Hyperactivation of p21ras and PI3K cooperate to alter murine and human neurofibromatosis type 1-haploinsufficient osteoclast functions
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Kinase AKT controls innate immune cell development and functionThe haploinsufficient hematopoietic microenvironment is critical to the pathological fracture repair in murine models of neurofibromatosis type 1In vitro model of bone to facilitate measurement of adhesion forces and super-resolution imaging of osteoclastsRas dependent paracrine secretion of osteopontin by Nf1+/- osteoblasts promote osteoclast activation in a neurofibromatosis type I murine model.Generalized metabolic bone disease in Neurofibromatosis type INf1 Haploinsufficiency Alters Myeloid Lineage Commitment and Function, Leading to Deranged Skeletal Homeostasis.Activating transcription factor 4 regulates osteoclast differentiation in mice.Bone mineral density in children and young adults with neurofibromatosis type 1Decreased bone mineralization in children with Noonan syndrome: another consequence of dysregulated RAS MAPKinase pathway?Development of severe skeletal defects in induced SHP-2-deficient adult mice: a model of skeletal malformation in humans with SHP-2 mutationsLocal low-dose lovastatin delivery improves the bone-healing defect caused by Nf1 loss of function in osteoblasts.Dystrophic spinal deformities in a neurofibromatosis type 1 murine model.Mice lacking Nf1 in osteochondroprogenitor cells display skeletal dysplasia similar to patients with neurofibromatosis type I.Erk1 positively regulates osteoclast differentiation and bone resorptive activityEvidence of increased bone resorption in neurofibromatosis type 1 using urinary pyridinium crosslink analysisBone resorption in syndromes of the Ras/MAPK pathway.Pediatric 25-hydroxyvitamin D concentrations in neurofibromatosis type 1Loss of Cbl-PI3K interaction enhances osteoclast survival due to p21-Ras mediated PI3K activation independent of Cbl-bc-Fms signaling mediates neurofibromatosis Type-1 osteoclast gain-in-functions.Pathway crosstalk between Ras/Raf and PI3K in promotion of M-CSF-induced MEK/ERK-mediated osteoclast survivalPlexiform neurofibroma genesis: questions of Nf1 gene dose and hyperactive mast cellsNeurofibroma-associated macrophages play roles in tumor growth and response to pharmacological inhibition.Heterozygous inactivation of the Nf1 gene in myeloid cells enhances neointima formation via a rosuvastatin-sensitive cellular pathwayPathogenesis of plexiform neurofibroma: tumor-stromal/hematopoietic interactions in tumor progression.The p85alpha subunit of class IA phosphatidylinositol 3-kinase regulates the expression of multiple genes involved in osteoclast maturation and migration.Interleukin 8/KC enhances G-CSF induced hematopoietic stem/progenitor cell mobilization in Fancg deficient mice.How does the Schwann cell lineage form tumors in NF1?Neurofibromin-deficient myeloid cells are critical mediators of aneurysm formation in vivo.The ecology of brain tumors: lessons learned from neurofibromatosis-1.The musculoskeletal phenotype of the RASopathies.The regulation of osteoclast function and bone resorption by small GTPasesAberrant Myeloid Differentiation Contributes to the Development of Osteoporosis in Neurofibromatosis Type 1.Primary osteopathy of vertebrae in a neurofibromatosis type 1 murine model.Nf1+/- mice have increased neointima formation via hyperactivation of a Gleevec sensitive molecular pathway.Hyperactive Ras/MAPK signaling is critical for tibial nonunion fracture in neurofibromin-deficient mice.Bone mineral metabolism in patients with neurofibromatosis type 1 (von Recklingausen disease).Hyperactive transforming growth factor-β1 signaling potentiates skeletal defects in a neurofibromatosis type 1 mouse model.The reduced osteogenic potential of Nf1-deficient osteoprogenitors is EGFR-independent.The generalized bone phenotype in children with neurofibromatosis 1: a sibling matched case-control study.Multiple increased osteoclast functions in individuals with neurofibromatosis type 1.
P2860
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P2860
Hyperactivation of p21ras and PI3K cooperate to alter murine and human neurofibromatosis type 1-haploinsufficient osteoclast functions
description
2006 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2006
@ast
im Oktober 2006 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2006/11/01)
@sk
vědecký článek publikovaný v roce 2006
@cs
wetenschappelijk artikel (gepubliceerd op 2006/11/01)
@nl
наукова стаття, опублікована в листопаді 2006
@uk
مقالة علمية (نشرت في نوفمبر 2006)
@ar
name
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@ast
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@en
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@nl
type
label
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@ast
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@en
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@nl
prefLabel
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@ast
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@en
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@nl
P2093
P2860
P921
P356
P1476
Hyperactivation of p21ras and ...... ufficient osteoclast functions
@en
P2093
Alexander G Robling
D Wade Clapp
David A Ingram
Feng-Chun Yang
Jincheng Yan
Todd D Nebesio
Trent Morgan
Xiaohong Li
P2860
P304
P356
10.1172/JCI29092
P407
P577
2006-10-19T00:00:00Z