Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations. - Wikidata - wikimedia - TriplyDB

Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations.

Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations.

http://www.wikidata.org/entity/Q33425920

about

Systemic VHL gene functions and the VHL disease Pancreas-specific Cre driver lines and considerations for their prudent use Elimination of von Hippel-Lindau function perturbs pancreas endocrine homeostasis in mice Insights into the Pathogenesis of Pancreatic Cystic Neoplasms.Conditional deletion of p53 and Rb in the renin-expressing compartment of the pancreas leads to a highly penetrant metastatic pancreatic neuroendocrine carcinoma.Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice Primary cilia in pancreatic development and disease.Mouse models of inherited cancer syndromes The multifaceted von Hippel-Lindau tumour suppressor protein.EAF2 loss enhances angiogenic effects of Von Hippel-Lindau heterozygosity on the murine liver and prostate.Whole-exome sequencing of neoplastic cysts of the pancreas reveals recurrent mutations in components of ubiquitin-dependent pathways.Hypoxia-inducible factor 1 activation from adipose protein 2-cre mediated knockout of von Hippel-Lindau gene leads to embryonic lethality.Complex cellular functions of the von Hippel-Lindau tumor suppressor gene: insights from model organisms.Von Hippel-Lindau disease (VHL): a need for a murine model with retinal hemangioblastoma VHLdb: A database of von Hippel-Lindau protein interactors and mutations.Genetic modification of hypoxia signaling in animal models and its effect on cancer.Pancreatic cyst development: insights from von Hippel-Lindau disease.Stabilization of HIF-2α impacts pancreas growth

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Deciphering von Hippel-Lindau (VHL/Vhl)-associated pancreatic manifestations by inactivating Vhl in specific pancreatic cell populations.

http://www.wikidata.org/entity/Q33425920

description

2009 nî lūn-bûn

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2009 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2009 թվականի ապրիլին հրատարակված գիտական հոդված

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2009年の論文

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年学术文章

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2009年學術文章

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name

Deciphering von Hippel-Lindau ...... c pancreatic cell populations.

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Deciphering von Hippel-Lindau ...... c pancreatic cell populations.

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Deciphering von Hippel-Lindau ...... c pancreatic cell populations.

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Deciphering von Hippel-Lindau ...... c pancreatic cell populations.

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Deciphering von Hippel-Lindau ...... c pancreatic cell populations.

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JOURNAL.PONE.0004897

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Deciphering von Hippel-Lindau ...... c pancreatic cell populations.

@en

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Arianne Wilson

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Asha Adem

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David M Harlan

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Dominique Lorang

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H-C Jennifer Shen

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Irina A Lubensky

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Klaus Pechhold

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Kris Ylaya

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Laura S Schmidt

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Mei He

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P2860

The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

Vhlh gene deletion induces Hif-1-mediated cell death in thymocytes

pVHL function is essential for endothelial extracellular matrix deposition.

von Hippel-Lindau disease-associated hemangioblastomas are derived from embryologic multipotent cells

Identification of the von Hippel-Lindau disease tumor suppressor gene

Direct evidence for the pancreatic lineage: NGN3+ cells are islet progenitors and are distinct from duct progenitors

Contrasting properties of hypoxia-inducible factor 1 (HIF-1) and HIF-2 in von Hippel-Lindau-associated renal cell carcinoma.

Contrasting effects on HIF-1alpha regulation by disease-causing pVHL mutations correlate with patterns of tumourigenesis in von Hippel-Lindau disease.

The von Hippel-Lindau protein interacts with heteronuclear ribonucleoprotein a2 and regulates its expression.

Vascular tumors in livers with targeted inactivation of the von Hippel-Lindau tumor suppressor.

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e4897

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scholarly article

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10.1371/JOURNAL.PONE.0004897

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Stephen M. Hewitt

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2009-04-02T00:00:00Z

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