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1 fewer patients have simple cysts or acquired cystic kidney disease.
2 sufficient to exacerbate the pathogenesis of cystic kidney disease.
3  kidneys, renal agenesis, hydronephrosis and cystic kidney disease.
4 mprove therapeutic efficacy in patients with cystic kidney disease.
5 everity, we generated a single-cell atlas of cystic kidney disease.
6 iation persisted only for recipients without cystic kidney disease.
7 ved in epithelial-mesenchymal transition and cystic kidney disease.
8  patient affected with progressive medullary cystic kidney disease.
9 ation is associated with the pathogenesis of cystic kidney disease.
10 cific treatments available for patients with cystic kidney disease.
11 n has been implicated in the pathogenesis of cystic kidney disease.
12 riably associated with retinal dystrophy and cystic kidney disease.
13 idney size, which is an index of severity of cystic kidney disease.
14 ent of these localization motifs may lead to cystic kidney disease.
15 idism halts late-stage progression of rodent cystic kidney disease.
16 dney homeostasis, the loss of which leads to cystic kidney disease.
17 rk of ciliary dysfunction analogous to human cystic kidney disease.
18 sive polycystic kidney disease, or medullary cystic kidney disease.
19 mplications toward mitochondrial fitness and cystic kidney disease.
20 that block the assembly of these cilia cause cystic kidney disease.
21 to UUO is similar in a number of respects to cystic kidney disease.
22 h polycystic liver disease and in some cases cystic kidney disease.
23  had variants in other genes associated with cystic kidney disease.
24  the diversity of immune cell involvement in cystic kidney disease.
25 n PKD1, PKD2, or other genes associated with cystic kidney disease.
26 a similar manner to that observed in various cystic kidney diseases.
27 he abnormal planar cell polarity observed in cystic kidney diseases.
28  has helped advance a new unifying theory of cystic kidney diseases.
29 cilia development, cilia function, and human cystic kidney diseases.
30 genes that are known to be involved in human cystic kidney diseases.
31  and pkd2, are already associated with human cystic kidney diseases.
32 %] vs 10 530 [35%]), and less likely to have cystic kidney disease (2530 [6%] vs 4600 [15%]).
33 o 2.42, 95% confidence interval: 1.53-3.85), cystic kidney disease (3.03, 1.26-7.31), and nephrolithi
34  focal segmental glomerulosclerosis (18.0%), cystic kidney disease (9.0%), alternative complement pat
35               Mutations of HNF-1beta produce cystic kidney disease, a phenotype associated with dereg
36  cell carcinoma in association with acquired cystic kidney disease (ACKD).
37 mpared with those with glomerulonephritis or cystic kidney disease (adjusted hazard ratio [aHR], 0.96
38 of ESKD, including (1) glomerulonephritis or cystic kidney disease (adjusted subhazard ratio [aSHR],
39 ile nephronophthisis, an autosomal recessive cystic kidney disease afflicting children and young adul
40 set CKD, focal segmental glomerulosclerosis, cystic kidney disease, alternative complement pathway-as
41             Defects in primary cilia lead to cystic kidney disease, although the ciliary mechanisms t
42 pients with and without primary diagnoses of cystic kidney disease and for transplants from African A
43 e polaris (Tg737), a protein associated with cystic kidney disease and left-right axis patterning def
44 uently associated with nephronophthisis-like cystic kidney disease and other organ manifestations.
45 ronophthisis (NPH) is an autosomal-recessive cystic kidney disease and represents the most common gen
46 re Nephronophthisis (NPHP), characterized by cystic kidney disease and retinal degeneration, and Meck
47 have been linked to human diseases including cystic kidney disease and retinitis pigmentosa.
48 study reveals segment-specific mechanisms in cystic kidney disease and suggests Grhl2 as a modifier o
49 ing another link between proteins mutated in cystic kidney disease and their localization to cilia an
50 an aminopeptidase XPNPEP3 is associated with cystic kidney disease and TNF-TNFR2 cellular signaling.
51 anism that links the Hh signaling pathway to cystic kidney diseases and can open new avenues for the
52  that are elucidating the genetic defects of cystic kidney diseases and providing clues about the pat
53 (DKD), loss of bicaudal C is associated with cystic kidney diseases and Y-box binding protein 1 has b
54 Variable features include retinal dystrophy, cystic kidney disease, and liver fibrosis.
55 fier role for the 'trans' polycystin gene in cystic kidney disease, and support a contribution from t
56 on and function are the predominant cause of cystic kidney disease, and that the genes identified her
57  The jck mouse is another model of recessive cystic kidney disease, and this mouse harbors a missense
58                   Animal models of inherited cystic kidney disease are useful for study of the pathog
59 e complex, support the unifying concept that cystic kidney diseases are "ciliopathies".
