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1 und accumulated in the lysosomes of proximal renal tubular cells.
2 th phosphorylation of RB and AKT in cultured renal tubular cells.
3  impact of the SARS-CoV-2 infection upon the renal tubular cells.
4 IS down-regulated C/EBPbeta in primary human renal tubular cells.
5 aimed at repressing HIF-1alpha expression in renal tubular cells.
6 g was examined in Intu-knockdown and control renal tubular cells.
7  a regulator of mitochondrial dysfunction in renal tubular cells.
8 iates albumin-induced profibrotic effects in renal tubular cells.
9 rker for detecting ER stress in podocytes or renal tubular cells.
10 abundantly expressed in podocytes but not in renal tubular cells.
11 nction caused by ischemic or toxic injury to renal tubular cells.
12 ion and fibrosis that is highly expressed in renal tubular cells.
13 ot induce apoptosis or regulated necrosis of renal tubular cells.
14  Gas6 receptor Axl in the apical membrane of renal tubular cells.
15 pathways leading to apoptosis or survival in renal tubular cells.
16 l-mesenchymal transition induced by FGF-2 in renal tubular cells.
17 n in mouse inner medullary collecting duct-3 renal tubular cells.
18 rkers of M2 macrophages when cocultured with renal tubular cells.
19 ithelial sodium channel alpha, ENaCalpha, in renal tubular cells.
20 s a critical role in TGF-beta-induced EMT of renal tubular cells.
21  created by knocking out Tsc1 in a subset of renal tubular cells.
22 glucose-induced mitochondrial dysfunction in renal tubular cells.
23 s on the viability of islets, podocytes, and renal tubular cells.
24  the mechanism that enables viral entry into renal tubular cells.
25 eases in GAPDH and pax2 abundance in NRK-52E renal tubular cells.
26 ss 1 phosphatidylinositol 3-kinase (PI3K) in renal tubular cells.
27 or against oxidative and apoptotic damage in renal tubular cells.
28 lates membrane potential and K+ secretion in renal tubular cells.
29  an integral part of the injury phenotype of renal tubular cells.
30  beta-tubulin colocalize to primary cilia of renal tubular cells.
31 ) crystal-binding proteins on the surface of renal tubular cells.
32 nal protection required both macrophages and renal tubular cells.
33 a occludens (ZA) induced by ATP depletion of renal tubular cells.
34    Similar results were obtained in cultured renal tubular cells.
35                                  In cultured renal tubular cells, 20 microM cisplatin induced approxi
36 nockdown suppressed scratch wound healing in renal tubular cells, accompanied by the abnormality of c
37 chemia is characterized by disruption of the renal tubular cell actin cytoskeleton, this study was co
38 ysiological osmoregulatory mechanism whereby renal tubular cells adjust to the intraluminal hyperosmo
39    beta 1 integrin-mediated adhesion between renal tubular cells after anoxic injury.
40 port to show that HSC can differentiate into renal tubular cells after I/R injury.
41 in the kidney and most likely is degraded in renal tubular cells after reabsorption.
42 romising therapeutic strategy for protecting renal tubular cells against cisplatin-induced AKI by enh
43 was found for cell fusion between indigenous renal tubular cells and BMDC, but this was infrequent an
44 ll types including the vascular endothelium, renal tubular cells and erythrocytes.
45                               Whereas murine renal tubular cells and freshly isolated renal tubules r
46 sue remodeling using cultured human proximal renal tubular cells and half-nephrectomized mice treated
47  cisplatin accumulates preferentially in the renal tubular cells and is a frequent cause of drug-indu
48   NGAL is a glycoprotein released by damaged renal tubular cells and is a sensitive maker of both cli
49 ciated with the apical membranes of cultured renal tubular cells and is bound to membrane skeletal el
50 ecific receptors located on osteoblastic and renal tubular cells and is fully functional as the N-ter
51 ologic analysis revealed Pals1 expression in renal tubular cells and podocytes of human kidneys.
