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


Noggin, NOG
The secreted polypeptide, encoded by this gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, this protein may have a principal role in creating morphogenic gradients. The protein appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of the ortholog suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation. Recently, several dominant human NOG mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) were identified; both SYM1 and SYNS1 have multiple joint fusion as their principal feature, and map to the same region (17q22) as this gene. All of these mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of this human gene is highly homologous to that of Xenopus, rat and mouse. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, BMP4, V1a, HAD, Smad1
Papers using Noggin antibodies
Stem cell-based cell therapy in neurological diseases: a review.
Najbauer Joseph, In PLoS ONE, 2008
... B27 [all from Gibco, Gland Island, NY], supplemented with 100 ng/ml mouse or human recombinant Noggin (R&D Systems) or 200 nM Dorsomorphin (BIOMOL, Plymouth Meeting, PA) as ...
Structural basis for the inhibition of activin signaling by follistatin
Hogan Brigid L. M, In PLoS Biology, 2005
... K14-Noggin transgenic mice have been described ...
Papers on Noggin
Functional polymer-dependent 3D culture accelerates the differentiation of HepaRG cells into mature hepatocytes.
Suemizu et al., Kawasaki, Japan. In Hepatol Res, Feb 2016
To reveal the in vivo differentiation ability, we transplanted the 3D-cultured HepaRG spheroids into TK-NOG mice.
Neuroprotective effect of Myo/Nog cells in the stressed retina.
George-Weinstein et al., United States. In Exp Eye Res, Jan 2016
UNASSIGNED: Myo/Nog cells are essential for eye development in the chick embryo and respond to injury in adult tissues.
Neuroprotective Effects of Brain-Derived Neurotrophic Factor and Noggin-Modified Bone Mesenchymal Stem Cells in Focal Cerebral Ischemia in Rats.
Cheng et al., Tianjin, China. In J Stroke Cerebrovasc Dis, Dec 2015
In the present study, we tried to reveal the underlying mechanism of the improvement of neurological function after stroke by BMSCs transfected with brain-derived neurotrophic factor (BDNF) and/or Noggin.
BMP signalling: agony and antagony in the family.
Martin et al., Dublin, Ireland. In Trends Cell Biol, May 2015
Antagonists such as Noggin, Chordin, Gremlin (Grem1), and twisted gastrulation-1 (Twsg1) have been shown to inhibit BMP action in a range of different cell types and developmental stage-specific contexts.
The Hepatitis B Virus Genotype Affects the Persistence of Viral Replication in Immunodeficient NOG Mice.
Takehara et al., Suita, Japan. In Plos One, 2014
The purpose of this study was to elucidate the differences in HBV load and the persistence of viremia in vivo between genotypes A and C. METHODS: Immunodeficient NOG mice were transfected by hydrodynamic injection with the HBV expression plasmids pHBA1.2 or pHBC1.2,
The Bone Morphogenetic Proteins and Their Antagonists.
Rider et al., London, United Kingdom. In Vitam Horm, 2014
One mechanism for enabling tight spatiotemporal control of their activities is through a number of antagonist proteins, including Noggin, Follistatin, Chordin, Twisted gastrulation (TSG), and the seven members of the Cerberus and Dan family.
Endothelial Notch activity promotes angiogenesis and osteogenesis in bone.
Adams et al., Münster, Germany. In Nature, 2014
On the basis of a series of genetic experiments, we conclude that skeletal defects in these mutants involved defective angiocrine release of Noggin from endothelial cells, which is positively regulated by Notch.
Somites without a clock.
Stern et al., London, United Kingdom. In Science, 2014
Non-somite mesoderm treated with Noggin generates many somites that form simultaneously, without cyclic expression of Notch-pathway genes, yet have normal size, shape, and fate.
An introduction of genetics in otosclerosis: a systematic review.
