ライフサイエンスコーパス: M cell

1 ranslocation through antigen-sampling cells (M cells).

2 role in selective sensory processing in the M-cell.

3 llometry compared with the earlier-generated M cells.

4 MNV strains was reduced in mice depleted of M cells.

5 Virus particles have been observed within M cells.

6 ylate cyclase AC3 underlies PDF signaling in M cells.

7 mal transition (EMT) of FAE enterocytes into M cells.

8 hesis that prions cross the nasal mucosa via M cells.

9 t marks epithelial transdifferentiation into M cells.

10 primary gene that dictates directionality in M cells.

11 med that S Typhi also preferentially targets M cells.

12 mucosa through enterocytes in the absence of M cells.

13 increasing the exposure time of cecal patch M cells.

14 ich facilitate adherence of S Typhimurium to M cells.

15 ired for preferential accumulation of GUS in M cells.

16 f CA and pyruvate,orthophosphate dikinase in M cells.

17 , such as Peyer's patches, and mature GP2(+) M cells.

18 of mice conditionally depleted of microfold (M) cells.

19 neration also vary between BS and mesophyll (M) cells.

20 nd HL-60 (14.5+/-1.75 mF/m(2), 0.76+/-0.12 S/m) cells.

21 n and spindle pole integrity specifically in mES cells.

22 ies in weak TF binding sites can function in mES cells.

23 icantly reduced at these sites in Vezf1(-/-) mES cells.

24 xtensive proliferation of Hif1alpha-targeted mES cells.

25 stress led to oct3/4 gene downregulation in mES cells.

26 sociates with spindle-associated proteins in mES cells.

27 tical spindle-associated protein in mouse ES(mES) cells.

28 d) was identified within a limited number of M cells 15 to 180 min following inoculation, but not in

29 and timing ensure reliable activation of the M-cell, a feedforward excitatory motif that may extend t

30 Like M-cell ablations, bilateral ablations of spiral fiber ne

31 through tail stimulation [5-7] and ablating M-cells abolishes short-latency tail-elicited startles [

32 timulation of splenic B cells, where Atad5(+/m) cells accumulated in the S phase of the cell cycle an

33 icited startles [8, 9], we hypothesized that M-cell activity was necessary for S-start generation.

34 The M-cell adhesion molecules junctional adhesion molecule-A

35 eld potentials recorded on activation of the M-cell, allowing unequivocal physiological identificatio

36 e sex drive rhythm (MSDR) is mediated by the M cells along with DN1 neurons, a cluster of clock neuro

37 several isotypes was also reduced in Atad5(+/m) cells, although the types of end-joining pathways wer

38 Both serovars can adhere to and invade M cells and enterocytes, and it has been assumed that S

39 pe, such that mat2 is the preferred donor in M cells and mat3 is the preferred donor in P cells.

40 ocalizes to loci expressed preferentially in M cells and to retrotransposon LTRs.

41 deletion resulted in increased adherence to M cells and, as expected, decreased adherence to Caco-2

42 quivocal physiological identification of the M-cell and of its feedback and reciprocal inhibitory net

43 y to rescue the lethality of Brca2-deficient mES cells and their effect on sensitivity to DNA-damagin

44 usters of clock neurons-morning oscillators (M cells) and evening oscillators (E cells)-are largely r

45 ect of Hif1alpha on telomerase regulation in mES cells, and imply that Hif1alpha may have a physiolog

46 he temporal resolution of essential genes in mES cells, and to identify novel genes that control spro

47 Microfold (M) cells, antigen-sampling cells in the intestine, were

48 Transcellular dendrites scanned the M-cell apical surface and the gut luminal content; they

49 CT-induced nasal-associated lymphoid tissue M cells appear to be generated from ciliated Foxj1(+)PGR

50 PP, isolated lymphoid follicle, and villous M cells are all derived from intestinal crypt stem cells

51 m epithelial cells bearing microvilli, while M cells are more susceptible to microbial adhesion.

52 These data demonstrate that M cells are required for the pathogenesis of two unrelat

53 M cells are specialized epithelial cells mediating immun

54 data are consistent with a model whereby PP M cells are the primary route by which MNV crosses the i

55 PP type M cells are thought to be dependent on cytokines, includ

56 Microfold (M) cells are epithelial cells present in mucosal tissues

57 Microfold (M) cells are specialized intestinal epithelial cells tha

58 Although CD11c(med) cells are associated with the initiation of vascula

59 Whereas TCRgammadelta(med) cells are mostly CD2(+)CD8(-) and CD2(+)CD8(+), TCR

60 d spiral fiber neurons, which project to the M-cell axon hillock.

