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1 e a promising treatment for SCLT1-associated cystic kidney.
2 mase-like AngII generating capacity in ADPKD cystic kidneys.
3 erstitial abnormalities and smaller cysts in cystic kidneys.
4 -1) that was significantly underexpressed in cystic kidneys.
5 pes indicative of defective cilia, including cystic kidneys.
6 at survives shows hydrocephalus and severely cystic kidneys.
7 o distal tubular segments in both normal and cystic kidneys.
8 of certain components of the pathway causing cystic kidneys.
9 doses sufficient to reduce phospho-ERK1/2 in cystic kidneys.
10 t deletion of the mouse Cby1 gene results in cystic kidneys, a phenotype common to ciliopathies, and
11 eterotaxy, cardiopulmonary malformations and cystic kidneys, a syndrome also characteristic of mutati
12 letion of TAZ in zebrafish also results in a cystic kidney accompanied by overexpression of PC2.
13 r Pkd2) and structure (Tg737) play a role in cystic kidney and aneurysm through survivin downregulati
14                                      In PKD2 cystic kidney and liver, we find polycystin-2 expression
15 nerated zebrafish mutants for pkd1 and noted cystic kidney and mTOR activation in pkd1a mutants, sugg
16 Affected individuals typically develop large cystic kidneys and approximately one half develop end-st
17 ockout mice resulted in development of multi-cystic kidneys and cardiac hypertrophy in some mice.
18 ethal condition with skeletal abnormalities, cystic kidneys and CNS malformation.
19 disruption of the PKD1 gene in mice leads to cystic kidneys and embryonic or perinatal death.
20 ebrafish caused ciliary paralysis leading to cystic kidneys and otolith defects and that knockdown in
21       The mice die shortly after birth, with cystic kidneys and proteinaceous debris throughout the l
22                                              Cystic kidneys and vascular aneurysms are clinical manif
23  Knockdown of ift80 in zebrafish resulted in cystic kidneys, and knockdown in Tetrahymena thermophila
24   Analysis of these adults revealed severely cystic kidneys associated with the presence of renal ade
25  characteristic imaging findings (echogenic, cystic kidney at US that did not function at scintigraph
26            Fz3 was expressed on the cilia of cystic kidneys but barely detected on the cilia of norma
27                       Macrophages infiltrate cystic kidneys, but the role of these and other inflamma
28 bit typical ciliopathy phenotypes, including cystic kidney, cleft palate and polydactyly.
29             Thus, proximal tubular injury in cystic kidneys closely parallels that observed with uret
30 es were observed in heterozygotes, including cystic kidney, craniofacial malformations, microphthalmi
31  cell carcinoma in association with acquired cystic kidney disease (ACKD).
32 y represented among the basal body proteome: cystic kidney disease (especially nephronophthisis) synd
33 ile nephronophthisis, an autosomal recessive cystic kidney disease afflicting children and young adul
34 e polaris (Tg737), a protein associated with cystic kidney disease and left-right axis patterning def
35 ronophthisis (NPH) is an autosomal-recessive cystic kidney disease and represents the most common gen
36 re Nephronophthisis (NPHP), characterized by cystic kidney disease and retinal degeneration, and Meck
37 have been linked to human diseases including cystic kidney disease and retinitis pigmentosa.
38 ing another link between proteins mutated in cystic kidney disease and their localization to cilia an
39 an aminopeptidase XPNPEP3 is associated with cystic kidney disease and TNF-TNFR2 cellular signaling.
40                   Animal models of inherited cystic kidney disease are useful for study of the pathog
41                     Mutant mice present with cystic kidney disease as neonates.
42 was also dramatically up-regulated in murine cystic kidney disease epithelia [jck/jck (nek8) and Ift8
43 ation in pkd2, one of two autosomal dominant cystic kidney disease genes, did not show increased risk
44                                              Cystic kidney disease has been linked to mutations in th
45  A-related kinase, Nek8, are associated with cystic kidney disease in both humans and mice, with Nek8
46 ssive polycystic kidney disease (ARPKD) as a cystic kidney disease in which lesions are localized to
47 Jouberin (Jbn) protein in mouse leads to the cystic kidney disease nephronophthisis, owing to an unex
48                                              Cystic kidney disease represents a major cause of end-st
49 e of the simple mendelian disorder medullary cystic kidney disease type 1 (MCKD1), mapped more than a
50 nile hyperuricemic nephropathy and medullary cystic kidney disease type 2.
