ライフサイエンスコーパス: Henle

1 tured human epithelial cell lines: HEp-2 and Henle-407.

2 ak cone density, rod-free zone diameter, and Henle fiber layer.

3 vea, consistent with loss in cone nuclei and Henle's fiber layer.

4 es between the outer nuclear layer (ONL) and Henle's fiber layer (HFL) were well defined, showing tha

5 lphaKG) transport in the proximal tubule and Henle's loop from reabsorption (acid load) to secretion

6 ned by the greater length of the cone axons (Henle fibers) in wider foveas.

7 P2RY5 is expressed in both Henle's and Huxley's layers of the inner root sheath of

8 125I-labeled IpaC binds cultured Henle 407 intestinal cells with an apparent dissociation

9 f serovar Typhimurium to enter into cultured Henle-407 cells or to induce macrophage cell death.

10 r invasion or multiplication within cultured Henle cells; the shuA mutant invaded and produced normal

11 nths, foveal cone cell bodies stack >6 deep, Henle fiber layer (HFL) thickens, and IS/OS length equal

12 orum was noninvasive for cultured epithelial Henle 407, chick kidney, chick ovary, and budgerigar abd

13 molarity conditions and is less invasive for Henle 407 cells.

14 neal birefringence using SLP-VCC can fail if Henle's layer is disrupted by macular disease.

15 nels are essential for NaCl re-absorption in Henle's loop and for potassium secretion by the stria va

16 different genes with increased expression in Henle cells were identified.

17 which was defective for plaque formation in Henle cell monolayers, had a reduced amount of IcsA dete

18 ponding to SSPiM appeared more frequently in Henle's fiber layer (HFL) than the inner nuclear layer (

19 vitro and during the first 3 h of growth in Henle cells in vivo.

20 ssion when S. flexneri was intracellular (in Henle cells) than when S. flexneri was extracellular (in

21 p and surA mutants failed to form plaques in Henle cell monolayers and were defective in cell surface

22 neri pst mutant to form wild-type plaques in Henle cell monolayers may be due to aberrant expression

23 flexneri pst mutant forms smaller plaques in Henle cell monolayers than does the parental strain.

24 localization or the formation of plaques in Henle cell monolayers.

25 tH promoters was higher when Shigella was in Henle cells than when it was in L broth.

26 ize corneal birefringence based on an intact Henle's layer.

27 C, are translocated into cultured intestinal Henle-407 cells.

28 eria could direct protein translocation into Henle-407 cells as this process occurred in the presence

29 that were cultured with, but did not invade, Henle cells (extracellular).

30 The degP mutant SM1100 invaded Henle cells at wild-type levels and induced apoptosis in

31 ing infection of human epithelial cell lines Henle 407, HEp-2, and HeLa.

32 delineate the axons of photoreceptor nuclei, Henle's fiber layer (HFL).

33 taining of the infundibulum, isthmus, and of Henle's layer of the inner root sheath of the lower anag

34 gulates the cortical thick ascending limb of Henle (cTALH) COX-2 expression via a p38-dependent pathw

35 surrounding cortical thick ascending limb of Henle (cTALH).

36 tion of PTH1R in the thick ascending limb of Henle (TAL) and in distal convoluted tubules (DCTs): Ksp

37 expressed along the thick ascending limb of Henle (TAL), designated NKCC2A, NKCC2B, and NKCC2F.

38 r conductance in the thick ascending limb of Henle (TAL).

39 ed, primarily in the thick ascending limb of Henle (TAL).

40 nel expressed in the thick ascending limb of Henle (TALH) and throughout the distal nephron of the ki

41 o examine whether the thin ascending limb of Henle (tALH) decreases its luminal solute concentration

42 permeability in the thin descending limb of Henle (TDLH) is required for formation of a concentrated

43 reabsorption in the thick ascending limb of Henle and a less well defined role in the inner medullar

44 alizes to the apical thick ascending limb of Henle and BSC2/NKCC1 which was isolated from a mouse IMC

45 lecting duct and the thick ascending limb of Henle and is strongly gated by internal pH in the physio

46 ey in proximal tubule and descending limb of Henle epithelia and in vasa recta endothelia.

47 oid gland and kidney thick ascending limb of Henle to sense and respond to alterations in serum calci

48 changer [NHE3]), the thick ascending limb of Henle's loop (the bumetanide-sensitive Na-K-2Cl cotransp

49 thelial cells of the thick ascending limb of Henle's loop and of the macula densa.

50 alt transport in the thick ascending limb of Henle's loop and/or the distal convoluted tubule, and th

51 ts or in a medullary thick ascending limb of Henle's loop cell line.