61 a previously described mouse embryonic stem (mES) cell-based functional assay to characterize eight B

62 DSBs, TLC1 RNA remains nucleolar in most G2/M cells but accumulates in the nucleoplasm and colocaliz

63 madelta(hi) cells can generate TCRgammadelta(med) cells but never the opposite.

64 In summary, MD cells can sense alterations in local tissue metabolis

65 ion is the thymus, where a few TCRgammadelta(med) cells can be induced to TCRgammadelta(hi) but only

66 In mucosal tissues, epithelial M cells capture and transport microbes across the barrie

67 left and right sides, cannot be explained by M-cell circuit models.

68 anslocation through a human-derived in vitro M-cell coculture system in comparison to espF(O127) and

69 y macrophages, (ii) translocation through an M-cell coculture system, and (iii) uptake by and translo

70 E-induced arrest and introducing AR into PC3-M cells confers 2-ME-induced mitotic arrest.

71 introduced stably into mouse embryonic stem (mES) cells containing a conditional allele of Lig3 that

72 Adherence to M cells could be further enhanced by introduction of the

73 In contrast with intestinal PP M cells, CT-induced nasal-associated lymphoid tissue M c

74 apmer antisense oligonucleotides (ASOs) in T(m), cell culture and animal experiments and compare them

75 In lymphoma cell lines, IMGN529 induced G2/M cell cycle arrest after internalization and lysosomal

76 oresistant EOC cells through induction of G2/M cell cycle arrest and apoptotic cell death.

77 PBD drug induces DNA damage, resulting in G2/M cell cycle arrest and cell death.

78 uce microtubule fragmentation, leading to G2/M cell cycle arrest and intrinsic apoptosis.

79 CQL5 display a slow proliferation rate, a G2/M cell cycle arrest and late S-phase cycling defects.

80 triggered enhanced apoptosis, and induced G2/M cell cycle arrest and more overall cytotoxicity than i

81 duced growth inhibition, apoptosis, and G(2)-M cell cycle arrest associated with upregulation of p21(

82 y appears to be a principal mechanism for G2/M cell cycle arrest by p53.

83 tial oil and aqueous infusion resulted in G2/M cell cycle arrest in a dose-dependent manner.

84 In cell culture models, WFA exerts G(2)/M cell cycle arrest in a p27(Kip1)- and Skp2-dependent m

85 ogated the apoptotic effects, but not the G2/M cell cycle arrest induced by JA.

86 In somatic cells, a permanent G2/M cell cycle arrest is induced in the second cell cycle

87 strate for the first time that HNE caused G2/M cell cycle arrest of hepatocellular carcinoma HepG2 (p

88 nt activation after DNA damage results in G2/M cell cycle arrest that allows time for DNA repair befo

89 ited proliferation of GBM cells through a G2/M cell cycle arrest via inhibition of polo-like kinase 1

90 tosis, abolished cytarabine-induced S and G2/M cell cycle arrest, and cooperated with cytarabine in i

91 events CARP-1 binding with APC-2, causes G(2)M cell cycle arrest, and induces apoptosis with an IC(50

92 Phycocyanin induces G2/M cell cycle arrest, apoptotic and autophagic cell death

93 PRDM1 in PRDM1-null NK cell lines led to G2/M cell cycle arrest, increased apoptosis, and a strong n

94 4-HNE induced G(2)-M cell cycle arrest, led to formation gammaH2AX foci, an

95 reduction of H4 K16 acetylation, severe G(2)/M cell cycle arrest, massive chromosome aberration, and

96 ecreases cell proliferation by inducing G(2)/M cell cycle arrest, whereas BAFF has no effect on cell

97 resulted in dose-dependent apoptosis and G2/M cell cycle arrest, which was associated with the activ

98 Vpr is an accessory protein that induces G2/M cell cycle arrest.

99 otype, actin cytoskeleton remodeling, and G2/M cell cycle arrest.

100 m by which p53 can enforce and maintain a G2/M cell cycle arrest.

101 E1-null NK cell line led to apoptosis and G2/M cell cycle arrest.

102 iting tubulin polymerization and inducing G2/M cell cycle arrest.

103 tin were mediated by Src through inducing G2/M cell cycle arrest.

104 inhibition of Cdc2 kinase and subsequent G2/M cell cycle arrest.

