ライフサイエンスコーパス: K cell

1 ce that express insulin, via a transgene, in K cells.

2 We developed mice lacking GIP-producing K cells.

3 d to endothelial cells, the precursor of the KS cell.

4 r (M), parvocellular (P), and koniocellular (K) cells.

5 psulated O1:K1 or O1:K2 cells but not for O1:K- cells.

6 -treated O1:K1 or O1:K2 cells but not for O1:K- cells.

7 ocalizes at the jagged protrusions in double KD cells.

8 ng autocrine factors to rescue the cortactin-KD cells.

9 increased growth and motility seen in the NM-kd cells.

10 %) of cell extensions were greater than FLNa KD cells.

11 ed, and proliferation was decreased in TRPC1-KD cells.

12 d greater fiber alignment compared with FLNa KD cells.

13 n of N-glycans was specifically decreased in KD cells.

14 icrovillus inclusions were observed in MYO5B-KD cells.

15 receptor agonist) remained effective in Cav1-KD cells.

16 ed in the culture supernatants from the beta-KD cells.

17 t melanoma that were down-regulated in Panx1-KD cells.

18 cells, but not on ECM produced by cortactin-KD cells.

19 of the cellular phenotypes observed in RPGR KD cells.

20 ted in apoptosis in primary and immortalized KS cells.

21 ificantly blocked the VEGF-induced growth of KS cells.

22 ated Src kinases such as Lyn, Fyn, or Hck in KS cells.

23 ctor (PDGF) may be important for survival of KS cells.

24 Tat upon its binding to surface receptors on KS cells.

25 wth factor A (VEGF-A), which is expressed by KS cells.

26 phatic endothelium, is robustly expressed in KS cells.

27 VEGF is an autocrine growth factor for AIDS-KS cells.

28 2-terminal kinase (JNK) signaling pathway in KS cells.

29 ic manner, enhances gp130-mediated growth of KS cells.

30 h was augmented significantly in Dex-treated KS cells.

31 endogenously present on the cell surface of KS cells.

32 kin-6 (IL-6), an autocrine growth factor for KS cells.

33 dominant angiogenic factor expressed in AIDS-KS cells.

34 cient in establishing lung tumors than BRMS1(KD) cells.

35 lie motility defects of cortactin-knockdown (KD) cells.

36 s and are overexpressed in Kaposi's sarcoma (KS) cells.

37 s and are overexpressed in Kaposi's sarcoma (KS) cells.

38 actors for AIDS-associated Kaposi's sarcoma (KS) cells.

39 r ADAR1 (ADAR1(kd)) compared to control (CON(kd)) cells.

40 n 293, BJAB, and BCBL-1 cells but not in SLK-KS(-) cells.

41 AIDS-associated Kaposi's sarcoma (KS) cell, a key element for development of KS lesions, p

42 SPL-KD cells accumulated intracellular and extracellular S1P

43 s C, which inhibits vesicle recycling, Myo1c-KD cells accumulated more E-cadherin-positive vesicles i

44 Supernatants from transfected KS cells activated NF-kappaB signaling in untransfected

45 oined breaks in M059-J as compared with M059-K cells after 30 h of incubation.

46 he expression of autocrine growth factors of KS cells after RA treatment.

47 Furthermore, JNK activity was increased in KS cells after VEGF or VRP stimulation.

48 Under differentiation conditions, SPL-KD cells also demonstrated delayed induction of 3 myogen

49 Sec61beta-KD cells also exhibited altered ATP7A cellular distribut

50 I-E(k)]) and immunohistochemical (donor [I-E(k)+] cell) analyses.

51 d mouse preproinsulin II from a transgene in K cells and nontransgenic NOD mice (controls); pancreas

52 Thirty-four per cent of K cells and only 9 % of P and 6 % of M cells responded p

53 Wortmannin radiosensitized to killing M059-K cells and strongly inhibited DNA DSB rejoining.

54 nucleation, was observed in the N-WASP/WAVE2 KD cells and was shown to be required for the N-WASP/WAV

