Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent - Wikidata - wikimedia - TriplyDB

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

http://www.wikidata.org/entity/Q35078672

about

Notch regulation of bone development and remodeling and related skeletal disorders Physiological notch signaling maintains bone homeostasis via RBPjk and Hey upstream of NFATc1 Truncating mutations in the last exon of NOTCH3 cause lateral meningocele syndrome Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone.MiR-199b-5p inhibits osteogenic differentiation in ligamentum flavum cells by targeting JAG1 and modulating the Notch signalling pathway.RBP-Jκ-dependent Notch signaling is required for murine articular cartilage and joint maintenance.Chondrocyte-specific pathology during skeletal growth and therapeutics in a murine model of pseudoachondroplasia Notch activation as a driver of osteogenic sarcoma.NOTCH-Mediated Maintenance and Expansion of Human Bone Marrow Stromal/Stem Cells: A Technology Designed for Orthopedic Regenerative Medicine.Transient gamma-secretase inhibition accelerates and enhances fracture repair likely via Notch signaling modulation TNF-induced osteoclastogenesis and inflammatory bone resorption are inhibited by transcription factor RBP-J.Cartilage-specific RBPjκ-dependent and -independent Notch signals regulate cartilage and bone development Notch signaling in skeletal health and disease.Canonical Notch activation in osteocytes causes osteopetrosis.Notch gain of function inhibits chondrocyte differentiation via Rbpj-dependent suppression of Sox9.Development of the endochondral skeleton Notch signaling in postnatal joint chondrocytes, but not subchondral osteoblasts, is required for articular cartilage and joint maintenance NOTCH signaling in skeletal progenitors is critical for fracture repair.Yunis-Varón syndrome is caused by mutations in FIG4, encoding a phosphoinositide phosphatase Anabolic actions of Notch on mature bone.Notch Signaling and the Skeleton.Systemic inhibition of canonical Notch signaling results in sustained callus inflammation and alters multiple phases of fracture healing.Hairy and Enhancer of Split-related with YRPW motif (HEY)2 regulates bone remodeling in mice Notch signaling in skeletal stem cells.Notch1 and Notch2 expression in osteoblast precursors regulates femoral microarchitecture Notch signaling and bone remodeling.Notch signaling pathway promotes osteogenic differentiation of mesenchymal stem cells by enhancing BMP9/Smad signaling.Molecular genetics of osteosarcoma.Notch signaling components are upregulated during both endochondral and intramembranous bone regeneration.Loss of Notch3 Signaling Enhances Osteogenesis of Mesenchymal Stem Cells from Mandibular Torus.TNF and Bone Remodeling.Jagged1 immobilization to an osteoconductive polymer activates the Notch signaling pathway and induces osteogenesis.Hairy and Enhancer of Split-Related With YRPW Motif-Like (HeyL) Is Dispensable for Bone Remodeling in Mice.Notch signaling pathways in human thoracic ossification of the ligamentum flavum.The Notch Ligand Jagged1 Regulates the Osteoblastic Lineage by Maintaining the Osteoprogenitor Pool.

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P2860

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

http://www.wikidata.org/entity/Q35078672

description

2010 nî lūn-bûn

@nan

2010 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հոտեմբերին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

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2010年論文

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2010年論文

@zh-tw

2010年论文

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name

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

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Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

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type

label

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

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Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

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prefLabel

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

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Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

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P1433

Journal of Bone and Mineral Research

P1476

Osteosclerosis owing to Notch gain of function is solely Rbpj-dependent

@en

P2093

Brendan Lee

http://www.w3.org/2001/XMLSchema#string

Brian Dawson

http://www.w3.org/2001/XMLSchema#string

Elda Munivez

http://www.w3.org/2001/XMLSchema#string

Shan Chen

http://www.w3.org/2001/XMLSchema#string

Tao Yang

http://www.w3.org/2001/XMLSchema#string

Terry Bertin

http://www.w3.org/2001/XMLSchema#string

P2860

Soluble Jagged 1 represses the function of its transmembrane form to induce the formation of the Src-dependent chord-like phenotype

Notch1 augments NF-kappaB activity by facilitating its nuclear retention

Notch3 and pre-TCR interaction unveils distinct NF-kappaB pathways in T-cell development and leukemia.

TAN-1, the human homolog of the Drosophila notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms

Mutation of the fucose-specific beta1,3 N-acetylglucosaminyltransferase LFNG results in abnormal formation of the spine

Notch signaling controls multiple steps of pancreatic differentiation

Direct inhibition of the NOTCH transcription factor complex

Doubly truncated FosB isoform (Delta2DeltaFosB) induces osteosclerosis in transgenic mice and modulates expression and phosphorylation of Smads in osteoblasts independent of intrinsic AP-1 activity

Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass

The association of Notch2 and NF-kappaB accelerates RANKL-induced osteoclastogenesis

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2175-2183

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10.1002/JBMR.115

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10

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25

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44627347

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20499347

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3126919

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