52 NF-kappaB pathway in thick ascending limb of Henle's loop cells of UAKD mice was detected by increase

53 yonic kidney 293 and thick ascending limb of Henle's loop cells that were transfected with mutant uro

54 lls and immortalized thick ascending limb of Henle's loop cells with wild-type and mutated uromodulin

55 n ascending limb and thick ascending limb of Henle's loop has increased greatly over the last decade.

56 the proximal tubule, thick ascending limb of Henle's loop, and cortical and medullary collecting duct

57 proximal tubule, the thick ascending limb of Henle's loop, and the collecting duct.

58 luted tubule and the thick ascending limb of Henle's loop, respectively.

59 apical domain of the thick ascending limb of Henle's loop, the connecting tubule, and in some, but no

60 collecting duct and thick ascending limb of Henle's loop.

61 reabsorption in the thick ascending limb of Henle's loop.

62 asma membrane of the thick ascending limb of Henle's loop.

63 ane of the mammalian thick ascending limb of Henle's loop.

64 ined specifically to thick ascending limb of Henle's loop.

65 the proximal tubule, thin descending limb of Henle, and vasa recta; AQP2, AQP3, and AQP4 in the colle

66 nt in differentiated thick ascending limb of Henle, collecting duct, and stroma; however, it disappea

67 on restricted to the thick ascending limb of Henle, distal convoluted, connecting and cortical collec

68 ptake pathway in the thick ascending limb of Henle, is expressed in three different full-length splic

69 cotransporter of the thick ascending limb of Henle, the Na-Cl cotransporter of the distal convoluted

70 port activity in the thick ascending limb of Henle.

71 proximal tubules and thin descending limb of Henle.

72 a and cortex and in thin descending limbs of Henle's loop in inner medulla.

73 cal membrane of the thick ascending limbs of Henle's loop was strong, whereas outer medullary collect

74 ules, predominantly thick ascending limbs of Henle's loop.

75 highly expressed in thick ascending limbs of Henle's loops and collecting ducts and weakly expressed

76 ecting tubules, and thin descending limbs of Henle's loops.

77 ollecting ducts and thick ascending limbs of Henle's loops.

78 the transport of iron occurs in the loop of Henle (LH) and collecting duct system.

79 n proximal stop flow pressure during loop of Henle (LH) perfusion at 40 nl/min with artificial tubula

80 ctivation of ion transporters in the loop of Henle (NKCC2) and distal nephron (NCC, ENaC, and pendrin

81 y in the thick ascending limb of the loop of Henle (TAL).

82 ific contribution of thick ascending loop of Henle (TALH) -derived HO-1, we generated a transgenic mo

83 lume delivery to the thick ascending loop of Henle (TALH) and macula densa, providing the error signa

84 n in the thick ascending limb of the loop of Henle (TALH) in vivo was examined in anaesthetized rats

85 interstitial fluid resorbed from the loop of Henle and collecting ducts.

86 ged or upregulated, and those in the loop of Henle and distal tubule lineages were downregulated.

87 d in the thick ascending limb of the loop of Henle and excreted in the urine.

88 II, to stimulate sodium transport in loop of Henle and the distal nephron, and to induce hypertension

89 m-chloride transporter in the kidney loop of Henle and the KCC2 potassium-chloride transporter in neu

90 ation was significantly elevated and loop of Henle Cl absorption was reduced in microperfused superfi

91 TGF responses to an increase in loop of Henle flow rate from 0 to 30 nl/min, whether determined

92 erulotubular balance response in the loop of Henle is accompanied by increased Na,K-ATPase activity.

93 Cl- transport in the loop of Henle is responsible for reclamation of 25-40% of the fi

94 al medicine because they inhibit the loop of Henle Na-K-2Cl cotransporter with much higher affinity.

95 se in THP-, NKCC2- and AQP1-positive loop of Henle nephron segments in mutant DeltaSRM kidneys.

96 hange significantly during prolonged loop of Henle perfusion in e-5'NT/CD73(+/+) mice, a complete dis

97 essure in response to an increase in loop of Henle perfusion rate from 0 to 30 nl/min was comparable

98 In separate experiments, loop of Henle perfusion with 50 microM ouabain decreased TGF res

99 o assessment of proximal tubular and loop of Henle sodium handling, to assess sodium exit after loop

100 ly reabsorbed in proximal tubule and loop of Henle) to the distal nephron in quantities equal to inge

101 al for the coordinated growth of the loop of Henle, a medullary extension of the nephron that elongat

102 ule, the thick ascending limb of the loop of Henle, and the distal convoluted tubule.