55 growth factor-beta (TGF-beta) is produced by KS cells and has pleiotropic effects, including inhibiti

56 functional role in VEGF-induced signaling in KS cells and may act to link pathways from the VEGF rece

57 bFGF is highly expressed also by in situ KS cells and mediates KS-like lesion formation after ino

58 AIDS-KS cells and primary tumor tissues also expressed high l

59 nduces the spindle morphology distinctive of KS cells and promotes the formation of abnormal vascular

60 1 inhibitor MgcRacGAP is decreased in double-KD cells, and the barrier development and Rac1 activatio

61 igration was suppressed in GOLPH3 knockdown (KD) cells, and the suppression was restored by a re-intr

62 OM-induced DNA-binding activity of STAT3 in KS cells, and Dex further increased this activity.

63 tors and endogenous bFGF on proliferation of KS cells, and underlying intracellular events have remai

64 sphorylation of a similar set of proteins in KS cells, and which was augmented significantly in Dex-t

65 en together, lead us to conclude that mutant K cells are defective in part of the GPI transamidase ma

66 Intestinal K cells are glucose-responsive endocrine cells that migh

67 in three-dimensional collagen I gels, ACTN4 KD cells are more polarized compared with cells in which

68 Mesenchymal phenotypes observed in BRMS1(KD) cells are dependent on RelA/p65, the transcriptional

69 lating such cytokine-driven proliferation of KS cells are not well characterized.

70 inically important to determine whether AIDS-KS cells are resistant to apoptosis via the Fas system.

71 These findings demonstrate that AIDS-KS cells are resistant to Fas-mediated apoptosis and sug

72 AIDS-KS cells are resistant to killing by chemotherapeutic dr

73 lt-1-VEGF receptor that is down-regulated in KS cells as compared with endothelial cells.

74 esults show that within the CO blobs: 1) all K cell axons contain glutamate, and the vast majority of

75 little is known of specific interactions in KS cells between glucocorticoid and gp130-related growth

76 y, expression of Ii in M12.C3 cells or SaI/A(k) cells blocked the MHC class II interactions with cell

77 In TRPC1-KD cells, both hypoxia-inducible factor 1alpha expressio

78 band LFPs) are linked to high spike rates in K cells (but not P cells or M cells), on multisecond tim

79 Rescue of cortactin-KD cells by expression of cortactin-binding domain mutan

80 otent IFN-beta transcript induction in ADAR1(kd) cells by all three viruses; in contrast, in ADAR1-su

81 Complementation of ADAR1(kd) cells by expression of either p150 WT isoform or the

82 nthetic analogs inhibit the proliferation of KS cells by inhibiting the mRNA and protein levels of in

83 idence that anti-bFGF Ab abolished growth of KS cells by preventing S phase entry of the cell cycle,

84 ious results these findings suggest that the K cells consist of several classes, some of which could

85 Increased growth of the C(ko) virus in PKR(kd) cells correlated with increased viral protein expres

86 in resistance, reducing hormone release from K cells could lead to weight loss and increased insulin

87 In contrast to WT cells, FLNa knockdown (KD) cells could not completely maintain tension when mat

88 aches infer CHPs using either single-cell or k-cell data alone, and typically within a single populat

89 However, integrating both single- and k-cell data may reap additional benefits, and quantifyin

90 applying it to jointly generated single- and k-cell data to reveal CHP differences in several key inf

91 well as experimentally generated single- and k-cell data, we found situations where each data type wo

92 ile CHP information contained in single- and k-cell data.

93 f differentiation (culture days 14-21), beta-KD cells demonstrated increased levels of insoluble alph

94 rdinately reducing circulating levels of all K cell-derived hormones are unknown.