52    In vitro, SCFAs modulated inflammation in renal tubular cells and podocytes under hyperglycemic co
53 asure the significant uptake of polymyxin in renal tubular cells and provides crucial information for
54 d ADV may cause mitochondrial dysfunction in renal tubular cells and reprogramming of glucose metabol
55         We showed that CLUH was expressed in renal tubular cells and that its expression and activity
56  = 3) showed increased elastin expression in renal tubular cells and the interstitium but not glomeru
57 e proteins shows a predominant expression in renal tubular cells and the localization of immunoreacti
58  present on the surface of oligodendrocytes, renal tubular cells, and certain tumor cells.
59  in immortalized patient NPHP1 urine-derived renal tubular cells, and improved ciliary and kidney phe
60  production during the cold storage of human renal tubular cells, and to define the roles of extrinsi
61 Bax and Bak from proximal tubules attenuated renal tubular cell apoptosis and suppressed renal inters
62  delivery of HSP72 inhibits ischemia-induced renal tubular cell apoptosis by preventing NF-kappaB act
63 ll death per se, it dramatically potentiated renal tubular cell apoptosis initiated by other death cu
64 production, with increased kidney injury and renal tubular cell apoptosis.
65 utralization also inhibited ischemia-induced renal tubular cell apoptosis.
66 anscription, and subsequent ischemia-induced renal tubular cell apoptosis.
67  common in sepsis but presents focally; most renal tubular cells appear normal.
68          Myofibroblasts produced from EMT of renal tubular cells are responsible for the deposition o
69 y involved in the circadian clock system, in renal tubular cells (Bmal1(lox/lox)/Pax8-rtTA/LC1 mice).
70 e also demonstrated a role for endostatin in renal tubular cell branching morphogenesis and show that
71  growth factor (EGF) causes proliferation in renal tubular cells but, when it is combined with transf
72 -beta) plays an essential role in the EMT of renal tubular cells, but the molecular mechanism governi
73 he regenerative capacity of actively cycling renal tubular cells by decreasing the number of cells in
74                    In summary, activation of renal tubular cells by infiltrating T cells can amplify
75  altered exposure of Ax-II on the surface of renal tubular cells could promote crystal retention and
76 t of miR-26a on apoptosis was evaluated in a renal tubular cell culture.
77 ional intervention reduced hemolysis-related renal tubular cell damage, hepatocyte damage, ileal leak
78 f mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, rem
79 nistered to donor or recipient decreased the renal tubular cell death, inflammation, and MHC II expre
80 f persistent Cav-EGFR-ERK signaling mediates renal tubular cell dedifferentiation and identifies a no
81  with acute tubular necrosis, apoptosis, and renal tubular cell desquamation, with toxic vacuolizatio
82                                              Renal tubular cells do not express any of the known HIV-
83 mmed necrosis (necroptosis), which occurs in renal tubular cells during AKI.
84                                              Renal tubular cells elicit adaptive responses following
85 e of C5b-9 in complement-mediated effects on renal tubular cells exposed to proteinuric urine, equiva
86                 We show that Pkd1 -deficient renal tubular cells express high levels of cGAS, the mai
87     Functionally, OTUD5 deletion intensifies renal tubular cell ferroptosis and exacerbates acute kid
88 obin, resulting in increased endothelial and renal tubular cell free iron, which is associated with r
89 ent results demonstrate that TMIGD1 protects renal tubular cells from renal injury in different model
90 t mediates internalization of the virus into renal tubular cells, from which the virus can be rescued
91 f type I interferons, such as keratinocytes, renal tubular cells, glial cells and synovial stromal ce
92 n of renal vessels and induces hypertension, renal tubular cell hypertrophy, and podocyte apoptosis.
93 he expression of membrane sodium channels in renal tubular cells in a manner dependent on the metabol
94 ty is associated with a beneficial effect on renal tubular cells in AKI.
95 owed iron accumulation on the apical side of renal tubular cells in Heph/Cp KO mice.
96  Factor H was present on the urinary side of renal tubular cells in proteinuric, but not in normal re
97 d secreted by immune cells, hepatocytes, and renal tubular cells in various pathologic states.
