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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 IF (p), IHC (p) - ABIN873145
Song, Cui, Yu, Liu, Liu, Yang, He, Zhang: Expression characteristics of BMP2, BMPR-IA and Noggin in different stages of hair follicle in yak skin. in General and comparative endocrinology 2017
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
studies support previous work that suggest Noggin is an important suppressor of the differentiation of osteoblast lineage cells in bone metastases; now it is also shown that this protein can be induced in bone cells themselves by factors derived from prostate cancer cells
Report of a novel missense NOG mutation and phenotypic variability in an Indian family where multiple members were affected with tarsal-carpal coalition syndrome with multiple synostoses and proximal symphalangism.
Study suggested that the NOGGIN rs227731 polymorphism may increase nonsyndromic cleft lip with or without palate risk in Caucasians and may have no significant association in the Chinese population (meta-analysis).
The clinical presentation of the reported mutation corresponds with previous case reports of families with NOG mutation. In this family, surgery with stapedectomy had lasting effect without renewed fixation of the stapes in a follow up period of 18 months-38 years.
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 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.
By next-generation and Sanger sequencing analyses, study identified two novel mutations, c.559C>G (p.P178A) and c.682T>A (p.C228S), in the proximal symphalangism and atypical multiple synostosis syndrome families, respectively.
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, 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]
Even though gremlin 1 and noggin were not widely expressed in adult tissues, in a subset of organs their expression pattern indicated a potential role in normal tissue homeostasis as well as in malignancies.
A novel heterozygous change of p. R42T [c.C124A (CCC > ACC)] leading to a proline was identified in a family with multiple synostoses syndrome.
NOggin attenuates BMP4-mediated transdifferentiation of human valve interstitial cells towards an osteogenic-like phenotype in aortic valve sclerosis.
Mutations in the NOG gene are commonly found in congenital stapes ankylosis with symphalangism, but not in otosclerosis.
Noggin suppression decreased viability and BMP-2-induced osteogenic differentiation of human mesenchymal stem cells.
Noggin null mice display cutaneous syndactyly and impaired interdigital mesenchyme specification. Failure of webbing regression was caused by lack of cell cycle exit and interdigital apoptosis. Noggin null mutants have increased Indian hedgehog (Ihh) expression in cartilage condensations leading to aberrant extension of IHH downstream signaling into the interdigital mesenchyme.
Down-regulation of Noggin and miR-138 cooperatively promoted osteogenic differentiation of mesenchymal stem cells.
the absence of Noggin, and consequently BMP hypersignaling, leads to the decrease of the number of muscle progenitor cells and their phenotypic shift towards adipocytes in vitro.
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, Noggin, and Numb proteins. we found that Shh and Noggin could affect motor performance and that these proteins could be associated with both TDP-43 and Numb
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
endogenous Bmp2, Bmp4, 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 signaling emanating from the interzone.
Taken together, these results show that hair follicle development in Trps1 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 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.
Noggin antagonizes BMP, which is required in presumptive notochord cells for mammalian foregut morphogenesis
Noggin is expressed constantly in Meckel's cartilage (MC) and in the absence of Noggin, MC is significantly thickened attributing to dramatically elevated cell proliferation rate associated with enhanced phosphorylation of Smad1/5/8.
MiR-200c represses noggin in dental epithelial-like cells.
Noggin stimulates myogenesis from dorsal aorta progenitors.
Bone morphogenetic proteins and noggin have different roles in the processes of glial scar formation and neurorestoration in the ischemic brain.
Myo/Nog cells are the primary source of noggin in telogen hair follicles.
Noggin inactivation causes osteopenia, suggesting that BMP in excess have a detrimental effect on bone or that noggin has a BMP-independent role in skeletal homeostasis.
noggin 1, differently from noggin 2 and noggin 4, is expressed during all phases of Xenopus laevis retinal development. Gain-of-function experiments by electroporation in the optic vesicle show that overexpression of noggin 1 significantly decreases the number of bipolar cells in the inner nuclear layer of the retina, without significantly affecting the generation of the other retinal cell types.
a new role for Noggin1 in determining specific anterior neural structures by the modulation of TGFbeta and SHH signaling.
The data provide a quantitative basis for modeling the process of Noggin1 diffusion in embryonic tissues, considering its interaction with heparan sulfate proteoglycans.
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 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, Noggin, beta-Catenin, and Cerberus 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 and MATER 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