Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.1681/ASN.2009040421

http://scihub22266oqcxt.onion/10.1681/ASN.2009040421
suck pdf from google scholar
20075061!2831854!20075061
unlimited free pdf from europmc20075061    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
pmid20075061      J+Am+Soc+Nephrol 2010 ; 21 (3): 489-97
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Rapamycin ameliorates PKD resulting from conditional inactivation of Pkd1 #MMPMID20075061
  • Shillingford JM; Piontek KB; Germino GG; Weimbs T
  • J Am Soc Nephrol 2010[Mar]; 21 (3): 489-97 PMID20075061show ga
  • Aberrant activation of the mammalian target of rapamycin (mTOR) pathway occurs in polycystic kidney disease (PKD). mTOR inhibitors, such as rapamycin, are highly effective in several rodent models of PKD, but these models result from mutations in genes other than Pkd1 and Pkd2, which are the primary genes responsible for human autosomal dominant PKD. To address this limitation, we tested the efficacy of rapamycin in a mouse model that results from conditional inactivation of Pkd1. Mosaic deletion of Pkd1 resulted in PKD and replicated characteristic features of human PKD including aberrant mTOR activation, epithelial proliferation and apoptosis, and progressive fibrosis. Treatment with rapamycin was highly effective: It reduced cyst growth, preserved renal function, inhibited epithelial cell proliferation, increased apoptosis of cyst-lining cells, and inhibited fibrosis. These data provide in vivo evidence that rapamycin is effective in a human-orthologous mouse model of PKD.
  • |Animals[MESH]
  • |Apoptosis/physiology[MESH]
  • |Blood Urea Nitrogen[MESH]
  • |Cell Division/physiology[MESH]
  • |Disease Models, Animal[MESH]
  • |Fibrosis[MESH]
  • |Gene Expression/drug effects[MESH]
  • |Humans[MESH]
  • |Immunosuppressive Agents/pharmacology[MESH]
  • |Intermediate Filament Proteins/genetics[MESH]
  • |Intracellular Signaling Peptides and Proteins/metabolism[MESH]
  • |Kidney Tubules, Collecting/pathology/physiopathology[MESH]
  • |Kidney Tubules, Distal/pathology/physiopathology[MESH]
  • |Mice[MESH]
  • |Mosaicism[MESH]
  • |Nerve Tissue Proteins/genetics[MESH]
  • |Nestin[MESH]
  • |Phenotype[MESH]
  • |Polycystic Kidney Diseases/*genetics/pathology/*physiopathology[MESH]
  • |Protein Serine-Threonine Kinases/metabolism[MESH]
  • |Sirolimus/*pharmacology[MESH]
  • |TOR Serine-Threonine Kinases[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box