Smad4 is required for maintaining normal murine postnatal bone homeostasis - Wikidata - wikimedia - TriplyDB

Smad4 is required for maintaining normal murine postnatal bone homeostasis

Smad4 is required for maintaining normal murine postnatal bone homeostasis

http://www.wikidata.org/entity/Q37217038

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TGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and disease TGF-β and BMP signaling in osteoblast differentiation and bone formation Targeting WW domains linker of HECT-type ubiquitin ligase Smurf1 for activation by CKIP-1 Non-virus-mediated transfer of siRNAs against Runx2 and Smad4 inhibit heterotopic ossification in rats.An integrative genetics approach to identify candidate genes regulating BMD: combining linkage, gene expression, and association.Smad signaling in skeletal development and regeneration.Dual roles of smad proteins in the conversion from myoblasts to osteoblastic cells by bone morphogenetic proteins.Quantitative trait loci, genes, and polymorphisms that regulate bone mineral density in mouse SHIP1 regulates MSC numbers and their osteolineage commitment by limiting induction of the PI3K/Akt/β-catenin/Id2 axis.Mutations at a single codon in Mad homology 2 domain of SMAD4 cause Myhre syndrome.An atypical canonical bone morphogenetic protein (BMP) signaling pathway regulates Msh homeobox 1 (Msx1) expression during odontogenesis.Bone Morphogenetic Protein (BMP) signaling in development and human diseases Genetic mouse models for bone studies--strengths and limitations PfSMAD4 plays a role in biomineralization and can transduce bone morphogenetic protein-2 signals in the pearl oyster Pinctada fucata.BST2 Mediates Osteoblast Differentiation via the BMP2 Signaling Pathway in Human Alveolar-Derived Bone Marrow Stromal Cells Dual function of Bmpr1a signaling in restricting preosteoblast proliferation and stimulating osteoblast activity in mouse Development of the endochondral skeleton Transforming growth factor-beta-regulated miR-24 promotes skeletal muscle differentiation.Disruption of Wnt/β-catenin signaling in odontoblasts and cementoblasts arrests tooth root development in postnatal mouse teeth.Wntless regulates dentin apposition and root elongation in the mandibular molar Osterix regulates tooth root formation in a site-specific manner Overexpression of H1 calponin in osteoblast lineage cells leads to a decrease in bone mass by disrupting osteoblast function and promoting osteoclast formation.Embryonic ablation of osteoblast Smad4 interrupts matrix synthesis in response to canonical Wnt signaling and causes an osteogenesis-imperfecta-like phenotype.Smad4 controls bone homeostasis through regulation of osteoblast/osteocyte viability.Requirement of Smad4-mediated signaling in odontoblast differentiation and dentin matrix formation.Smad4 is required to inhibit osteoclastogenesis and maintain bone mass.Disruption of Smad4 in odontoblasts causes multiple keratocystic odontogenic tumors and tooth malformation in mice.Constitutive activation of smoothened leads to impaired developments of postnatal bone in mice.Myhre syndrome.Smad4 in osteoblasts exerts a differential impact on HSC fate depending on osteoblast maturation stage.Chondrodysplasias and TGFβ signaling.Maturation of cortical bone suppresses periosteal osteoprogenitor proliferation in a paracrine manner.Skeletal metastases from breast cancer: pathogenesis of bone tropism and treatment strategy.SMAD4 Loss Is Associated with Cetuximab Resistance and Induction of MAPK/JNK Activation in Head and Neck Cancer Cells.BMP signalling in skeletal development, disease and repair.BMP9 a possible alternative drug for the recently withdrawn BMP7? New perspectives for (re-)implementation by personalized medicine.A Reciprocal Interaction between β-Catenin and Osterix in Cementogenesis.Differential involvement of Wnt signaling in Bmp regulation of cancellous versus periosteal bone growth.Mesenchymal TGF-β signaling orchestrates dental epithelial stem cell homeostasis through Wnt signaling.BmpR1A is a major type 1 BMP receptor for BMP-Smad signaling during skull development.

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P2860

Smad4 is required for maintaining normal murine postnatal bone homeostasis

http://www.wikidata.org/entity/Q37217038

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 05 June 2007

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Smad4 is required for maintaining normal murine postnatal bone homeostasis

@en

Smad4 is required for maintaining normal murine postnatal bone homeostasis.

@nl

type

label

Smad4 is required for maintaining normal murine postnatal bone homeostasis

@en

Smad4 is required for maintaining normal murine postnatal bone homeostasis.

@nl

prefLabel

Smad4 is required for maintaining normal murine postnatal bone homeostasis

@en

Smad4 is required for maintaining normal murine postnatal bone homeostasis.

@nl

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Journal of Cell Science

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Smad4 is required for maintaining normal murine postnatal bone homeostasis

@en

P2093

Di Chen

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

Fuyu Lin

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

Haifeng Wan

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

Haihong Liu

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

Jian Wang

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

Jishuai Zhang

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

Jun Ding

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

Ning Hou

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

Ruifu Yang

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

Tujun Weng

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

P2860

Novel regulators of bone formation: molecular clones and activities

A human chondrodysplasia due to a mutation in a TGF-beta superfamily member

A RUNX2/PEBP2alpha A/CBFA1 mutation displaying impaired transactivation and Smad interaction in cleidocranial dysplasia

Linkage of osteoporosis to chromosome 20p12 and association to BMP2

Generalized lacZ expression with the ROSA26 Cre reporter strain

Smad-dependent and Smad-independent pathways in TGF-beta family signalling

Disruption of human limb morphogenesis by a dominant negative mutation in CDMP1

Limb alterations in brachypodism mice due to mutations in a new member of the TGF beta-superfamily

Bone morphogenetic protein type IA receptor signaling regulates postnatal osteoblast function and bone remodeling

Bone morphogenetic protein-4 is required for mesoderm formation and patterning in the mouse

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2162-2170

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scholarly article

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10.1242/JCS.03466

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P433

Pt 13

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120

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2007-06-05T00:00:00Z

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6285605

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17550966

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2692485

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