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1 cytoskeleton and junction remodeling in the tubular epithelium.
2 ered to Bowman's capsule and infiltrated the tubular epithelium.
3 docytes and the brush border of the proximal tubular epithelium.
4 l component C3, principally expressed by the tubular epithelium.
5 g the structural and functional integrity of tubular epithelium.
6 s and might facilitate the recovery of renal tubular epithelium.
7 nd were intimately associated with the renal tubular epithelium.
8 y of nonhematologic tissues, including renal tubular epithelium.
9 rafts is isometric vacuolization of proximal tubular epithelium.
10 n and proliferate to re-establish the normal tubular epithelium.
11 ion is predominantly found in the collecting tubular epithelium.
12 14% that of wild-type mice and is limited to tubular epithelium.
13 graft functional elements such as the renal tubular epithelium.
14 coronary and intrarenal vessels and in renal tubular epithelium.
15 primitive inner ear cells, and seminiferous tubular epithelium.
16 increased in renal glomeruli and induced in tubular epithelium.
17 pression remains in most, if not all, of the tubular epithelium.
18 ithrombin was found only within the proximal tubular epithelium.
19 and fewer cells than normal are converted to tubular epithelium.
20 s and on the apical surface of the trachea's tubular epithelium.
21 epithelium (11 of 11 cases), proximal renal tubular epithelium (5 of 5 cases), colonic ganglion cell
24 xclusively in the degenerated, dilated renal tubular epithelium after unilateral ureteral obstruction
25 esults suggest that TGFbeta signaling in the tubular epithelium alone is sufficient to cause acute tu
26 odel, activation of TGFbeta signaling in the tubular epithelium alone was sufficient to cause AKI cha
27 ion reveals increased Nox4 expression in the tubular epithelium also during obstructive nephropathy.
29 dextran-labeled cells were restricted to the tubular epithelium and excluded from the interstitium.
30 normal transition of induced mesenchyme into tubular epithelium and full growth and branching of the
31 aining was diminished in the nuclei of renal tubular epithelium and interstitium after obstructive in
32 butes to the maintenance and repair of renal tubular epithelium and may be a novel therapeutic target
33 hed podocytes crawling on the surface of the tubular epithelium and occasionally, in contact with per
34 tegration and necrosis of the renal proximal tubular epithelium and of the intestinal mucosal epithel
36 in mediating cell dedifferentiation of renal tubular epithelium and suggest that EMT is a multistep p
37 tes to renal IRI by a direct effect on renal tubular epithelium and that this effect is independent o
38 e mAb prevented the deposition of C3b on the tubular epithelium and the generation of systemic C3a af
39 chanistically interesting features in kidney tubular epithelium, and that somatic mutation may play a
40 asts, a loss of functional microvilli on the tubular epithelium, and varying degrees of chronic inter
41 ression of a complement inhibitor within the tubular epithelium appears to be a critical factor permi
42 cells in crescents, parietal epithelium, and tubular epithelium, as well as by infiltrating leukocyte
43 erentiation of the condensed mesenchyme into tubular epithelium, as well as the rate of growth and br
44 pha production specifically within the renal tubular epithelium attenuated the AKI and the increase i
45 in is expressed in the human embryonic renal tubular epithelium beginning on approximately day 75 to
46 2 activation and its nuclear accumulation in tubular epithelium, but it restored SnoN protein abundan
47 n DNA fragmentation and cell death in kidney tubular epithelium, but the endonucleases responsible fo
48 n of HIV-1-specific proviral DNA and mRNA in tubular epithelium cells, argue strongly for localized r
49 e with a targeted deletion for Alk3 in their tubular epithelium did not respond to therapy with THR-1
50 t of CD8 effectors that infiltrate the graft tubular epithelium during clinical rejection episodes, p
51 ndings of increased synthesis of C3 in human tubular epithelium exposed to high concentrations of pro
54 ased in rejected kidney, particularly in the tubular epithelium; however, enzymatic activity was sign
55 low expression of PAI-1 mRNA and protein in tubular epithelium in beta6(-/-) UUO kidneys, with incre
56 ta-catenin is induced predominantly in renal tubular epithelium in CKD, surprisingly, depletion of tu
57 of proliferating cell nuclear antigen in the tubular epithelium, inflammatory cell infiltrate, and ne
61 Recently we have established that the kidney tubular epithelium is repaired by surviving epithelial c
62 ent morphogenesis and differentiation of the tubular epithelium lead to the establishment of a functi
64 intercalation of cells into the plane of the tubular epithelium maintained the normal tubular morphol
65 olycystin-1 from its basolateral location in tubular epithelium may alter critical pathways controlli
66 ed that NRP mediates attachment to the renal tubular epithelium of Ca stone crystals through an elect
68 mmunostaining for nitrotyrosine localized to tubular epithelium of chronically rejected human renal a
69 ion of clusterin mRNA occurred mostly in the tubular epithelium of dilated, convoluted proximal tubul
70 Nlrp3 and Asc were highly expressed in renal tubular epithelium of humans and mice, and the absence o
75 ly for the formation of the undifferentiated tubular epithelium of the nascent pancreatic rudiment an
77 t receptor 1-related protein y (Crry) in the tubular epithelium preceded activation of the alternativ
78 w that complement inhibitors targeted to the tubular epithelium protect against tubulointerstitial in
79 transgene expression was localized to kidney tubular epithelium rather than vascular endothelial cell
81 borne by albumin into endocytosing proximal tubular epithelium results in the synthesis and release
82 gastrointestinal mucosal and renal proximal tubular epithelium, the Gb3 receptor glycolipid of the r
84 cused on the transformation of the organized tubular epithelium to the myofibroblastic phenotype, a p
86 ion of RANTES was localized primarily to the tubular epithelium, underscoring a role for tubular cell
87 he transition of nascent epithelial cells to tubular epithelium was derived, helping to reconcile in
89 esponse in PVAN is partly coordinated by the tubular epithelium, whereas in TCMR, this may be control
90 seen by a profound increase in proliferating tubular epithelium, which coincided with increased hepat
91 t-AKI, and activates RA signaling in injured tubular epithelium, which in turn promotes alternatively
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