103 tinct distribution pattern along the loop of Henle, but the functional significance of this organizat

104 ific transcripts in proximal tubule, loop of Henle, distal convoluted tubule, and cortical and medull

105 4 expression in the proximal tubule, loop of Henle, distal tubule, and collecting duct and suggest th

106 ortant in sodium reabsorption in the loop of Henle, is maintained or even increased in Foxa1-deficien

107 proximal tubule (S1/S2 segment), the loop of Henle, the intercalated cells of the distal convoluted t

108 d in the thick ascending limb of the loop of Henle, whereas it is transcellular in the distal convolu

109 in the proximal convoluted tubule or loop of Henle.

110 n in the thick ascending limb of the loop of Henle.

111 sodium exit from the proximal tubule/loop of Henle.

112 ting duct predominantly but also the loop of Henle.

113 s of the thick ascending limb of the loop of Henle.

114 ollecting ducts, distal tubules, and loop of Henle.

115 rogenitor cells and formation of the loop of Henle.

116 tics can curtail their action in the loop of Henle.

117 t in the thick ascending limb of the loop of Henle; and claudin-4, -7, and -8 as determinants of coll

118 eabsorbed in the proximal tubule and loop of Henle; and, second, a stimulus to sodium-cation exchange

119 the basement membranes of the thin loops of Henle and spreads from there through the interstitium to

120 luted tubules, collecting ducts and loops of Henle as well as within the cytoplasm of tubule-delineat

121 subset of thin descending limbs of loops of Henle expressed the transgene.

122 ater absorption along microperfused loops of Henle of NKCC2A-/- mice were unchanged at normal flow ra

123 educed in microperfused superficial loops of Henle of NKCC2B-deficient mice.

124 in anaesthetized rats by perfusing loops of Henle of superficial nephrons with solutions containing

125 the kidney within the lumen of the loops of Henle, but no intracellular storage sites were identifie

126 RNA in the epithelial layers of the loops of Henle, distal tubules, and the collecting ducts of the k

127 duced kidney cysts primarily in the loops of Henle, whereas inactivation in adult mice did not lead t

128 by the thick ascending limb of the loops of Henle.

129 mal tubules and descending limbs of loops of Henle.

130 e phospholipase C, PC-PLC, promotes lysis of Henle 407 cell primary vacuoles in the absence of LLO.

131 -type S. flexneri in confluent monolayers of Henle and Caco-2 cells.

132 not form plaques in confluent monolayers of Henle cells, indicating an inability of this mutant to s

133 rate (EPFR) measurements during perfusion of Henle's loop.

134 channel of the thick ascending limb (TAL) of Henle is critical for Ca(++) reabsorption in the kidney.

135 The thick ascending limb (TAL) of Henle's loop drives paracellular Na(+), Ca(2+), and Mg(2

136 In the thick ascending limb (TAL) of Henle's loop, chloride is reabsorbed transcellularly, wh

137 orption by the thick ascending limb (TAL) of Henle's loop.

138 tro but exhibited normal plaque formation on Henle cell monolayers.

139 the isc mutant was unable to form plaques on Henle cell monolayers because the strain was noninvasive

140 sitA mntH mutant formed wild-type plaques on Henle cell monolayers but had a reduced ability to survi

141 media in vitro but formed smaller plaques on Henle cell monolayers than the parent strain.

142 ron chelator but formed wild-type plaques on Henle cell monolayers, indicating that the sitA mutant w

143 h the suf mutant formed wild-type plaques on Henle cell monolayers, the isc mutant was unable to form

144 eoB iucD) formed slightly smaller plaques on Henle cell monolayers.

145 sitA, feoB, and iucD did not form plaques on Henle cell monolayers.

146 nt SNGFR, SNGFR was manipulated by perfusing Henle's loop to alter TGF activity.

147 also strong labeling of the outer plexiform (Henle fiber) layer with anti-GSTP1.

148 inal thickness, and outer nuclear layer plus Henle fiber layer (ONL+HFL) thickness were measured usin

149 ckness measurements included the ONL and the Henle fiber layer (ONL + HFL), and were obtained using s

150 tion between the outer nuclear layer and the Henle fiber layer.

151 formed by the outer plexiform (OPL) and the Henle fiber layers (HFL): 5.0 x 10(-3) mm(2) vs 15.9 x 1

152 nteraction of carotenoids and tubulin in the Henle's fiber layer could play an important role in the

153 e determined from a polarimetry image of the Henle fiber layer.

154 e determined from a polarimetry image of the Henle fiber layer.

155 bsequent experimental inoculation study, the Henle-Koch-Evans postulates were fulfilled for M. alliga

156 ates that it survived and divided within the Henle cell cytoplasm, but the dksA mutant cells were elo

157 al orientation and size were consistent with Henle fibers.

158 promoters increased when Shigella was within Henle cells, and our data suggest that the intracellular