95 (VEGF) molecule in large quantities in AIDS-KS cell-derived conditioned medium (AIDS-KS-CM) (12.1-21

96 ice metastasized, whereas tumors made by 231-kd cells did not.

97 cells depleted of both CGN and CGNL1 (double-KD cells) display normal Rac1 activation and tight junct

98 CDT-treated GMSM-K cells displayed cell cycle arrest at the S phase of gr

99 SPRY2 KD cells displayed impaired mitochondrial fusion and cel

100 The switch from low-to-high spike rates in K cells does not degrade their visual signalling capacit

101 this challenge is to measure random pools of k cells (e.g., 10) to increase sensitivity, followed by

102 on and that crowding is sufficient for scrib(KD) cell elimination.

103 NOD mice with intestinal K cells engineered to express insulin have reduced blood

104 sal cell surface by control cells, cortactin-KD cells exhibit defective FN secretion and abnormal FN

105 At matched eccentricities, K cells exhibited lower spatial and intermediate tempora

106 GMSM-K cells exhibited morphological alterations and a rapid

107 Consistent with this proposition, ACSL1 kd cells exhibited a decrease in activation and phosphor

108 Interestingly, we found that the B1-KD cells exhibited increased microtubule dynamics as com

109 In addition, the NM-kd cells exhibited marked reduction in the expression of

110 Finally, CD133 KD cells exhibited poorer tumor growth in vivo.

111 Furthermore, B1-KD cells exhibited significantly lower intracellular bin

112 Atm(KD/-) cells exhibited proliferation defects and genomic

113 We now report that KS cells express a recently identified focal adhesion ki

114 Although all KS cells express Fas on the cell surface, these cells we

115 alysis revealed that all three types of AIDS-KS cells express high levels of FAP-1 mRNA, and treatmen

116 We have observed that AIDS-KS cells express high levels of receptors for immune reg

117 Here we demonstrate that AIDS-KS cells express surface interleukin-4 (IL-4) receptors,

118 mRNA by RT-PCR revealed that all three AIDS-KS cells express very low levels of bcl-2 mRNA.

119 As detected on Northern blots, AIDS-KS cells expressed major 3.9-kb VEGF-specific mRNA.

120 However, none of the three types of KS cells expressed soluble Fas mRNA as determined by rev

121 nd dual immunofluorescence staining in MYO5B-KD cells expressing mutant forms of MYO5B, we observed t

122 Finally, enhanced apoptosis in ADAR1(kd) cells following infection with wild type and V(ko) v

123 retin response." To determine the role(s) of K cells for the incretin response and type 2 diabetes me

124 N(kd)) and protein kinase PKR-deficient (PKR(kd)) cells for IFN-beta induction following infection wi

125 o W cells in cat lateral geniculate nucleus, K cells form three pairs of layers in macaques.

126 r studies suggested that spindle-shaped AIDS-KS cells from various AIDS-KS lesions play important rol

127 impairs pancreatic beta cell and intestinal K cell function despite significant weight loss.

128 resence of the DNA of HHV-8 in the nuclei of KS cells further supports the possibility that this agen

129 Xenograft Panx1-KD cells grown within the chorioallantoic membrane of av

130 now obtained evidence that TNF-alpha-induced KS cell growth and ERK1/2 activation are mediated exclus

131 Furthermore, Axl knockdown inhibits KS cell growth and invasion.

132 VEGF mRNA and protein production and inhibit KS cell growth in a dose-dependent manner.

133 Kaposi's sarcoma (KS), and retinoids inhibit KS cell growth in vitro.

134 Thus, glucocorticoids enhance KS cell growth through the regulation of TGF-beta activa

135 Second, KS cell growth was inhibited by VDR agonist 1alpha,25 di

136 ding to selective synergistic stimulation of KS cell growth with Dex and the gp130-related growth fac

137 ut not synergistic effects on stimulation of KS cell growth with IL-1beta or TNF-alpha, the signals o

138 and interruption of Notch signaling inhibits KS cell growth.