105 ranscription and abrogates ATF5-induced G(2)/M cell cycle blockade and inhibition of cell proliferati

106 serine 79 (S79) is required to activate G(2)/M cell cycle blockade.

107 ow BRCA1 E3 ligase activity regulates the G2/M cell cycle checkpoint and, thus, contributes to mainte

108 ow BRCA1 E3 ligase activity regulates the G2/M cell cycle checkpoint and, thus, contributes to mainte

109 AB2IP-deficient cells enforced a robust G(2)-M cell cycle checkpoint compared with control cells.

110 Thus targeting DNA replication and G2-M cell cycle checkpoint simultaneously by cisplatin and

111 hibition of ATR or CHK1, but also defects G2-M cell cycle checkpoint.

112 es to simultaneously control the G1/S and G2/M cell cycle checkpoints through transcriptional inducti

113 and cellular gene expression, activates G(2)-M cell cycle checkpoints, and is essential for viral spr

114 cycle progression, focusing on the G1 and G2/M cell cycle checkpoints, as well as on related essentia

115 fic repression of translation of the core G2/M cell cycle component cycB during the specialized cell

116 leading to an irreversible arrest in the G2/M cell cycle phase and delayed apoptosis.

117 t are not identical to, those causing the G2/M cell cycle phenotype.

118 ent data showing that BRCA1 ubiquitinates G2/M cell cycle proteins, cyclin B and Cdc25C, leading to t

119 s are derepressed in cells stalled at the G2/M cell cycle stage after knockdown of FACT, but not in G

120 histone chaperone activity by FACT at the G2/M cell cycle stage which could affect transcription elon

121 brucei, with derepression specific to the G2/M cell cycle stage.

122 agments on FGF1-mediated signaling during G2/M cell cycle transition.

123 pore complex components and regulators of G2/M cell cycle transition.

124 birinapant alone also induced significant G2-M cell-cycle arrest and cell death in UM-SCC-46 cells.

125 ni anemia pathway, including a pronounced G2-M cell-cycle arrest and chromosomal radial formation.

126 < 0.0001), corresponding with a prolonged G2-M cell-cycle arrest and increased apoptosis following ra

127 ll cultures, Mif deletion led to enhanced G2/M cell-cycle arrest and increased expression of the CDK

128 Tivantinib treatment induced a G(2)-M cell-cycle arrest in EBC1 cells similarly to vincristi

129 but not 5-azacytidine, also produced a G(2)/M cell-cycle arrest in HMC-1 cells.

130 f telomeric DNA and eventually a specific G2/M cell-cycle arrest known as senescence.

131 s by enhancing the DNA-damage response, G(2)/M cell-cycle arrest, and apoptosis.

132 air inhibitors, accumulation of DNA DSBs, G2-M cell-cycle arrest, and induction of apoptosis.

133 les Myc-induced proliferation, triggering G2/M cell-cycle arrest, polyploidy, and apoptosis.

134 rora kinase inhibitors (AKi) leading to G(2)-M cell-cycle arrest.

135 viability through caspase activation and G2/M cell-cycle arrest.

136 ition of CDK2 and cyclin A expression and G2-M cell-cycle arrest.

137 ression of Plk2 restored sensitivity to G(2)-M cell-cycle blockade and cytotoxicity triggered by pacl

138 i-dependent knockdown of Plk2 abrogated G(2)-M cell-cycle blockade by paclitaxel, conferring resistan

139 Consequently, GSCs exhibit rapid G2-M cell-cycle checkpoint activation and enhanced DNA repa

140 s and, consequently, induced apoptosis or G2/M cell-cycle delay in normal cells to protect them from

141 ignaling genes and down-regulation of the G2/M cell-cycle marker gene, CYCB1;1 TCP20 and NLP6&7 also

142 f the checkpoint kinases 1/2, an aberrant G2/M cell-cycle progression and induction of myeloid differ

143 riant, we demonstrate a role for TORC2 in G2/M cell-cycle progression.

144 mple, PP M cells frequently appeared to form M cell-DC functional units, whereas villous M cells did

145 Moreover, lack of Sik3 in M cells decreases the amplitude of PERIOD (PER) cycling

146 Furthermore, our results show that T(M) cells defective in rapid recall ability have less diA

147 sm and cell viability using mouse fibroblast MS cells deficient in the murine IGF-II receptor and cor

148 eases as naive CD8(+) T cells develop into T(M) cells, demonstrating a novel correlation between the

149 ensory afferents synapsing directly onto the M-cell dendrites [3].

