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1 mplications toward mitochondrial fitness and cystic kidney disease.
2 ved in epithelial-mesenchymal transition and cystic kidney disease.
3 ation is associated with the pathogenesis of cystic kidney disease.
4 cific treatments available for patients with cystic kidney disease.
5 n has been implicated in the pathogenesis of cystic kidney disease.
6 riably associated with retinal dystrophy and cystic kidney disease.
7 idney size, which is an index of severity of cystic kidney disease.
8 ent of these localization motifs may lead to cystic kidney disease.
9 idism halts late-stage progression of rodent cystic kidney disease.
10 dney homeostasis, the loss of which leads to cystic kidney disease.
11 sufficient to exacerbate the pathogenesis of cystic kidney disease.
12 rk of ciliary dysfunction analogous to human cystic kidney disease.
13 kidneys, renal agenesis, hydronephrosis and cystic kidney disease.
14 sive polycystic kidney disease, or medullary cystic kidney disease.
15 that block the assembly of these cilia cause cystic kidney disease.
16 to UUO is similar in a number of respects to cystic kidney disease.
17 he abnormal planar cell polarity observed in cystic kidney diseases.
18 has helped advance a new unifying theory of cystic kidney diseases.
19 cilia development, cilia function, and human cystic kidney diseases.
20 genes that are known to be involved in human cystic kidney diseases.
21 and pkd2, are already associated with human cystic kidney diseases.
23 ile nephronophthisis, an autosomal recessive cystic kidney disease afflicting children and young adul
25 e polaris (Tg737), a protein associated with cystic kidney disease and left-right axis patterning def
26 ronophthisis (NPH) is an autosomal-recessive cystic kidney disease and represents the most common gen
27 re Nephronophthisis (NPHP), characterized by cystic kidney disease and retinal degeneration, and Meck
29 ing another link between proteins mutated in cystic kidney disease and their localization to cilia an
30 an aminopeptidase XPNPEP3 is associated with cystic kidney disease and TNF-TNFR2 cellular signaling.
31 anism that links the Hh signaling pathway to cystic kidney diseases and can open new avenues for the
32 that are elucidating the genetic defects of cystic kidney diseases and providing clues about the pat
34 fier role for the 'trans' polycystin gene in cystic kidney disease, and support a contribution from t
35 on and function are the predominant cause of cystic kidney disease, and that the genes identified her
36 The jck mouse is another model of recessive cystic kidney disease, and this mouse harbors a missense
40 t recipients, especially those with acquired cystic kidney disease, are at increased risk for renal c
41 anism for dysregulation of cAMP signaling in cystic kidney diseases arising from different gene mutat
43 ontributed to a unifying theory that defines cystic kidney diseases as "ciliopathies." The theory is
44 ants, these pathological alterations include cystic kidney disease, biliary and pancreatic duct abnor
45 st formation may guide potential therapy for cystic kidney diseases by targeting the structural and f
46 e pronephros) is simple and genes that cause cystic kidney diseases (CKD) in humans, cause pronephric
48 ominant polycystic kidney disease, medullary cystic kidney disease, diabetic nephropathy, or CKD of u
49 was also dramatically up-regulated in murine cystic kidney disease epithelia [jck/jck (nek8) and Ift8
50 y represented among the basal body proteome: cystic kidney disease (especially nephronophthisis) synd
51 ation in pkd2, one of two autosomal dominant cystic kidney disease genes, did not show increased risk
54 l development, as well as diseases including cystic kidney disease, hydrocephalus and situs inversus.
55 A-related kinase, Nek8, are associated with cystic kidney disease in both humans and mice, with Nek8
56 ssive polycystic kidney disease (ARPKD) as a cystic kidney disease in which lesions are localized to
57 he products of all genes that are mutated in cystic kidney diseases in humans, mice, or zebrafish are
59 hronophthisis (NPHP), an autosomal-recessive cystic kidney disease, is the most frequent genetic caus
60 al manifestation of JBTS is a juvenile-onset cystic kidney disease, known as nephronophthisis, typica
61 hronophthisis (NPHP), an autosomal recessive cystic kidney disease, leads to chronic renal failure in
62 homologues associated with diseases such as cystic kidney disease, male sterility, and hydrocephalus
63 h as the miR-17 approximately 92 cluster and cystic kidney disease, miR-92a and von Hippel-Lindau syn
64 Jouberin (Jbn) protein in mouse leads to the cystic kidney disease nephronophthisis, owing to an unex
66 on the finding that all proteins mutated in cystic kidney diseases of humans or animal models are ex
67 sts inhibit cystogenesis in animal models of cystic kidney diseases, presumably by downregulating cAM
68 d long term and developed slowly progressive cystic kidney disease, renal fibrosis, and hydronephrosi
70 hronophthisis (NPHP), an autosomal recessive cystic kidney disease, represents the most frequent gene
71 anscriptional control in the pathogenesis of cystic kidney disease, retinal degeneration, and central
72 fied in association with inherited causes of cystic kidney disease, the molecular mechanisms that reg
73 e of the simple mendelian disorder medullary cystic kidney disease type 1 (MCKD1), mapped more than a
75 which harbors candidate genes for medullary cystic kidney disease, whereas mouse Rhbg is syntenic on
76 HP) comprises a group of autosomal recessive cystic kidney diseases, which constitute the most freque
78 We report that loss of murine Thm1 causes cystic kidney disease, with persistent proliferation of
79 s a critical role in situs determination and cystic kidney disease, yet its exact function remains un
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