The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
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Differentially expressed genes in autosomal dominant osteopetrosis type II osteoclasts reveal known and novel pathways for osteoclast biologyBoning up on autophagy: the role of autophagy in skeletal biologyPaget disease of bone-associated UBA domain mutations of SQSTM1 exert distinct effects on protein structure and functionAlternative splicing in osteoclasts and Paget's disease of bone.Emerging strategies and therapies for treatment of Paget's disease of bone.Role of NF-κB in the skeletonMutant p62P392L stimulation of osteoclast differentiation in Paget's disease of boneAutophagy proteins regulate the secretory component of osteoclastic bone resorption.Polymorphisms in autophagy genes are associated with paget disease of bone.Paget's Disease of Bone: A Review of Epidemiology, Pathophysiology and ManagementLipid-enriched diet rescues lethality and slows down progression in a murine model of VCP-associated disease.Gene expression profile in osteoclasts from patients with Paget's disease of bone.The adaptor protein p62/SQSTM1 in osteoclast signaling pathways.Pathogenesis of Paget disease of bone.Osteosarcoma: Molecular Pathogenesis and iPSC Modeling.Further Evidence of Contrasting Phenotypes Caused by Reciprocal Deletions and Duplications: Duplication of NSD1 Causes Growth Retardation and Microcephaly.Behavioral effects of SQSTM1/p62 overexpression in mice: support for a mitochondrial role in depression and anxietyAutophagy and 3-Phosphoinositide-Dependent Kinase 1 (PDK1)-Related Kinome in Pagetic Osteoclasts.Effect of a rare genetic variant of TM7SF4 gene on osteoclasts of patients with Paget's disease of bone.Lipopolysaccharide (LPS)-Induced Autophagy Is Responsible for Enhanced Osteoclastogenesis.Transgenic mice expressing mutant forms VCP/p97 recapitulate the full spectrum of IBMPFD including degeneration in muscle, brain and bone.A point mutation in the ubiquitin-associated domain of SQSMT1 is sufficient to cause a Paget's disease-like disorder in mice.Autophagy: a new player in skeletal maintenance?Modulation of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) receptors in a human osteoclast model in vitro.p62/sequestosome 1 deficiency accelerates osteoclastogenesis in vitro and leads to Paget's disease-like bone phenotypes in mice.Zoledronic acid prevents pagetic-like lesions and accelerated bone loss in the p62 mouse model of Paget's diseaseRab GTPases in Osteoclastic Endomembrane SystemsCan zebrafish be a valid model to study Paget's disease of bone?
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P2860
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 09 July 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@en
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@nl
type
label
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@en
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@nl
prefLabel
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@en
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@nl
P2093
P2860
P356
P1476
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.
@en
P2093
Estelle Chamoux
Jacques P Brown
Jean Morissette
Julie Couture
Martine Bisson
Sophie Roux
P2860
P304
P356
10.1210/ME.2009-0066
P577
2009-07-09T00:00:00Z