Development of severe skeletal defects in induced SHP-2-deficient adult mice: a model of skeletal malformation in humans with SHP-2 mutations (Q34611774)

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English	Development of severe skeletal defects in induced SHP-2-deficient adult mice: a model of skeletal malformation in humans with SHP-2 mutations	scientific article

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scholarly article

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16 January 2020

Development of severe skeletal defects in induced SHP-2-deficient adult mice: a model of skeletal malformation in humans with SHP-2 mutations (English)

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16 January 2020

Timothy J Bauler

1

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16 January 2020

author name string

Nobuhiro Kamiya

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16 January 2020

Philip E Lapinski

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16 January 2020

Eric Langewisch

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16 January 2020

Yuji Mishina

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16 January 2020

John E Wilkinson

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16 January 2020

Gen-Sheng Feng

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16 January 2020

Philip D King

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16 January 2020

publication date

10 November 2010

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16 January 2020

Disease Models & Mechanisms

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16 January 2020

4

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16 January 2020

2

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16 January 2020

228-239

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16 January 2020

Shp2 acts downstream of SDF-1alpha/CXCR4 in guiding granule cell migration during cerebellar development

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Protein tyrosine phosphatase SHP-2: a proto-oncogene product that promotes Ras activation

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Coordinated regulation by Shp2 tyrosine phosphatase of signaling events controlling insulin biosynthesis in pancreatic beta-cells

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Deletion of Shp2 tyrosine phosphatase in muscle leads to dilated cardiomyopathy, insulin resistance, and premature death

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Leopard syndrome

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Development of diabesity in mice with neuronal deletion of Shp2 tyrosine phosphatase.

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How do Shp2 mutations that oppositely influence its biochemical activity result in syndromes with overlapping symptoms?

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Shp2-mediated molecular signaling in control of embryonic stem cell self-renewal and differentiation

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Hyperactivation of p21ras and PI3K cooperate to alter murine and human neurofibromatosis type 1-haploinsufficient osteoclast functions

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Conditional deletion of Shp2 in the mammary gland leads to impaired lobulo-alveolar outgrowth and attenuated Stat5 activation

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Ras-MAPK signaling in osteogenic differentiation: friend or foe?

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Concerted functions of Gab1 and Shp2 in liver regeneration and hepatoprotection

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7 July 2018

Reduced phosphatase activity of SHP-2 in LEOPARD syndrome: consequences for PI3K binding on Gab1

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7 July 2018

PTPN11 (Shp2) mutations in LEOPARD syndrome have dominant negative, not activating, effects

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7 July 2018

Diversity and functional consequences of germline and somatic PTPN11 mutations in human disease

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7 July 2018

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7 July 2018

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7 July 2018

Neuronal Shp2 tyrosine phosphatase controls energy balance and metabolism

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7 July 2018

Noonan syndrome-associated SHP2/PTPN11 mutants cause EGF-dependent prolonged GAB1 binding and sustained ERK2/MAPK1 activation

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Grouping of multiple-lentigines/LEOPARD and Noonan syndromes on the PTPN11 gene

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Mutations in PTPN11, encoding the protein tyrosine phosphatase SHP-2, cause Noonan syndrome

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A clinical study of Noonan syndrome

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26 October 2018

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1 reference

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12 December 2020

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inferred from PubMed ID database lookup

Neurofibromin and its inactivation of Ras are prerequisites for osteoblast functioning

1 reference

https://pubmed.ncbi.nlm.nih.gov/21068439

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

CFU-GM-derived cells form osteoclasts at a very high efficiency

1 reference

https://pubmed.ncbi.nlm.nih.gov/21068439

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.1242/DMM.006130

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16 January 2020

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16 January 2020

1 reference

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16 January 2020

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