51             Defects in primary cilia lead to cystic kidney disease, although the ciliary mechanisms t
52 Variable features include retinal dystrophy, cystic kidney disease, and liver fibrosis.
53 fier role for the 'trans' polycystin gene in cystic kidney disease, and support a contribution from t
54 on and function are the predominant cause of cystic kidney disease, and that the genes identified her
55  The jck mouse is another model of recessive cystic kidney disease, and this mouse harbors a missense
56 t recipients, especially those with acquired cystic kidney disease, are at increased risk for renal c
57 ants, these pathological alterations include cystic kidney disease, biliary and pancreatic duct abnor
58 ominant polycystic kidney disease, medullary cystic kidney disease, diabetic nephropathy, or CKD of u
59 l development, as well as diseases including cystic kidney disease, hydrocephalus and situs inversus.
60 hronophthisis (NPHP), an autosomal-recessive cystic kidney disease, is the most frequent genetic caus
61         Nephronophthisis (NPHP), a recessive cystic kidney disease, is the most frequent genetic caus
62 al manifestation of JBTS is a juvenile-onset cystic kidney disease, known as nephronophthisis, typica
63 hronophthisis (NPHP), an autosomal recessive cystic kidney disease, leads to chronic renal failure in
64  homologues associated with diseases such as cystic kidney disease, male sterility, and hydrocephalus
65 h as the miR-17 approximately 92 cluster and cystic kidney disease, miR-92a and von Hippel-Lindau syn
66 8 being the NPHP9 gene in the human juvenile cystic kidney disease, nephronophthisis.
67 d long term and developed slowly progressive cystic kidney disease, renal fibrosis, and hydronephrosi
68 hronophthisis (NPHP), an autosomal recessive cystic kidney disease, represents the most frequent gene
69 anscriptional control in the pathogenesis of cystic kidney disease, retinal degeneration, and central
70 fied in association with inherited causes of cystic kidney disease, the molecular mechanisms that reg
71  which harbors candidate genes for medullary cystic kidney disease, whereas mouse Rhbg is syntenic on
72             In addition, mutant mice develop cystic kidney disease, with markedly increased tubule di
73    We report that loss of murine Thm1 causes cystic kidney disease, with persistent proliferation of
74 s a critical role in situs determination and cystic kidney disease, yet its exact function remains un
75 mplications toward mitochondrial fitness and cystic kidney disease.
76 sive polycystic kidney disease, or medullary cystic kidney disease.
77 that block the assembly of these cilia cause cystic kidney disease.
78 sufficient to exacerbate the pathogenesis of cystic kidney disease.
79 to UUO is similar in a number of respects to cystic kidney disease.
80  kidneys, renal agenesis, hydronephrosis and cystic kidney disease.
81 ved in epithelial-mesenchymal transition and cystic kidney disease.
82 ation is associated with the pathogenesis of cystic kidney disease.
83 cific treatments available for patients with cystic kidney disease.
84 n has been implicated in the pathogenesis of cystic kidney disease.
85 riably associated with retinal dystrophy and cystic kidney disease.
86 idney size, which is an index of severity of cystic kidney disease.
87 ent of these localization motifs may lead to cystic kidney disease.
88 idism halts late-stage progression of rodent cystic kidney disease.
89 dney homeostasis, the loss of which leads to cystic kidney disease.
90 rk of ciliary dysfunction analogous to human cystic kidney disease.
91 e pronephros) is simple and genes that cause cystic kidney diseases (CKD) in humans, cause pronephric
92                                              Cystic kidney diseases (CKDs) affect millions of people
93 anism that links the Hh signaling pathway to cystic kidney diseases and can open new avenues for the
94  that are elucidating the genetic defects of cystic kidney diseases and providing clues about the pat
95 e complex, support the unifying concept that cystic kidney diseases are "ciliopathies".
96                                              Cystic kidney diseases are common renal disorders charac
97 anism for dysregulation of cAMP signaling in cystic kidney diseases arising from different gene mutat
98 ontributed to a unifying theory that defines cystic kidney diseases as "ciliopathies." The theory is
99 st formation may guide potential therapy for cystic kidney diseases by targeting the structural and f
100                      Patients with inherited cystic kidney diseases have progressive cystic dilation
101 he products of all genes that are mutated in cystic kidney diseases in humans, mice, or zebrafish are
102  on the finding that all proteins mutated in cystic kidney diseases of humans or animal models are ex
103 sts inhibit cystogenesis in animal models of cystic kidney diseases, presumably by downregulating cAM
104 HP) comprises a group of autosomal recessive cystic kidney diseases, which constitute the most freque
105 cilia development, cilia function, and human cystic kidney diseases.