139 In contrast, in caveolin-1 KD (Cav1-KD) cells, >87% of adiponectin-induced nCDase activation

140 K cells in different K LGN layers differed in spatial, t

141 retin hormone secreted from gastrointestinal K cells in response to food intake, has an important rol

142 IP/DT mice demonstrate an important role for K cells in the regulation of body weight and insulin sen

143 We show that TGF-beta is produced by KS cells in both the latent and active forms, and that T

144 Furthermore, growth of KS cells in nude mice was specifically inhibited by VEGF

145 -HSA inhibited migration and invasion of the KS cells in vitro in response to various growth factors.

146 be important in growth and proliferation of KS cells in vitro, particularly Oncostatin M, hepatocyte

147 f which have been shown to promote growth of KS cells in vitro.

148 to acquire the features of KS spindle cells (KS cells) including spindle morphology, marker expressio

149 Analysis of KD cells indicates that FADD is necessary for Fas-L- or

150 observed in response to infection of miR-126 KD cells, indicating that miR-126 plays an important rol

151 dlin-1 also failed to rescue electrotaxis in KS cells, indicating that both integrin and lipid bindin

152 adation, showed activity in vitro to inhibit KS cell invasion.

153 The K cell is a specific sub-type of enteroendocrine cell lo

154 he fidelity of visual signals transmitted by K cells is improved, probably because K cell responses b

155 onstrate that in vivo, Akt activation within KS cells is potently down-regulated in areas adjacent to

156 VEGF production by KS cells is promoted synergistically by inflammatory cyt

157 es granulocyte lineage commitment in PU.1(kd/kd) cells lacking the PU.1 distal enhancer and does not

158 The MODE-K cell line could also present alpha GalCer to primary m

159 terized a murine myoblast SPL-knockdown (SPL-KD) cell line lacking SPL.

160 In contrast, CD16/Jak2-K cell lines exhibited increased expression of bcl-2 and

161 Two such iPLA2beta knockdown (iPLA2beta-KD) cell lines express less than 20% of the iPLA2beta of

162 We constructed stable knockdown (KD) cell lines for five epithelium-expressed miRNAs (miR

163 It was first shown that KS cell lines and primary tumor tissue express high leve

164 In this study, we show that AIDS-KS cell lines express higher levels of vascular endothel

165 It was thus studied for its activity in KS cell lines in vitro and in vivo to determine whether

166 KS cell lines lacking KSHV also have elevated Axl expres

167 In this regard, two KS cell lines that were previously refractory to native

168 ANUP is a strong growth inhibitor for KS cell lines, but has little or no effect on fibroblast

169 Two tumorigenic AIDS-KS cell lines, KS Y-1 and KS-imm, expressed 4560 and 948

170 found that GCs directly induce the growth of KS cell lines.

171 uantitative enhancement of expression in the KS cell lines.

172 Act D treatment of AIDS-KS cells markedly and selectively down-regulated Bcl-xL

173 Thus, K cells may maintain long-term function of neurons and b

174 ion of antiapoptotic characteristics by AIDS-KS cells may contribute to their prolonged survival.

175 Surprisingly, ACTN4 KD cells migrate faster than the ones expressing the scr

176 )1 (primary targets of the Notch pathway) in KS cell nuclei.

177 K cell number, GIP transcripts, and plasma GIP levels we

178 Dibenzazepine also increased K cell numbers, resulting in increased gastric inhibitor

179 (GIP) is a 42-amino acid peptide produced by K cells of the mammalian proximal small intestine and is

180 GIP is expressed in K cells of the small intestine and in cells of the subma

181 in normal lung in a pattern compatible with K-cells of the diffuse neuroendocrine system.