150 odality-dependent membrane specialization in M-cell dendrites suited for processing stimuli of differ

151 pism, reovirus infection was also reduced in M cell-depleted mice.

152 activity screen using mouse embryonic stem (mES) cell-derived neuronal precursors.

153 M cell development is associated with B lymphocytes in a

154 M cell-DC functional units, whereas villous M cells did not consistently engage underlying DC.

155 In a cell culture model of M cell differentiation, we found lymphotoxin/tumor necro

156 ults are consistent with a two-step model of M cell differentiation, with initial CD137-independent c

157 sion dynamics of early mouse embryonic stem (mES) cell differentiation, uncovering discrete transitio

158 d for capturing luminal microbial particles; M cells display a unique apical membrane lacking microvi

159 define the importance of Peyer's patch (PP) M cells during MNV pathogenesis, we used a model of BALB

160 However, how some T(E/M) cells escape regulation and cause autoimmune disease

161 22, and Il26) in CCR6(+), but not CCR6(-), T(M) cells, even in CCR6(+) cells lacking IL-17 expression

162 Salt-inducible kinase 3 (SIK3) expression in M cells exhibit a short period of MSDR but a long period

163 ncreasing structural stiffness (2 to 100+ mN/m), cells exhibited decreases in migration speed and ave

164 Importantly, PC-M cells expressed surface markers associated with pericy

165 Our findings show that the M-cells fire simultaneously to generate the S-start.

166 ins and happens asynchronously always in the M cell first.

167 types were clearly distinct; for example, PP M cells frequently appeared to form M cell-DC functional

168 al factor controlling the differentiation of M cells from RANK-expressing intestinal epithelial precu

169 ptive transfer experiments revealed that T(E/M) cells from anti-IL-7Ralpha-treated mice had lost thei

170 B lymphocytes are critical to M cell function by forming a basolateral pocket and poss

171 Moreover, PC-M cells had pericyte-like functionality being capable of

172 M cells have also been suggested as a portal for pathoge

173 Multiple phenotypic subsets of M cells have now been described, all sharing a unique ap

174 M-cells have been proposed as evolutionary ancestors of

175 ed the balance of regulatory T cells and T(E/M) cells, hence promoting cell-extrinsic regulation and

176 d: (i) in vivo biotinylation system setup in mES cells; (ii) affinity purification of multiprotein co

177 ation of sialyl Lewis X-expressing B16-FTIII-M cells in E/P-selectin doubly-deficient mice.

178 but more uniform distribution between BS and M cells in Mo17.

179 CT causes induction of new M cells in the airway and intestine without cell divisio

180 while the latter were preferably taken up by M cells in the follicle-associated epithelium (FAE) regi

181 hus, our work demonstrates the importance of M cells in the pathogenesis of enteric viruses irrespect

182 avium subsp. paratuberculosis interacts with M cells in the Peyer's patches of the small intestine.

183 phage to the lung colonization of B16-FTIII-M cells in vivo in the mouse.

184 lines, raising the possibility that CD137 on M cells in vivo might interact with CD137L expressed by

185 -R stimulates cAMP increases in vitro and in M cells in vivo.

186 ndicate that spiral fiber neurons excite the M-cell in a lateralized manner.

187 eurons are essential for the function of the M-cell in response to sensory cues and suggest that conv

188 striosomal cells (S cells) and matrix cells (M cells) in cats with (3) H-thymidine and followed their

189 Peyer patch and cecal patch microfold cells (M cells) in vivo.

190 ce the targeted uptake from microfold cells (M-cells) in Peyer's patches of small intestine.

191 For that, we studied the Mauthner cells (M-cells) in the goldfish startle circuit, which receive

192 n covariations of multiple leaf (S(mes)) and M cell (including cell wall thickness) structural traits

193 82 expressed genes; 14,972 were expressed in M cells, including 53 M-enriched transcription factor (T

194 epigenomic dataset in mouse embryonic stem (mES) cells, including DNA methylation (MeDIP-seq and MRE

195 The goldfish M-cell initial segment/axon hillock is surrounded by a c

196 produced by a tonic (intrinsic) reduction in M-cell input resistance, likely mediated by a Cl(-) cond

197 n of stg and/or introduction of lpf enhanced M cell invasion as well, leading to significant increase

198 HELQ-knockout cells, and accumulation of G2/M cells is reduced.

199 onstitutive and inducible differentiation of M cells is toward strictly defined context-dependent phe

200 cating that the diAcH3 level of individual T(M) cells is a useful marker for assessing their function

201 s that are crucial in ensuring that only one M-cell is active and that it fires only once.

