recognition mechanism driven by the flexibility of a loop at the interface of the SET and postSET region in NSD1 protein.
Nuclear localization and interaction with COP1 are required for STO/BBX24 function during photomorphogenesis.
Rodríguez-Franco et al., Freiburg, Germany. In Plant Physiol, 2011
Mutations in the region responsible for the interaction with COP1 revealed that a physical interaction of the proteins is also required for degradation of BBX24 in the light and for normal photomorphogenesis.
NSD1 PHD domains bind methylated H3K4 and H3K9 using interactions disrupted by point mutations in human sotos syndrome.
Kamps et al., San Diego, United States. In Hum Mutat, 2011
data suggest that Sotos point mutations in NSD1 PHD domains disrupt its transcriptional regulation by interfering with its ability to bind epigenetic marks and recruit cofactors.
Nanostructured arrays of semiconducting octahedral molecular sieves by pulsed-laser deposition.
Suib et al., United States. In Nat Mater, 2010
The parallel fibres interact strongly with the substrate and grow epitaxially along <110>(STO) with lattice misfits of less than 4%, whereas the inclined fibres are oriented with (301) parallel to the substrate surface.
NUP98-NSD1 links H3K36 methylation to Hox-A gene activation and leukaemogenesis.
Kamps et al., San Diego, United States. In Nat Cell Biol, 2007
study shows that NUP98-NSD1 induces acute myeloid leukemia in vivo, sustains self-renewal of myeloid stem cells in vitro, and enforces expression of the HoxA7, HoxA9, HoxA10 and Meis1 proto-oncogenes
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