98 is effects of kaempferol and esculetin using renal tubular cells in vitro and in vivo in a mouse Unil
99           Consistently, in cisplatin-injured renal tubular cells in vitro, lithium enhanced autophagi
100  viability of islets and HK-2 human proximal renal tubular cells in vitro.
101  renal tubular cells, penetrated live murine renal tubular cells in vivo, and localized in the cell n
102 , isolated tumor cells as well as in primary renal tubular cells, in which HIF was stabilized, we det
103 ng by TRIM59 plays a significant role in the renal tubular cell injury caused by SARS-CoV-2, which su
104                                              Renal tubular cell injury causes dysregulation of SR-B1,
105 which was coincident with renal dysfunction, renal tubular cell injury/apoptosis, and proliferation.
106                     CLUH loss of function in renal tubular cells is associated with mitochondrial dys
107 lation and concentration of polymyxin within renal tubular cells is essential for the development of
108 capacity for autophagy in both podocytes and renal tubular cells is markedly impaired in type 2 diabe
109 primary cultures treated with cyclosporin A, renal tubular cells isolated from Nupr1-deficient mice e
110 d the dedifferentiation and proliferation of renal tubular cells, key regenerative processes in injur
111 using fluorescence-activated cell sorting of renal tubular cells labeled with segment-specific fluore
112 found on the surface of lysosomes and that a renal tubular cell line deficient in OCRL accumulated su
113 ling and caused cellular injury in the human renal tubular cell line.
114  in a doxycycline-regulated Smad7-expressing renal tubular cell line.
115 ced (thermal stress, 43 degrees Cx1 hour) in renal tubular cells (LLC-PK1) with Western blot confirma
116                                     Death of renal tubular cells may occur by apoptosis during develo
117       Renal biopsy data further suggest that renal tubular cells may serve as reservoir for HIV-1.
118  ATP depletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was obs
119 entified that bound membranes of fixed human renal tubular cells, penetrated live murine renal tubula
120 lting in decreased mouse survival, decreased renal tubular cell proliferation and decreased renal rep
121             Primary cilia dysfunction alters renal tubular cell proliferation and differentiation and
122 UN levels, and was associated with increased renal tubular cell proliferation and plasma lactate leve
123       JMJD3 inhibition by GSKJ4 also reduced renal tubular cell proliferation and suppressed expressi
124 ulated proinflammatory macrophages, promoted renal tubular cell proliferation.
125                         Knockdown of Fat1 in renal tubular cells reduces migration, decreases active
126 r in situ We now show that EV from adult rat renal tubular cells significantly improved renal functio
127 important role as an epigenetic regulator of renal tubular cell survival and regenerative pathways fo
128  indices of glomerular injury or to suppress renal tubular cell TGF-beta in D.
129 parameters in D, as well as the increases in renal tubular cell TGF-beta seen in D.
130                      2-OHE had no effects on renal tubular cell TGF-beta, but it significantly reduce
131                                           In renal tubular cells, TGF-beta1 administration upregulate
132 tein fibronectin in high glucose-conditioned renal tubular cells than in normal glucose cells.
133         In all cases, renal cysts arise from renal tubular cells that lose the capacity to produce Pk
134 nhibitors might modulate glucose influx into renal tubular cells, thereby regulating the metabolic co
135                     HIF-2alpha activation in renal tubular cells upregulated mRNA and protein express
136 ated A2-restricted peptides most abundant in renal tubular cells, we identified 2 immunogenic kidney
137                                        Human renal tubular cells were cold-stored at 4 degrees C for
138 s of patients shedding polyomavirus-infected renal tubular cells were compared with those of patients
139 ransforming growth factor-beta (TGF-beta) in renal tubular cells were significantly higher in PAN nep
140      The objective was to determine in human renal tubular cells whether apoptosis is specific for re
141 cyte-macrophage colony-stimulating factor by renal tubular cells, which directly stimulates expressio
142     Albumin induced features of ER stress in renal tubular cells with ATF3/ATF4 activation.
143 of the native kidneys of this patient showed renal tubular cells with intranuclear inclusions charact
144 on of cell cycle pathways was seen in murine renal tubular cells with NOTCH overexpression, and molec

 
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