60                                              Cystic kidney diseases are common renal disorders charac
61 t recipients, especially those with acquired cystic kidney disease, are at increased risk for renal c
62 anism for dysregulation of cAMP signaling in cystic kidney diseases arising from different gene mutat
63                     Mutant mice present with cystic kidney disease as neonates.
64 ontributed to a unifying theory that defines cystic kidney diseases as "ciliopathies." The theory is
65 ants, these pathological alterations include cystic kidney disease, biliary and pancreatic duct abnor
66 st formation may guide potential therapy for cystic kidney diseases by targeting the structural and f
67 e pronephros) is simple and genes that cause cystic kidney diseases (CKD) in humans, cause pronephric
68                                              Cystic kidney diseases (CKDs) affect millions of people
69            Rats with spontaneous progressive cystic kidney disease (Cy/+ (IU)) and normal littermates
70 gotes were significantly more likely to have cystic kidney disease, defined as four or more kidney cy
71  However, these mice eventually succumbed to cystic kidney disease despite mTORC1 inactivation.
72 ominant polycystic kidney disease, medullary cystic kidney disease, diabetic nephropathy, or CKD of u
73 was also dramatically up-regulated in murine cystic kidney disease epithelia [jck/jck (nek8) and Ift8
74 y represented among the basal body proteome: cystic kidney disease (especially nephronophthisis) synd
75 ation in pkd2, one of two autosomal dominant cystic kidney disease genes, did not show increased risk
76                   Analysis of the UK Biobank cystic kidney disease group showed probands with IFT140
77                               Progression of cystic kidney disease has been linked to activation of t
78                                              Cystic kidney disease has been linked to mutations in th
79 the native kidneys, particularly if acquired cystic kidney disease has developed during prolonged dia
80                      Patients with inherited cystic kidney diseases have progressive cystic dilation
81 l development, as well as diseases including cystic kidney disease, hydrocephalus and situs inversus.
82  PKD1, PKD2, and other genes associated with cystic kidney disease (ie, ALG8, ALG9, DNAJB11, GANAB, H
83 ygous for ALG8 PTVs are at increased risk of cystic kidney disease in a large, unselected health syst
84  A-related kinase, Nek8, are associated with cystic kidney disease in both humans and mice, with Nek8
85 snd (alias Barttin) as a genetic modifier of cystic kidney disease in Joubert syndrome, using a Cep29
86 ssive polycystic kidney disease (ARPKD) as a cystic kidney disease in which lesions are localized to
87 he products of all genes that are mutated in cystic kidney diseases in humans, mice, or zebrafish are
88                   Macrophage accumulation in cystic kidney disease is not directly regulated by the c
89         Nephronophthisis (NPHP), a recessive cystic kidney disease, is the most frequent genetic caus
90 hronophthisis (NPHP), an autosomal-recessive cystic kidney disease, is the most frequent genetic caus
91 al manifestation of JBTS is a juvenile-onset cystic kidney disease, known as nephronophthisis, typica
92 hronophthisis (NPHP), an autosomal recessive cystic kidney disease, leads to chronic renal failure in
93  homologues associated with diseases such as cystic kidney disease, male sterility, and hydrocephalus
94                          Some glomerular and cystic kidney diseases might benefit from disease-specif
95 h as the miR-17 approximately 92 cluster and cystic kidney disease, miR-92a and von Hippel-Lindau syn
96  monoallelic individuals uniformly exhibited cystic kidney disease (mostly neonatal) without consiste
97 ped on behalf of the Network for Early Onset Cystic Kidney Disease (NEOCYST) by an international grou
98 Jouberin (Jbn) protein in mouse leads to the cystic kidney disease nephronophthisis, owing to an unex
99 8 being the NPHP9 gene in the human juvenile cystic kidney disease, nephronophthisis.
100  on the finding that all proteins mutated in cystic kidney diseases of humans or animal models are ex
101 s in ALG8 result in increased risk of a mild cystic kidney disease phenotype.
102 sts inhibit cystogenesis in animal models of cystic kidney diseases, presumably by downregulating cAM
103                              Analyses of the cystic kidney disease probands of Genomics England 100K
104       However, the specific role of GRHL2 in cystic kidney disease remains unknown.
105 d long term and developed slowly progressive cystic kidney disease, renal fibrosis, and hydronephrosi
106                                              Cystic kidney disease represents a major cause of end-st
107 hronophthisis (NPHP), an autosomal recessive cystic kidney disease, represents the most frequent gene
108 anscriptional control in the pathogenesis of cystic kidney disease, retinal degeneration, and central
109 mples with ADPKD and generating a transgenic cystic kidney disease (TCKD) mouse model by overexpressi
110 fied in association with inherited causes of cystic kidney disease, the molecular mechanisms that reg
111 e of the simple mendelian disorder medullary cystic kidney disease type 1 (MCKD1), mapped more than a
112 nile hyperuricemic nephropathy and medullary cystic kidney disease type 2.
113 transcription factor Grhl2 in the context of cystic kidney disease was examined through analysis of i
114  which harbors candidate genes for medullary cystic kidney disease, whereas mouse Rhbg is syntenic on
115 HP) comprises a group of autosomal recessive cystic kidney diseases, which constitute the most freque
116             In addition, mutant mice develop cystic kidney disease, with markedly increased tubule di
117    We report that loss of murine Thm1 causes cystic kidney disease, with persistent proliferation of
118 s a critical role in situs determination and cystic kidney disease, yet its exact function remains un

 
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