106 genes that are known to be involved in human cystic kidney diseases.
107  and pkd2, are already associated with human cystic kidney diseases.
108 he abnormal planar cell polarity observed in cystic kidney diseases.
109  has helped advance a new unifying theory of cystic kidney diseases.
110 syndrome (JBTS) are a group of heterogeneous cystic kidney disorders with partially overlapping loci.
111  response that links replication stress with cystic kidney disorders.
112 ss of polarity and enhanced proliferation in cystic kidney epithelium.
113 schemia-reperfusion injury as a "third hit." Cystic kidneys exhibited striking upregulation and activ
114     arl13b was initially cloned as the novel cystic kidney gene scorpion (sco) in zebrafish and was s
115             Here, we show that the zebrafish cystic kidney gene seahorse is closely associated with c
116  GFR, and the progressive enlargement of the cystic kidneys in adult ADPKD.
117  whether loss of function of Arl13b leads to cystic kidneys in mammals, we generated a mouse model wi
118                 Treatment of mouse Pkd1-null cystic kidneys in organ culture with a c-Met pharmacolog
119 l cysts and management strategies for use of cystic kidneys in transplantation are presented.
120  Similar to autosomal dominant PKD, juvenile cystic kidney (jck) mice develop cysts in multiple nephr
121 ey disease (PKD) progression in the juvenile cystic kidney (jck) mutation can be influenced by an epi
122      The murine autosomal recessive juvenile cystic kidney (jck) mutation results in polycystic kidne
123 usion to map the recessive mutation juvenile cystic kidney (jck) to mouse chromosome 11 using an inte
124 odes a ciliary kinase, produces the juvenile cystic kidneys (jck) model of polycystic kidney disease,
125 g-lasting attenuation of PKD in the juvenile cystic kidneys (jck) mouse model of nephronophthisis by
126 sly showed slows cyst progression in a mouse cystic kidney model with neonatal inactivation of Pkd1,
127 ediator of cAMP signaling, in developing and cystic kidney models.
128 of polycystic kidney disease in the juvenile cystic kidney mouse.
129  kinase that is mutated in the jck (juvenile cystic kidneys) mouse, a model of autosomal recessive ju
130 idative stress, was shown to be increased in cystic kidneys of mice and rats in a pattern that reflec
131 eroxidase were also reduced in plasma and in cystic kidneys of mice and rats.
132 dney cells and promoted miR-21 expression in cystic kidneys of mice.
133 was also observed in Pkd2-/-placentae and in cystic kidneys of Pkd1cond/-; Meox2cre/+ mice.
134 ng was carried out using RNA from normal and cystic kidneys of the C57BL/6J-cpk mouse.
135 ed misregulation of multiple pathways in the cystic kidneys of this model.
136 cripts of Hedgehog target genes increased in cystic kidneys of two other orthologous mouse mutants, j
137 the perinatal period with massively enlarged cystic kidneys, pancreatic ductal cysts and pulmonary hy
138                            Surprisingly, the cystic kidney pathology in these mutants is dependent on
139 nction, supporting the idea that the lack of cystic kidney phenotype in human patients with ARL13B mu
140  Flcn knockout mice did not rescue the multi-cystic kidney phenotype.
141 d to result from increased expression by the cystic kidneys predominantly in the second and third pos
142 somal-recessive ciliopathies presenting with cystic kidneys, retinal degeneration, and cerebellar/neu
143 ive of the timing of Pkd1 gene inactivation, cystic kidneys showed enhanced uptake of (13)C-glucose a
144 n ventral body curvature, hydrocephalus, and cystic kidneys, similar to the effects of knocking down
145 nfantile nephronophthisis is associated with cystic kidneys, situs inversus, and INVS mutations.
146 lial cells, causing the development of large cystic kidneys that characterize autosomal dominant poly
147 otypes ranging from retinal degeneration and cystic kidneys to neural tube defects.
148 ctivation on the enlargement and function of cystic kidneys was evaluated.
149 expression levels and activity in normal and cystic kidneys were far greater for MMP-2.
150 n humans, Pax2 is also expressed in juvenile cystic kidneys where it correlates with cell proliferati
151 els of sphingoid base-containing isoforms in cystic kidneys, whereas changes were subtle for Gb4Cer-c
152 c-Myc upregulates miR-17 approximately 92 in cystic kidneys, which in turn aggravates cyst growth by
153  before postnatal day 13 results in severely cystic kidneys within 3 weeks, whereas inactivation at d

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