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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
13 r Pkd2) and structure (Tg737) play a role in cystic kidney and aneurysm through survivin downregulati
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.
20 ebrafish caused ciliary paralysis leading to cystic kidneys and otolith defects and that knockdown in
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
30 es were observed in heterozygotes, including cystic kidney, craniofacial malformations, microphthalmi
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
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.
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
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
49 e of the simple mendelian disorder medullary cystic kidney disease type 1 (MCKD1), mapped more than a
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
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
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
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
91 e pronephros) is simple and genes that cause cystic kidney diseases (CKD) in humans, cause pronephric
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
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
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
110 syndrome (JBTS) are a group of heterogeneous cystic kidney disorders with partially overlapping loci.
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
117 whether loss of function of Arl13b leads to cystic kidneys in mammals, we generated a mouse model wi
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,
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
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
139 nction, supporting the idea that the lack of cystic kidney phenotype in human patients with ARL13B mu
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
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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