نتایج جستجو برای: pkd1

تعداد نتایج: 895  

Journal: :Journal of the American Society of Nephrology : JASN 2010
Saori Nishio Xin Tian Anna Rachel Gallagher Zhiheng Yu Vishal Patel Peter Igarashi Stefan Somlo

Polycystic kidney disease (PKD) can arise from either developmental or postdevelopmental processes. Recessive PKD, caused by mutations in PKHD1, is a developmental defect, whereas dominant PKD, caused by mutations in PKD1 or PKD2, occurs by a cellular recessive mechanism in mature kidneys. Oriented cell division is a feature of planar cell polarity that describes the orientation of the mitotic ...

Journal: :Human molecular genetics 1997
R Sandford B Sgotto S Aparicio S Brenner M Vaudin R K Wilson S Chissoe K Pepin A Bateman C Chothia J Hughes P Harris

PKD1 is the major locus of the common genetic disorder autosomal dominant polycystic kidney disease (ADPKD). Analysis of the predicted protein sequence of the human PKD1 gene, polycystin, shows a large molecule with a unique arrangement of extracellular domains and multiple putative transmembrane regions. The precise function of polycystin remains unclear with a paucity of mutations to define k...

Journal: :Journal of the American Society of Nephrology : JASN 2010
Michelle Liu Sally Shi Sean Senthilnathan Julie Yu Elliot Wu Carsten Bergmann Klaus Zerres Nadja Bogdanova Eliecer Coto Constantinos Deltas Alkis Pierides Kyproula Demetriou Olivier Devuyst Berenice Gitomer Marku Laakso Anne Lumiaho Klea Lamnissou Riccardo Magistroni Patrick Parfrey Martijn Breuning Dorien J M Peters Roser Torra Christopher G Winearls Vicente E Torres Peter C Harris Andrew D Paterson York Pei

Significant variation in the course of autosomal dominant polycystic kidney disease ( ADPKD) within families suggests the presence of effect modifiers. Recent studies of the variation within families harboring PKD1 mutations indicate that genetic background may account for 32 to 42% of the variance in estimated GFR (eGFR) before ESRD and 43 to 78% of the variance in age at ESRD onset, but the g...

2010
Sharon A. Matthews Maria N. Navarro Linda V. Sinclair Elizabeth Emslie Carmen Feijoo-Carnero Doreen A. Cantrell

Mammalian PKD (protein kinase D) isoforms have been implicated in the regulation of diverse biological processes in response to diacylglycerol and PKC (protein kinase C) signalling. To compare the functions of PKD1 and PKD2 in vivo, we generated mice deficient in either PKD1 or PKD2 enzymatic activity, via homozygous expression of PKD1(S744A/S748A) or PKD2(S707A/S711A) 'knockin' alleles. We als...

Journal: :American journal of physiology. Renal physiology 2011
Wouter N Leonhard Annemieke van der Wal Zlata Novalic Steven J Kunnen Ron T Gansevoort Martijn H Breuning Emile de Heer Dorien J M Peters

Autosomal dominant polycystic kidney disease (ADPKD) caused by mutations in either the PKD1 or PKD2 gene is a major cause of end-stage renal failure. A number of compounds targeting specific signaling pathways were able to inhibit cystogenesis in rodent models and are currently being tested in clinical trials. However, given the complex signaling in ADPKD, an ideal therapy would likely have to ...

Journal: :Human molecular genetics 1996
B Peral A C Ong J L San Millán V Gamble L Rees P C Harris

Autosomal dominant polycystic kidney disease (ADPKD) is the most common single gene disorder resulting in renal failure. It is generally an adult onset disease, but rarely, cases of severe childhood polycystic disease arise in ADPKD families. The clear clinical anticipation in these pedigrees has led to the suggestion that the mutation may be an unstable trinucleotide repeat. We have now identi...

Journal: :The Journal of clinical investigation 2010
Shan Qin Mary Taglienti Surya M Nauli Leah Contrino Ayumi Takakura Jing Zhou Jordan A Kreidberg

Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disorder that is caused by mutations at two loci, polycystin 1 (PKD1) and polycystin 2 (PKD2). It is characterized by the formation of multiple cysts in the kidneys that can lead to chronic renal failure. Previous studies have suggested a role for hyperactivation of mammalian target of rapamycin (mTOR) in cystogenesis, b...

Journal: :Nature Medicine 1995

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1999
L Tsiokas T Arnould C Zhu E Kim G Walz V P Sukhatme

The function(s) of the genes (PKD1 and PKD2) responsible for the majority of cases of autosomal dominant polycystic kidney disease is unknown. While PKD1 encodes a large integral membrane protein containing several structural motifs found in known proteins involved in cell-cell or cell-matrix interactions, PKD2 has homology to PKD1 and the major subunit of the voltage-activated Ca2+ channels. W...

Journal: :Human molecular genetics 1999
P C Harris

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutation of one of two genes: PKD1 (16p13.3) or PKD2 (4q13-23). PKD1 accounts for approximately 85% of pedigrees and is associated with significantly more severe cystic disease. The ADPKD genes encode proteins, polycystin-1 and polycystin-2, which are very different in size and structure, but which have a region of homology and m...

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