Craniosynostosis caused by Axin2 deficiency is mediated through distinct functions of beta-catenin in proliferation and differentiation. - Wikidata - awgldk - TriplyDB

Craniosynostosis caused by Axin2 deficiency is mediated through distinct functions of beta-catenin in proliferation and differentiation.

Craniosynostosis caused by Axin2 deficiency is mediated through distinct functions of beta-catenin in proliferation and differentiation.

http://www.wikidata.org/entity/Q35677733

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Disruption of SUMO-specific protease 2 induces mitochondria mediated neurodegeneration Signaling mechanisms implicated in cranial sutures pathophysiology: Craniosynostosis Functional relevance of the BMD-associated polymorphism rs312009: novel involvement of RUNX2 in LRP5 transcriptional regulation SUMO-specific protease 2 is essential for modulating p53-Mdm2 in development of trophoblast stem cell niches and lineages Augmenting endogenous Wnt signaling improves skin wound healing Axin2 regulates chondrocyte maturation and axial skeletal development Reciprocal regulation of Wnt and Gpr177/mouse Wntless is required for embryonic axis formation SUMO-specific protease 2 in Mdm2-mediated regulation of p53 Gpr177 deficiency impairs mammary development and prohibits Wnt-induced tumorigenesis.Manipulating gene activity in Wnt1-expressing precursors of neural epithelial and neural crest cells.Beta-catenin/T-cell factor signaling is activated during lung injury and promotes the survival and migration of alveolar epithelial cells Neural crest cell signaling pathways critical to cranial bone development and pathology.Expression of Gpr177, a Wnt trafficking regulator, in mouse embryogenesis The balance of WNT and FGF signaling influences mesenchymal stem cell fate during skeletal development.Runx2 is required for early stages of endochondral bone formation but delays final stages of bone repair in Axin2-deficient mice.Differential expression of extracellular matrix-mediated pathways in single-suture craniosynostosis Phospholipase C signaling via the parathyroid hormone (PTH)/PTH-related peptide receptor is essential for normal bone responses to PTH.β-catenin/cyclin D1 mediated development of suture mesenchyme in calvarial morphogenesis.Functional comparison of chronological and in vitro aging: differential role of the cytoskeleton and mitochondria in mesenchymal stromal cells Viable mice with compound mutations in the Wnt/Dvl pathway antagonists nkd1 and nkd2.Gpr177/mouse Wntless is essential for Wnt-mediated craniofacial and brain development.Jagged1 functions downstream of Twist1 in the specification of the coronal suture and the formation of a boundary between osteogenic and non-osteogenic cells Role of Wnt signaling in the biology of the periodontium.Association of AXIN2 with non-syndromic oral clefts in multiple populations.Frontal Bone Insufficiency in Gsk3β Mutant Mice.Wnt signaling regulates homeostasis of the periodontal ligament.Update on Wnt signaling in bone cell biology and bone disease.Wnt signaling and injury repair.Microarray gene expression profiling of osteoarthritic bone suggests altered bone remodelling, WNT and transforming growth factor-beta/bone morphogenic protein signalling.Wnt signaling in bone development and disease: making stronger bone with Wnts Transcriptome correlation analysis identifies two unique craniosynostosis subtypes associated with IRS1 activation.Extraembryonic but not embryonic SUMO-specific protease 2 is required for heart development.Runx2 protein represses Axin2 expression in osteoblasts and is required for craniosynostosis in Axin2-deficient mice Gpr177, a novel locus for bone mineral density and osteoporosis, regulates osteogenesis and chondrogenesis in skeletal development Wnt signaling and skeletal development Augmentation of Smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice.Co-opted JNK/SAPK signaling in Wnt/beta-catenin-induced tumorigenesis.FOXOs attenuate bone formation by suppressing Wnt signaling.EphA4 as an effector of Twist1 in the guidance of osteogenic precursor cells during calvarial bone growth and in craniosynostosis Loss of Axin2 Causes Ocular Defects During Mouse Eye Development

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P2860

Craniosynostosis caused by Axin2 deficiency is mediated through distinct functions of beta-catenin in proliferation and differentiation.

http://www.wikidata.org/entity/Q35677733

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2006 nî lūn-bûn

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Craniosynostosis caused by Axi ...... iferation and differentiation.

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Developmental Biology

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Craniosynostosis caused by Axi ...... iferation and differentiation.

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Bo Liu

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Hsiao-Man Ivy Yu

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Wei Hsu

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P2860

TGF-beta signal transduction

A presenilin-1/gamma-secretase cleavage releases the E-cadherin intracellular domain and regulates disassembly of adherens junctions.

Essential role of BCL9-2 in the switch between beta-catenin's adhesive and transcriptional functions

A mutation in the LDL receptor-related protein 5 gene results in the autosomal dominant high-bone-mass trait

The Wnt signaling pathway in development and disease

LDL receptor-related protein 5 (LRP5) affects bone accrual and eye development

The mouse Fused locus encodes Axin, an inhibitor of the Wnt signaling pathway that regulates embryonic axis formation

Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis

Smad transcription factors

Identification of a domain of Axin that binds to the serine/threonine protein phosphatase 2A and a self-binding domain

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