202 The Mauthner cell (M-cell) is a command-like neuron in teleost fish whose f

203 Only 1 wedge had M-cell islands.

204 DNA element located adjacent to mat3, but in M cells it spreads across the silent mating-type region,

205 While virus particles have been observed in M cells, it is not known whether viruses use M cells to

206 Unlike common enterocytes, M cells lack an organized apical brush border, and are a

207 initial CD137-independent commitment to the M cell lineage followed by a CD137-CD137L interaction of

208 gh CD137; however, initial commitment to all M cell lineages is B lymphocyte and CD137 independent.

209 000 individual haploid mouse embryonic stem (mES) cell lines targeting 16,970 genes with genetically

210 LIF) and contribute to mouse embryonic stem (mES) cell maintenance of pluripotency and self-renewal.

211 t that inflammatory cytokine-induced PP type M cells may be a useful correlate of chronic intestinal

212 ggested that high affinity ligands targeting M cells may be used to deliver mucosal vaccines; here, w

213 convergent pathway that is essential for the M-cell-mediated startle behavior in larval zebrafish.

214 tion that spiral fiber neurons help activate M-cell-mediated startle behavior.

215 Using a tissue culture M cell model, we examined S Typhi strains with a deletio

216 alpha), did not have a significant effect on mES cell morphology, survival, or growth rate.

217 curs in PPs and involves cooperation between M cells of the follicle-associated epithelium and DCs of

218 me (SED), through the specialized epithelial M cells of the follicle-associated epithelium.

219 erentiated bundle sheath (BS) and mesophyll (M) cells of maize (Zea mays) leaves are specialized to a

220 Studies on the Mauthner cell (M-cell) of goldfish, Carassius auratus, have facilitated

221 The reticulospinal Mauthner cells (M-cells) of the startle circuit have been considered to

222 h spike rates in K cells (but not P cells or M cells), on multisecond timescales.

223 In Vezf1(-/-) mouse embryonic stem (mES) cells, our earlier data showed widespread changes i

224 , a lymphoid organ in which microfold cells (M cells) overlay an arrangement of B cells, T cells, and

225 M cells overlying intestinal Peyer's patches (PPs), isol

226 hat aids in the binding of these bacteria to M cells overlying Peyer's patches and subsequent entry i

227 We further show that in DKC1(m) cells, p53 IRES-dependent translation is impaired dur

228 es can have a dramatic effect on the in vivo M cell particle uptake independent of the action of targ

229 brain homogenate was identified adhering to M cells, passing between cells of the nasal mucosa, and

230 sal bacteria in Peyer's patches (PP) via the M cell pathway was mediated by their association with SI

231 At least three M cell phenotypes are known in the airways and intestine

232 The existence of diverse M cell phenotypes, especially inflammation-inducible M c

233 s in various functional categories, with the M cells playing more important roles in light reaction,

234 m increased developmental neuron loss in the M-cell population as it competes for limited termination

235 rmed that while induction of UEA-1+ putative M cell precursors was not CD137-dependent, full M cell t

236 gradients in S cells were still evident, but M cells, produced over mid to late prenatal ages, became

237 , while CD137-deficient mice produced UEA-1+ M cell progenitors in nasopharyngeal associated lymphoid

238 CD11c(hi)MHC II(med) cells promote endothelial cell quiescence in vitro

239 henotypes, especially inflammation-inducible M cells, provides an intriguing puzzle: some variants ma

240 ar average structural stiffness (25 +/- 5 mN/m), cells put out longer FAC lengths on smaller diameter

241 Following stimulation, memory T (T(M)) cells rapidly express many effector functions, a hal

242 The small increase in the P/M cell ratio in diurnal primates may result from increas

243 er, we conclude that SIK3-HDAC4 signaling in M cells regulates MSDR by regulating the molecular oscil

244 Surprisingly, IL-7-deprived diabetogenic T(E/M) cells remained present in the treated animals but sho

245 atches, which contain high numbers of mature M cells, renders BALB/c mice refractory to oral infectio

246 Although M cells represent a small proportion of the specialized

247 findings are consistent with the model that M cells represent the primary route by which MNV crosses

248 ptional changes following Gata6 induction in mES cells reveals step-wise pluripotency factor disengag

249 ne conversion observed during meiosis, where M cells serve as preferential donors of genetic informat

250 MNV- and reovirus-infected mice depleted of M cells showed reduced viral loads in the intestine.

251 per unit of leaf surface area (S(mes)), and M cell size; a second group included functional traits,

252 LysoDC extended dendrites through M-cell-specific transcellular pores to the gut lumen.

253 Elements sufficient for M-cell specificity in C(4) leaves are also present in bo

254 However, simultaneous M-cell spikes generated through direct current injection

255 s their excitability prior to the arrival of M-cell spikes in the tail.

