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Noggin rescues age-related stem cell loss in the brain of senescent mice with abnormally increased BMP6 causing neurodegenerative pathology.
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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.
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Down-regulation of Noggin and miR-138 cooperatively promoted osteogenic differentiation of mesenchymal stem cells.
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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.
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Bone morphogenetic protein signaling and its antagonism by NOGGIN play a role in osteoarthritis development.
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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.
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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
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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
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endogenous Bmp2, Bmp4, and Noggin transcript levels in postnatal bone and cartilage mirrored the activity of their respective reporters in these tissues
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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.
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Taken together, these results show that hair follicle development in Trps1 KO embryos is impaired directly or indirectly by decreased Noggin expression.
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BMP signaling was stimulated in adipose derived stem cells (ASCs) by downregulating noggin.
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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.
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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.
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Noggin antagonizes BMP, which is required in presumptive notochord cells for mammalian foregut morphogenesis
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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.
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MiR-200c represses noggin in dental epithelial-like cells.
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Noggin stimulates myogenesis from dorsal aorta progenitors.
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Bone morphogenetic proteins and noggin have different roles in the processes of glial scar formation and neurorestoration in the ischemic brain.
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Myo/Nog cells are the primary source of noggin in telogen hair follicles.