Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice - Wikidata - awgldk - TriplyDB

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

http://www.wikidata.org/entity/Q30842692

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Extracellular Signal-Regulated Kinase Signaling in CD4-Expressing Cells Inhibits Osteochondromas.Ptpn11 Deletion in CD4+ Cells Does Not Affect T Cell Development and Functions but Causes Cartilage Tumors in a T Cell-Independent Manner.

P2860

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Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

http://www.wikidata.org/entity/Q30842692

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2017 nî lūn-bûn

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2017 թուականի Մարտին հրատարակուած գիտական յօդուած

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2017 թվականի մարտին հրատարակված գիտական հոդված

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2017年の論文

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2017年学术文章

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2017年学术文章

@zh-cn

2017年学术文章

@zh-hans

2017年学术文章

@zh-my

2017年学术文章

@zh-sg

2017年學術文章

@yue

name

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@ast

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@en

type

label

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@ast

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@en

prefLabel

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@ast

Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@en

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FIMMU.2017.00343

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Frontiers in Immunology

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Unexpected Cartilage Phenotype in CD4-Cre-Conditional SOS-Deficient Mice

@en

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Connie L Sommers

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Devorah L Gallardo

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Jeffrey Baron

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Joshua A Kramer

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Julian C Lui

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Lawrence E Samelson

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Nicholas G Shakarishvili

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Nicolas Melis

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Robert L Kortum

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

Roberto Weigert

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P2860

The RASopathies: developmental syndromes of Ras/MAPK pathway dysregulation

The value of genomics in dissecting the RAS-network and in guiding therapeutics for RAS-driven cancers

Noonan syndrome

Sixteen years and counting: the current understanding of fibroblast growth factor receptor 3 (FGFR3) signaling in skeletal dysplasias

Mutation in Sos1 dominantly enhances a weak allele of the EGFR, demonstrating a requirement for Sos1 in EGFR signaling and development

Second-harmonic imaging microscopy for visualizing biomolecular arrays in cells, tissues and organisms.

Ras-guanine nucleotide exchange factor sos2 is dispensable for mouse growth and development.

Ras in cancer and developmental diseases

The ability of Sos1 to oligomerize the adaptor protein LAT is separable from its guanine nucleotide exchange activity in vivo.

Genetic inactivation of ERK1 and ERK2 in chondrocytes promotes bone growth and enlarges the spinal canal

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343

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scholarly article

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10.3389/FIMMU.2017.00343

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8

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Geoffrey Guittard

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2017-03-23T00:00:00Z

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28386265

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5362643

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