Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome - Wikidata - wikimedia - TriplyDB

Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome

Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome

http://www.wikidata.org/entity/Q35239339

about

WNT-5A: signaling and functions in health and disease 22q11 deletion syndrome: current perspective.Variants in the Regulatory Region of WNT5A Reduced Risk of Cardiac Conotruncal Malformations in the Chinese Population.Reduced dosage of β-catenin provides significant rescue of cardiac outflow tract anomalies in a Tbx1 conditional null mouse model of 22q11.2 deletion syndrome.DAAM1 and DAAM2 are co-required for myocardial maturation and sarcomere assembly Spatial regulation of cell cohesion by Wnt5a during second heart field progenitor deployment.Epithelial tension in the second heart field promotes mouse heart tube elongation.Atypical microdeletion in 22q11 deletion syndrome reveals new candidate causative genes: A case report and literature review.The heart tube forms and elongates through dynamic cell rearrangement coordinated with foregut extension.Bimodal regulation of Dishevelled function by Vangl2 during morphogenesis.Planar Cell Polarity Signaling in Mammalian Cardiac Morphogenesis.Septation of the Intrapericardial Arterial Trunks in the Early Human Embryonic Heart.

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P2860

Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome

http://www.wikidata.org/entity/Q35239339

description

2014 nî lūn-bûn

@nan

2014 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի նոյեմբերին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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name

Loss of Wnt5a disrupts second ...... ormations in DiGeorge syndrome

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Loss of Wnt5a disrupts second ...... ormations in DiGeorge syndrome

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Human Molecular Genetics

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Loss of Wnt5a disrupts second ...... ormations in DiGeorge syndrome

@en

P2093

Ding Li

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

Jianbo Wang

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

Magali Théveniau-Ruissy

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

Mary R Hutson

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Tanvi Sinha

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P2860

WNT5A mutations in patients with autosomal dominant Robinow syndrome

Planar cell polarity links axes of spatial dynamics in neural-tube closure

Generalized lacZ expression with the ROSA26 Cre reporter strain

A regulatory pathway involving Notch1/beta-catenin/Isl1 determines cardiac progenitor cell fate.

Ror2, encoding a receptor-like tyrosine kinase, is required for cartilage and growth plate development

Dominant mutations in ROR2, encoding an orphan receptor tyrosine kinase, cause brachydactyly type B

Isl1 identifies a cardiac progenitor population that proliferates prior to differentiation and contributes a majority of cells to the heart

DiGeorge syndrome phenotype in mice mutant for the T-box gene, Tbx1

Wnt/Frizzled activation of Rho regulates vertebrate gastrulation and requires a novel Formin homology protein Daam1

Mutations in VANGL1 associated with neural-tube defects

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1704-1716

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10.1093/HMG/DDU584

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6

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24

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4381755

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