182 iruses; in contrast, in ADAR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective

183 esian approach that can utilize single-cell, k-cell, or both simultaneously to infer CHPs within a si

184 The results indicate that KS cells overexpress activated Notch and interruption of

185 angiogenic properties, a key feature of the KS cell phenotype, and suggest a mechanism by which thes

186 Apo-2L induced apoptosis in >80% of AIDS-KS cells pretreated with Act D.

187 onse was absent in GIP/DT animals suggesting K cells produce GIP plus an additional incretin hormone.

188 In addition, the KS cell-produced basic fibroblast growth factor (bFGF) w

189 th the ERK1/2 signaling pathway required for KS cell proliferation.

190 on of ERK1/2, but also the TNF-alpha-induced KS cell proliferation.

191 ull activation of cyclin E-CDK2 activity and KS cell proliferation.

192 In TRPC1-KD cells, receptor-operated calcium entry was decreased.

193 In model C, d/b anti-k cells reduced chimerism to the background levels but f

194 Restoring NCX1 expression in beta-KD cells reduced migration rate and ERK1/2 activation, s

195 To reduce the number of functioning K cells, regulatory elements from the rat GIP promoter/g

196 Transfecting TRPC1 to TRPC1-KD cells rescued receptor expression, migration, and pro

197 Three possible mechanisms related to AIDS-KS cells, resistance to anti-Fas cytotoxicity were exami

198 ted by K cells is improved, probably because K cell responses become less rectified.

199 Expression of WT MYO5B in MYO5B-KD cells restored microvilli; however, expression of MYO

200 ding constitutively active IKK2 into the 231-kd cells restored the ability of TbetaRIII-deficient cel

201 ses of xenin-25, another peptide produced by K cells, restored the GIP-mediated insulin secretory res

202 PC-3 SRPK1-KD cells resulted in tumours that grew more slowly in xe

203 udies in wild-type mice with shRNA GRO-alpha KD cells revealed 2- to 4-fold impaired tumor growth, me

204 Tumors from MyD88-KD or TLR5-KD cells revealed the reduced production of neutrophil a

205 rosine phosphorylation of FGFR1 and FGFR2 on KS cells, reversed the inhibitory effects of anti-bFGF A

206 ic alpha and beta cells and intestinal L and K cells, secreting glucagon, insulin, and the incretins

207 We found that actinomycin D treatment of KS cells selectively abolished expression of mitogen-act

208 o the upper and lower tiers of layer IV, and K cells send axons to the cytochrome oxidase (CO) blobs

209 KS cells show synthesis of VEGF isoforms that are mitoge

210 reases in centre size with eccentricity, but K cells showed more scatter.

211 miR-126 KD cells showed lower expression of interleukin 8 (IL-8)

212 RPGR KD cells showed stronger actin filaments, associated wit

213 Furthermore, cortactin-KD cell speed defects were rescued on cell-free autocrin

214 ortical asynchrony precedes the increases in K cell spike rates by 1-3 s, implying causality.

215 SPL-KD cells successfully differentiated when treated with a

216 We found that RM from mutant K cells supported NH2-terminal processing of the nascent

217 The tagged PrP(C), when expressed in our PrP-KD cells, supports prion replication with the production

218 e highest relative affinities for Kd rescued Kd cell surface expression in T2 cells, while those expr

219 gamma was expressed as an approximately 230-kD cell surface protein, and differentiating ES clones t

220 iol)propionamide, specifically labeled a 160-kD cell surface protein, and the labeling was completely

221 AF-20, recognizes a rapidly internalized 180-kd cell-surface glycoprotein that is abundantly expresse

222 ntibody, 7.1, which recognizes a 220- to 240-kD cell-surface protein whose N-terminal amino acid sequ

223 ling is also known to play a pivotal role in KS cell survival and lytic phase entrance of KSHV.

224 stable short-hairpin RNA (shRNA) knockdown (KD) cells targeting these adaptors, TNF death-inducing s

225 s caused significantly less apoptosis in PKR(kd) cells than in PKR-sufficient cells.

