ライフサイエンスコーパス: tubular epithelia

1 in conferring apical character in Drosophila tubular epithelia.

2 n both the MDCK cyst model and in Drosophila tubular epithelia.

3 ly been identified in primary cilia in renal tubular epithelia.

4 thelial cells, is produced by glomerular and tubular epithelia.

5 n, capillary formation, and proliferation of tubular epithelia.

6 e induction of proinflammatory failed-repair tubular epithelia.

7 berrantly increased AGS3 expression in renal tubular epithelia affected by PKD and epithelial cell pr

8 t postischemic NF-kappaB activation in renal tubular epithelia aggravates tubular injury and exacerba

9 expressed in the apical membrane of proximal tubular epithelia and functions to reabsorb filtered pho

10 ced widespread NF-kappaB activation in renal tubular epithelia and in interstitial cells that peaked

11 PA) is expressed in glomerular podocytes and tubular epithelia and metabolizes angiotensin II (AngII)

12 NBCe1 variants expressed beyond the proximal tubular epithelia and potential limitations of pH correc

13 ey organoids have been described as strictly tubular epithelia and termed tubuloids.

14 Tip47-positive lipid droplets in glomeruli, tubular epithelia, and macrophages was accompanied by th

15 Tubular epithelia are a basic building block of organs a

16 Cells of the normal tubular epithelia are columnar and wedge-shaped, and cel

17 l disease-related fibroblasts originate from tubular epithelia at the site of injury.

18 Analysis of isolated tubular epithelia by FACS from bigenic SLC34a1-CreERt2;

19 Lineage tracing analysis of proximal tubular epithelia demonstrated that the tubular epitheli

20 stin-1 (PC1) or polycystin-2 (PC2), in which tubular epithelia form fluid-filled cysts.

21 ogical studies localized polycystin to renal tubular epithelia, hepatic bile ductules, and pancreatic

22 nserved mechanism that can elongate edgeless tubular epithelia in a process distinct from those that

23 In vivo, ILK was markedly induced in renal tubular epithelia in mouse models of chronic renal disea

24 APOL1 localized to proximal tubular epithelia in normal kidneys, FSGS, and HIVAN.

25 apical surfaces of epidermal cells and some tubular epithelia, including the excretory duct and pore

26 d that loss of mechanosensation in the renal tubular epithelia is a feature of PKD cysts.

27 d immature glomeruli, and the renal proximal tubular epithelia lacked proper localization of adhesion

28 53 and subsequent pro-apoptotic signaling in tubular epithelia of cisplatin-treated mice, leading to

29 culature, alongside renal tubules comprising tubular epithelia of different nephron segments.

30 The kidney tubular epithelia of KO animals were poorly differentiat

31 r patterns of lesion growth were observed in tubular epithelia of the liver and lung; this finding id

32 intensity of immunostaining was detected in tubular epithelia of the proximal tubule, thick ascendin

33 with tissue-specific deletion of Adora2b in tubular epithelia or vascular endothelia implicated endo

34 ad involution, and broaden and shorten other tubular epithelia (salivary glands, tracheae, and hindgu

35 mammalian airways are branching networks of tubular epithelia that deliver oxygen to the organism.

36 The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases

37 imal tubular epithelia demonstrated that the tubular epithelia that underwent multiple rounds of cell

38 d into a developing kidney and contribute to tubular epithelia, the ability to generate renal precurs

39 that the alpha8 integrin chain is induced in tubular epithelia undergoing dedifferentiation and contr

40 ell line, glomerulogenesis was abolished but tubular epithelia were expanded (0 glomeruli, 47 tubules

41 and a medullary region composed of elongated tubular epithelia where urine is concentrated.

42 ey rudiments, treated ES cells contribute to tubular epithelia with near 100% efficiency.