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1 d found no evidence of systemic infective or cystic disease.
2 treatment did not significantly reduce renal cystic disease.
3 x1Cre(+) allele causes a late onset of focal cystic disease.
4 ney and that acute kidney injury exacerbates cystic disease.
5 e cell cycle and proliferation, resulting in cystic disease.
6 is associated with significantly more severe cystic disease.
7 patients may be because of extensive hepatic cystic disease.
8 d patients with tuberous sclerosis and renal cystic disease.
9 ate of PAH secretion despite the presence of cystic disease.
10 romising strategy for the treatment of renal cystic diseases.
11 d progression in models orthologous to human cystic diseases.
12 have been implicated in the pathogenesis of cystic diseases.
13 out contiguous deletions had relatively mild cystic disease, 3 of whom had gross rearrangements of TS
14 rticoid metabolism result in recessive renal cystic disease, a developmental disorder of the kidney.
17 the administration of GME did not lessen the cystic disease and did not reverse the effects of BSO.
18 during embryogenesis develop profound renal cystic disease and die from renal failure within 3 weeks
19 1(-/-) or Pkd2(-/-) mice develop rapid renal cystic disease and exhibit embryonic lethality; this sup
20 ic knockdown of ILK strikingly reduced renal cystic disease and fibrosis and extended the life of pcy
21 that loss of Ift140 causes pronounced renal cystic disease and suggest that abnormalities in several
22 l polarity underlie TSC and ADPKD-associated cystic disease and targeting of this pathway may be of k
26 undertaken to further characterize the renal cystic disease as quantitative trait in this F2 cohort a
28 mpanied by a marked aggravation of the renal cystic disease, as reflected by kidney weights, histolog
32 other protein products of genes involved in cystic disease: Cystin, the product of the mouse cpk loc
33 neys results in rapid or slow progression of cystic disease depending on whether the animals are juve
34 ) is a lethal disorder associated with renal cystic disease, encephalocele, ductal plate malformation
35 marked variability was observed in the renal cystic disease expressed in F2 bpk/bpk homozygotes of a
38 for epithelial membrane antigen (EMA), gross cystic disease fluid protein-15 (GCDFP-15), cytokeratin
39 These studies identify a link between two cystic disease genes, HNF1beta (MODY5) and PKHD1 (ARPKD)
41 polarity and decreased expression of several cystic disease genes, some of which we identified as nov
45 le proteins whose functions are disrupted in cystic diseases have now been localized to the cilium or
46 ic approaches to slow the development of the cystic disease; however, little is known about the role
48 and XBP1 overexpression in vivo ameliorated cystic disease in a murine model with reduced PC1 functi
49 RAS inhibitors in slowing the progression of cystic disease in ADPKD are inconclusive, and we hypothe
55 d, although more than half developed hepatic cystic disease in later life, similar to the phenotype o
56 reatment with a proteasome inhibitor reduces cystic disease in orthologous gene models of human autos
57 deficiency in FPC increases the severity of cystic disease in Pkd2 mutants and down-regulates PC2 in
58 In addition, they cause an endothelial-lined cystic disease in the liver known as bacillary peliosis.
64 ml, respectively) on mTOR activity and renal cystic disease in two Pkd1-mutant mouse models at differ
70 least in some patients, the severity of the cystic disease is inversely correlated with the level of
71 ing approaches, earlier diagnosis of hepatic cystic disease is possible, and measurement of kidney an
72 o therapies are currently available to treat cystic diseases, making it imperative to dissect molecul
74 t Xpl mutant, in which polydactyly and renal cystic disease occurs, maps to the homologous region of
75 type of PCK AVP(-/-) rats and aggravated the cystic disease of PCK AVP(+/+) rats but did not induce c
76 have intermediate survival in the absence of cystic disease or renal failure, providing the first ind
77 concluded that the severity of the bpk renal cystic disease phenotype is modulated by multiple loci a
79 dk5 in the jck mice significantly attenuates cystic disease progression and is associated with shorte
82 this drug leads to amelioration of the renal cystic disease similar to genetic STAT6 inactivation.
83 zygotes; these mutants developed less severe cystic disease than jck homozygotes and provided genetic
84 dered were the extent and pattern of hepatic cystic disease, the degree of hepatic and renal dysfunct
85 orphogenesis in 3D renal cultures link renal cystic disease to apical organization defects, whereas c
86 one pair of sisters who were discordant for cystic disease, two mother- daughter pairs who were disc
88 tion of polycystins and that the severity of cystic disease was directly related to the length of tim
90 n 17 patients with constitutional deletions, cystic disease was severe, with early renal insufficienc
91 irm that a defect in the Nek8 gene can cause cystic disease, we performed a cross-species analysis: i
92 omas, and 22 (88%) had no or mild pancreatic cystic disease, which is substantially more than the gen
93 t88 gene leads to delayed, adult-onset renal cystic disease, which provides a window of opportunity t
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