226 ct a physiological profile of koniocellular (K) cells that might be linked to particular visual perce

227 denoviral retargeting to the FGF receptor in KS cells that are ordinarily transduction refractory to

228 hway plays a pivotal role in transmitting to KS cells the mitogenic signals of TNF-alpha.

229 HeLa cells stably deficient in ADAR1 ("ADAR1(kd) cells") through short hairpin RNA-mediated knockdown

230 th rough microsomal membranes (RM) of mutant K cells to further characterize the biosynthetic defect

231 cl-xL in Act D-induced sensitization of AIDS-KS cells to Apo-2L-mediated apoptosis.

232 lls or the single cytokines also induce AIDS-KS cells to produce and release basic fibroblast growth

233 SPL-KD cells transfected with mimics for miR-1 or miR-206 al

234 milar studies injecting GSI into established KS cell tumors on mice demonstrated growth inhibition or

235 The majority of the beta-KD cells underwent apoptosis around the polychromatophil

236 d the role of WRN in isogenic knockdown (WRN-KD) cells using a supF gene mutation reporter system fla

237 ed that ephrin B2 expression is required for KS cell viability by knock down with siRNA.

238 d efflux, their expression in 2008 Sec61beta-KD cells was analyzed; ATP7A was found to be 2- to 3-fol

239 quitinase closely related to Usp9x, in Usp9x KD cells was noted.

240 rowth factor, FGF2, the gene transduction of KS cells was enhanced 7.7-44 fold; recombinant adenoviru

241 ral isolates from cultured cutaneous primary KS cells was transmitted to an Epstein-Barr virus-negati

242 of RNA interference-mediated knockdown (PKR(kd) cells), we demonstrated that a reduction in PKR part

243 from the transgenic mice, insulin-producing K cells were not affected by the immune response and the

244 l intestine (Rie1), and mouse duodenum (MODE-K) cells were found to support only limited rotavirus re

245 telet-like particles (PLPs) produced by WDR1 KD cells were fewer in number but larger than PLPs produ

246 ility and lamellipodial defects of cortactin-KD cells were fully rescued by plating on increasing con

247 actor-independent proliferation of cortactin-KD cells were rescued by coculture with cortactin-expres

248 In polarized monolayers, Myo1c-knockdown (KD) cells were more sensitive to reduced calcium concent

249 AIDS-KS cells were relatively resistant to Apo-2L; however, A

250 signal-regulated kinases 1 and 2 (ERK1/2) in KS cells were significantly activated by TNF-alpha throu

251 Three isolates of AIDS-KS cells were studied.

252 B6)F(1) cells presensitized to CBA (d/b anti-k cells) were injected into (B6 x CBA)F(1) --> BALB/c mi

253 ndependent cell survival was stunted in CCN6 KD cells when treated with either human recombinant CCN6

254 mislocalization and aMTOC formation in MLL5-KD cells, whereas MLL5 mutants incapable of interacting

255 comparably induced formation of SG in ADAR1(kd) cells, whereas only the C(ko) mutant was an efficien

256 Reconstitution of class K cells with hGPI8 abolishes their accumulation of GPI p

257 ontrast, infection of miR-155 KD and miR-210 KD cells with the same organisms resulted in higher IL-8

258 high levels of FAP-1 mRNA, and treatment of KS cells with actinomycin D reduced the levels of FAP-1

259 Treatment of AIDS-KS cells with actinomycin D sensitized the tumor cells t

260 We observed that stimulation of KS cells with basic as well as RGD sequence-containing T

261 Moreover, in vivo xenograft studies with KS cells with or without KSHV infection showed that MAb1

262 Stimulation of KS cells with sIL-6R alpha/IL-6 or OM induced rapid tyro

263 Treatment of KS cells with VEGF-related protein (VRP), the ligand for

264 ddition of these nucleophiles to RM of class K cells yielded neither of these products.