Grolman et al., Utrecht, Netherlands. In Otolaryngol Head Neck Surg, 2014
These high-quality studies show that otosclerosis in Japanese patients is not linked to the NOG gene and that a polymorphism in the Sp1 binding site located on the COL1A1 gene is associated with otosclerosis as well as OTSC1.
5-Carboxy-8-hydroxyquinoline is a Broad Spectrum 2-Oxoglutarate Oxygenase Inhibitor which Causes Iron Translocation.
Kawamura et al., Oxford, United Kingdom. In Chem Sci, 2013
Using a representative 2OG oxygenase panel, we compare the inhibitory activities of 5-carboxy-8-hydroxyquinoline (IOX1) and 4-carboxy-8-hydroxyquinoline (4C8HQ) with that of two other commonly used 2OG oxygenase inhibitors, N-oxalylglycine (NOG) and 2,4-pyridinedicarboxylic acid (2,4-PDCA).
A novel mouse xenotransplantation model of EBV-T/NK-LPD and the application of the mouse model.
Imadome, In Nihon Rinsho Meneki Gakkai Kaishi, 2012
Here we show that intravenous injection of peripheral blood mononuclear cells (PBMCs) isolated from patients with CAEBV to NOD/Shi-scid/IL-2R γ(null) (NOG) mice leads to engraftment of EBV-infected T or NK cells.
Identification of NOG as a specific breast cancer bone metastasis-supporting gene.
Gomis et al., Barcelona, Spain. In J Biol Chem, 2012
Using genetic approaches, we show that when NOG is expressed in human breast cancer cells, it facilitates bone colonization by fostering osteoclast differentiation and bone degradation and also contributes to metastatic lesions reinitiation.
Combinatorial use of bone morphogenetic protein 6, noggin and SOST significantly predicts cancer progression.
Chan et al., Belfast, United Kingdom. In Cancer Sci, 2012
high BMP6 activity, defined by strong BMP6 expression with weak noggin or SOST expression, was associated with shorter survival in esophageal SCC patients; results suggest BMP6, noggin and SOST could be used in combination as a prognostic indicator in cancer progression
Molecular analysis of the Noggin (NOG) gene in holoprosencephaly patients.
Muenke et al., Bethesda, United States. In Mol Genet Metab, 2012
we conclude that mutations in the coding region of NOG are rare, and play at most an uncommon role in human Holoprosencephaly (HPE).
Myo/Nog cells in normal, wounded and tumor-bearing skin.
George-Weinstein et al., In Exp Dermatol, 2012
Myo/Nog cells are the primary source of noggin in telogen hair follicles.
Functional analysis of alleged NOGGIN mutation G92E disproves its pathogenic relevance.
Seemann et al., Berlin, Germany. In Plos One, 2011
p.G92E represents a rare polymorphism of the NOGGIN gene-- causing neither brachydactyly nor fibrodysplasia ossificans progressiva.
Genetic abnormalities in fibrodysplasia ossificans progressiva.
Tania et al., Taiwan. In Genes Genet Syst, 2011
The noggin (NOG) gene has also been reported in some studies.
Signaling through BMPR-IA regulates quiescence and long-term activity of neural stem cells in the adult hippocampus.
Gage et al., Los Angeles, United States. In Cell Stem Cell, 2010
In vivo, acute blockade of BMP signaling in the hippocampus by intracerebral infusion of Noggin first recruits quiescent NSCs into the cycle and increases neurogenesis; subsequently, it leads to decreased stem cell division and depletion of precursors and newborn neurons.
Highly efficient neural conversion of human ES and iPS cells by dual inhibition of SMAD signaling.
Studer et al., New York City, United States. In Nat Biotechnol, 2009
Here we report that the synergistic action of two inhibitors of SMAD signaling, Noggin and SB431542, is sufficient to induce rapid and complete neural conversion of >80% of hES cells under adherent culture conditions.
Establishment of HIV-1 resistance in CD4+ T cells by genome editing using zinc-finger nucleases.
June et al., Philadelphia, United States. In Nat Biotechnol, 2008
Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo in a NOG model of HIV infection.
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