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1 related patients with tuberous sclerosis and renal cystic disease.
2 -dose treatment did not significantly reduce renal cystic disease.
3 as a promising strategy for the treatment of renal cystic diseases.
4 lucocorticoid metabolism result in recessive renal cystic disease, a developmental disorder of the ki
5 f Pkd1 during embryogenesis develop profound renal cystic disease and die from renal failure within 3
6 Pkd1(-/-) or Pkd2(-/-) mice develop rapid renal cystic disease and exhibit embryonic lethality; th
7 specific knockdown of ILK strikingly reduced renal cystic disease and fibrosis and extended the life
8 dicate that loss of Ift140 causes pronounced renal cystic disease and suggest that abnormalities in s
11 y was undertaken to further characterize the renal cystic disease as quantitative trait in this F2 co
12 s accompanied by a marked aggravation of the renal cystic disease, as reflected by kidney weights, hi
13 simultaneous deletion of Gli2 attenuated the renal cystic disease associated with deletion of Thm1.
15 e (MKS) is a lethal disorder associated with renal cystic disease, encephalocele, ductal plate malfor
16 dies, marked variability was observed in the renal cystic disease expressed in F2 bpk/bpk homozygotes
26 60 ng/ml, respectively) on mTOR activity and renal cystic disease in two Pkd1-mutant mouse models at
30 ominant Xpl mutant, in which polydactyly and renal cystic disease occurs, maps to the homologous regi
31 It is concluded that the severity of the bpk renal cystic disease phenotype is modulated by multiple
35 with this drug leads to amelioration of the renal cystic disease similar to genetic STAT6 inactivati
36 lial morphogenesis in 3D renal cultures link renal cystic disease to apical organization defects, whe
37 lia ift88 gene leads to delayed, adult-onset renal cystic disease, which provides a window of opportu
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