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10篇 您的检索式：作者名="Pece N"

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		题名	作者	年代	出处	被引量
	1	Geoelectrical and seismic prospections in hydrogeology: Model and master curves for the evaluation of porosity and water saturation显示文摘	Carrara E Pece R Robertit N	1994	Pageoph1994，143，4：	1
	2	Molecular characterization and in situ localization of murine endoglin reveal that it is a transforming growth factor-beta binding protein of endothelial and stromal cells显示文摘	St-Jacques S Cymerman U Pece N	1994	Endocrinology1994，134，6：	1
	3	Identification of hereditary hemorrhagic telangiectasia type I in newborns by protein expression and mutation analysis of endoglin 显示文摘	Cymerman U Vera S Pece - Barbara N	2000	Pediatr Res2000，47，1：	1
	4	Molecular characterization and in situ localization of murine endoglin reveal that it is a transforming growth factor-beta binding protein of endothelial and stromal cells 显示文摘	St-Jacques S Cymerman U Pece N	1994	Endocrinology1994，134，6：	1
	5	Massive gastric dilatation and anuria resolved with naso-gastric tube decompression显示文摘	Ramón Peces Cristina Vega Carlos Peces Julio Trébol Juan A. González	2010	International Urology and Nephrology2010，，3：	1
	6	Autosomal dominant polycystic liver disease in a family without polycystic kidney disease associated with a novel missense protein kinase C substrate 80K-H mutation显示文摘Polycystic liver disease (PLD) is characterized by the presence of multiple bile duct-derived epithelial cysts scattered in the liver parenchyma. PLD can manifest itself in patients with severe autosomal dominant polycystic kidney disease (ADPKD). Isolated autosomal dominant polycystic liver disease (ADPLD) is genetically distinct from PLD associated with ADPKD, although it may have similar pathogenesis and clinical manifestations.Recently, mutations in two causative genes for ADPLD,independently from ADPKD, have been identified. We report here a family (a mother and her daughter) with a severe form of ADPLD not associated with ADPKD produced by a novel missense protein kinase C substrate 80K-H (PRKCSH) mutation (R281W). This mutation causes a severe phenotype, since the two affected subjects manifested signs of portal hypertension. Doppler sonography, computed tomography (CT) and magnetic resonance (MR) imaging are effective in documenting the underlying lesions in a non-invasive way.	Ramón Peces Joost PH Drenth Rene HM te Morsche Pedro González Carlos Peces	2005	World Journal of Gastroenterology2005，11，48：	1
	7	Regulation of Smurf2 ubiquitin ligase activity by anchoring the E2 to the HECT domain显示文摘	OGUNJIMI A A BRIANT D J PECE BARBARA N	2005	Mol Cell2005，19，3：	1
	8	Mutant endoglin in hereditary hemorrhagic telangiectasia type 1 is transiently expressed intracellularly and is not a dominant negative显示文摘	Pece N Vera S Cymerman U	1997	J Clin Invest1997，100，：	1
	9	Identification of hered- itary hemorrhagic telangiectasia type I in newborns by protein expres- sion and mutation analysis of endoglin 显示文摘	Cymennan U Vera S Pece - Barbara N	2000	Pediatr Res2000，47，：	1
	10	Molecular characterization and in situ localization of routine endoglin reveal that it is an transforming growth factor -13 binding protein of endothelial and stromal cells显示文摘	St-Jacques S Cymerman U Pece N	1994	Endocrinology1994，134，：	1

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