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Human Monoclonal NOG Primary Antibody for WB - ABIN967662
Choi, Stottmann, Yang, Meyers, Klingensmith: The bone morphogenetic protein antagonist noggin regulates mammalian cardiac morphogenesis. in Circulation research 2007
Show all 5 Pubmed References
Polyclonal NOG Primary Antibody for WB - ABIN540367
Gong, Krakow, Marcelino, Wilkin, Chitayat, Babul-Hirji, Hudgins, Cremers, Cremers, Brunner, Reinker, Rimoin, Cohn, Goodman, Reardon, Patton, Francomano, Warman: Heterozygous mutations in the gene encoding noggin affect human joint morphogenesis. in Nature genetics 1999
Show all 3 Pubmed References
Human Polyclonal NOG Primary Antibody for ICC, WB - ABIN343655
Zhao, Ji, Wang, Gu, Song, Zhang, Liu, Chen, Zhang: Cell surface proteomics analysis indicates a neural lineage bias of rat bone marrow mesenchymal stromal cells. in BioMed research international 2014
we describe a Danish family suffering from SYNS1 due to a novel NOG gene mutation (C230Y). We provide detailed clinical description of the family members presenting rare phenotype of the shoulders shared by affected individuals but no hearing loss, further adding to the phenotypic variability of the syndrome.
A New Subtype of Multiple Synostoses Syndrome Is Caused by a Mutation in GDF6 That Decreases Its Sensitivity to Noggin and Enhances Its Potency as a BMP Signal.
An imbalance between BMP-2 (show BMP2 Antibodies) and Noggin secretion induces abnormal osteogenic differentiation of ankylosing spondylitis-mesenchymal stem cells.
early noggin exposure may play a specific role in the directed differentiation of DA cells from human embryonic stem cells.
Novel p.W150C NOG mutation associated with proximal symphalangism and conductive hearing impairment was identified in a Chinese family.Impaired dimerization of mutant NOG is an important pathogenic mechanism for the NOG-related disorder.
No association between SPRY2 (show SPRY2 Antibodies), single-nucleotide polymorphisms, and nonsyndromic cleft lip with or without cleft palate risk were observed in this cohort of patients.
The study did not provide support for NOG being the causal gene at 17q22 in nonsyndromic cleft lip with or without cleft palate.
a novel NOG mutation in a Chinese family with proximal symphalangism
this study proposes that the decreased binding affinity of NOG with the p.R136C mutation to HSPG leads to an excess of bone morphogenetic protein signaling and underlies the proximal symphalangism and conductive hearing loss phenotype of carriers.
High-quality studies show that otosclerosis in Japanese patients is not linked to the NOG gene. [Review]
Bone morphogenetic protein signaling and its antagonism by NOGGIN play a role in osteoarthritis development.
We demonstrate that elevated BMP4 depletes PSM progenitors in vitro, phenocopying the Fgf3 mutant, suggesting that excessive BMP signals cause the Fgf3 axis defect. To test this in vivo we increased BMP signaling in Fgf3 mutants by removing one copy of Noggin, which encodes a BMP antagonist.
we observed a glial reaction and an activity-dependent modification of Shh (show SHH Antibodies), Noggin, and Numb (show NUMB Antibodies) proteins. we found that Shh (show SHH Antibodies) and Noggin could affect motor performance and that these proteins could be associated with both TDP-43 (show TARDBP Antibodies) and Numb (show NUMB Antibodies)
Molecular analysis demonstrated that ectopic Noggin-expressing regions in the early heart's pacemaker region, failed to express the potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4 (show HCN4 Antibodies)
endogenous Bmp2 (show BMP2 Antibodies), Bmp4 (show BMP4 Antibodies), and Noggin transcript levels in postnatal bone and cartilage mirrored the activity of their respective reporters in these tissues
A band of noggin-expressing cells insulates a region of proliferative chondrocytes from the influence of BMP signaling, allowing them to differentiate as articular cartilage upon exposure to Wnt (show WNT2 Antibodies) signaling emanating from the interzone.
Taken together, these results show that hair follicle development in Trps1 (show TRPS1 Antibodies) KO embryos is impaired directly or indirectly by decreased Noggin expression.
BMP signaling was stimulated in adipose derived stem cells (ASCs) by downregulating noggin.
The axial midline domain of Nog expression is critical to promote pharyngeal arch 1 development in early stages, necessary for adequate outgrowth of the mandibular bud.
Follistatin (show FST Antibodies) aids in maintaining proper somite size, and consequently sclerotome progenitor numbers, by preventing paraxial mesoderm from adopting an intermediate/lateral plate mesodermal fate in the Noggin-deficient state.
a new role for Noggin1 in determining specific anterior neural structures by the modulation of TGFbeta (show TGFB1 Antibodies) and SHH (show SHH Antibodies) signaling.
This allow one to compare the expression levels of Noggin1 and Noggin 2 constructs, to purify them on the affine immunosorbent and to show the activity of Noggin proteins by analyzing their ability to bind BMP4 (show BMP4 Antibodies) factor
Both Noggin proteins could induce a secondary head, including the forebrain. During normal development, Noggin1 mRNA was translated with low efficiency, providing sufficient Noggin1 only for antagonizing Bone morphogenetic protein.
A 2066 bp noggin 5' flanking sequence which recapitulates the roof-plate expression of endogenous gene in transgenic frog tadpoles has been identified; this roof-plate enhancer has been mapped to a sequence as short as 79 bp.
Noggin specifically blocks chondrogenic differentiation, rather than osteogenic differentiation, in mesodermal stem cell line C1 and skeletal cells.
Chordin (show CHRD Antibodies), Noggin, beta-Catenin (show CTNNB1 Antibodies), and Cerberus (show CER1 Antibodies) have roles in neural induction in Xenopus
X-epilectin expression is down-regulated by Noggin and tBR and that this effect is inhibited by BMP4 over-expression, suggesting X-epilectin expression is mediated by the BMP signalling pathway
maternal mRNA encoding noggin is enriched in animal tiers and at low concentrations in the C-tier, suggesting that the neural fates of C-tier blastomeres may be responsive to early signaling from their neighboring cells
Noggin did not affect oocyte nuclear maturation. Noggin supplementation up-regulated the expression of HSP70 (show HSP70 Antibodies) and MATER (show NLRP5 Antibodies) genes in matured oocytes.
Noggin, a cytokine inhibiting the BMP4 pathway, successfully upregulated the relative expression of NANOG mRNA in the ICM explants with respect to controls.
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.
symphalangism 1 (proximal)
, noggin 1
, noggin protein