ライフサイエンスコーパス: K cell

1 We developed mice lacking GIP-producing K cells.

2 otein-coupled receptors (GPCRs) expressed by K cells.

3 ding the alpha-subunit of Gs, selectively in K cells.

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

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

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

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

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

9 of the cellular phenotypes observed in RPGR KD cells.

10 ocalizes at the jagged protrusions in double KD cells.

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

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

13 but not RNA, expression was reduced in HOXA5-KD cells.

14 d that the EMT pathway was activated in Yap1-KD cells.

15 %) of cell extensions were greater than FLNa KD cells.

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

17 d greater fiber alignment compared with FLNa KD cells.

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

19 icrovillus inclusions were observed in MYO5B-KD cells.

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

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

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

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

24 ted in apoptosis in primary and immortalized KS cells.

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

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

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

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

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

30 phatic endothelium, is robustly expressed in KS cells.

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

32 2-terminal kinase (JNK) signaling pathway in KS cells.

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

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

35 endogenously present on the cell surface of KS cells.

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

37 dominant angiogenic factor expressed in AIDS-KS cells.

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

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

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

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

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

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

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

45 ar to that of conventional cell counting, of k(cells) = 0.85/day, and is extracted from initial cell

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

47 SPL-KD cells accumulated intracellular and extracellular S1P

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

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

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

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

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

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

54 Sec61beta-KD cells also exhibited altered ATP7A cellular distribut

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

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

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

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

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

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

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

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

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

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

65 1 inhibitor MgcRacGAP is decreased in double-KD cells, and the barrier development and Rac1 activatio

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

67 tes and conditioned media of ERK5-knockdown (KD) cells, and were reduced upon LTBP1 KD.

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

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

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

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

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

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

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

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

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

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

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

79 nb2, which is strikingly similar to Nesprin2-KD cells as assessed by quantitative PCR analysis.

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

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

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

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

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

85 In SMARCA4 KD cells, BRD4 distribution is reduced on 739 peaks afte

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

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

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

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

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

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

92 ion of hnRNP-E1 detected in ARIH1 knockdown (KD) cells compared to control suggests a role for ARIH1

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

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

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

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

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

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

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

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

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

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

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

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

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

106 NMIIB-KD cells display down-regulation of Gsc and Serpinb2, wh

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

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

109 SPRY2 KD cells displayed impaired mitochondrial fusion and cel

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

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

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

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

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

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

116 GMSM-K cells exhibited morphological alterations and a rapid

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 ease in AQP2 immunolabeling intensity in TAZ-KD cells following dDAVP stimulation.

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

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

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

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

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

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

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

140 R1 was highest in I-cells (cholecystokinin), K-cells (glucose-dependent insulinotropic polypeptide) a

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

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

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

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

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

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

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

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

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

150 and interruption of Notch signaling inhibits KS cell growth.

151 showed that acute or chronic stimulation of K cell Gs signaling greatly improved impaired glucose ho

152 del that allowed us to selectively stimulate K cell Gs signaling.

153 focused on the potential metabolic roles of K cell Gs.

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

155 tensions of these findings showed that ATG9A KD cells have intrinsic abnormalities in the actin cytos

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

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

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

159 roteome and ubiquitinome in USP11-knockdown (KD) cells in the presence of estradiol.

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

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

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

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

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

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

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

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

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

169 cell activation signature was detected at 1 K cell input and above in all protocols, with AmpliSeq s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 KS cell lines lacking KSHV also have elevated Axl expres

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

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

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

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

189 uantitative enhancement of expression in the KS cell lines.

190 in cancerous (N.G.P.) and non-cancerous (H.E.K.) cell lysate for H(2)O(2) detection (p = 0.0064 for E

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

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

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

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

195 Additionally, PN patients with AEC > 0.3 K cells/muL had higher Th2 markers (eotaxin, eotaxin-3,

196 )1 (primary targets of the Notch pathway) in KS cell nuclei.

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

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

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

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

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

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

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

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

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

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

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

208 oth IVi1 and Vb KD impair CcO activity, IVi1 KD cells produced higher levels of cellular and mitochon

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

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

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

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

213 lted in complete loss of cell division while KD cells provided evidence that Septin7 is essential for

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

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

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

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

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

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

220 rom specialized enteroendocrine cells (L and K cells, respectively).

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

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

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

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

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

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

227 RNA sequencing in LCC1 USP11-KD cells revealed significant suppression of cell-cycle-

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

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

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

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

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

233 KS cells show synthesis of VEGF isoforms that are mitoge

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

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

236 RPGR KD cells showed stronger actin filaments, associated wit

237 Stable PRMT1-knockdown (PRMT1-KD) cells showed reduced growth rates and cell cycle arr

238 In contrast, K cell-specific Gnas-KO mice displayed markedly reduced

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

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

241 SPL-KD cells successfully differentiated when treated with a

242 uman postmortem samples and PREPL knockdown (KD) cells suggest that PREPL expression modulates pathwa

243 ss of mitophagy that is observed in the IRGM KD cells, suggesting that IRGM regulates mitophagy throu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 to healthy controls possibly because of high K-cell turnover.

264 s-associated genes were up-regulated in LSD2-KD cells under adipogenic induction.

265 d 1985 differentially expressed genes in TAZ-KD cells under basal conditions and after dDAVP treatmen

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

267 revealed reduced NR4A1 protein levels in TAZ-KD cells upon dDAVP stimulation.

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

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

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

271 ing in promoting multilayer formation of Lgl-KD cells was further identified.

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

273 The osteoclastogenesis in IVi1 KD cells was reversed fully with an IL-6 inhibitor LMT-2

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

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

276 Using Sod1-KD cells we found that the WT-A4V heteromers formed high

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

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

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

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

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

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

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

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

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

286 Three isolates of AIDS-KS cells were studied.

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

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

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

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

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

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

293 Reconstitution of these KD cells with WT SKAP1, but not the SKAP1 S31 mutant, re

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

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

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

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

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

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

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