256 stage after knockdown of FACT, but not in G2/M cells stalled after knockdown of cyclin 6.

257 er the unique induction requirements of each M cell subset and functional differences, highlighting t

258 ns to follow the constitutive development of M cell subsets and their acute induction by cholera toxi

259 states of the Ccnb1 promoter among G1 and G2/M cells, suggesting cell cycle-independent origin of cel

260 es, leaf thickness (Thick(leaf)), mesophyll (M) cell surface area exposed to intercellular air space

261 administered microparticles also included an M-cell targeting ligand, Aleuria aurantia lectin, to enh

262 predicted that the enhancing effects of the M cell-targeting ligand only are enabled at high ionic s

263 effect was dependent on the presence of the M cell-targeting ligand.

264 Mucosal immune surveillance depends on M cells that reside in the epithelium overlying Peyer's

265 Human memory T cells (T(M) cells) that produce IL-17 or IL-22 are currently defi

266 Magnocellular (M) cells (the faster-conducting and achromatic pathway)

267 ynaptic sound response of the Mauthner cell (M-cell), the decision-making neuron of the startle circu

268 In WT mES cells, the elongating form of RNA pol II accumulates

269 ot affect other Gs-coupled GPCR signaling in M cells, they can be rescued, and they do not represent

270 -containing nanoparticles utilize epithelial M cells to enter Peyer's patches, small areas of the int

271 M cells, it is not known whether viruses use M cells to initiate a productive infection.

272 However, it is not known whether viruses use M cells to initiate a productive infection.

273 rium transforms primed epithelial cells into M cells to promote host colonization and invasion.

274 nesis of autoimmune diabetes by enabling T(E/M) cells to remain in a functionally competent state and

275 ifically targets antigen-sampling microfold (M) cells to translocate across the gut epithelium.

276 Switching Hif1alpha-targeted mES cells to a hypoxic environment largely restored Hif1

277 e largest resource of hemi/homozygous mutant mES cells to date and is available to all researchers.

278 is sufficient to direct GUS accumulation in M cells, transcripts encoding GUS are abundant in both M

279 ell precursors was not CD137-dependent, full M cell transcytosis function required expression of CD13

280 While these results support M cell transport of prions, larger amounts of infected b

281 Based on studies of M cell uptake under different ionic conditions, we hypot

282 m cells by performing a screen in murine ES (mES) cells using a shRNA expression library targeting mu

283 bling stimulus in preferentially stimulating M cells versus P cells.

284 ain an open chromatin structure in resting T(M) cells via epigenetic modifications.

285 s while preserving water; in addition, thick M cell walls may be beneficial for plant drought toleran

286 The induction of M cells was abrogated by anti-TNF-alpha blockade, sugges

287 In diurnal primates, the ratio of P to M cells was slightly but significantly higher than in no

288 nt nasopharyngeal associated lymphoid tissue M cells were defective in microparticle transcytosis.

289 ased numbers of Peyer's patch (PP) phenotype M cells were induced at the peak of inflammation in colo

290 oked postsynaptic potentials recorded in the M-cell were similarly attenuated after treatment with ei

291 an larynx carcinoma (HEp-2, ATCC, Rockville, MD) cells were used for bacterial adhesion assays.

292 ily contribute to the thylakoid membranes of M cells, whereas BS chloroplasts are mostly composed of

293 calize in renal tubules and in macula densa (MD) cells which modulate glomerular filtration rate (GFR

294 ne notable exception in mucosal epithelia is M cells, which are specialized for capturing luminal mic

295 ission yeast Schizosaccharomyces pombe P and M cells, which respectively express P and M factor phero

296 es are tuned by PI-3K signaling in CCR6(+) T(M) cells, which may contribute to chronic or autoimmune

297 gehog-responsive cephalic paraxial mesoderm (Mes) cells, which migrate rapidly to a supraorbital doma

298 The M-cell will continue to provide an unprecedented opportu

299 ge followed by a CD137-CD137L interaction of M cells with CD137-activated B lymphocytes or dendritic

300 A4 5' UTR abolishes enrichment of protein in M cells without affecting transcript abundance.