ライフサイエンスコーパス: M cell

1 d transcytotic cells called microfold cells (M cell).

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

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

4 tor B1 (SR-B1) as an EsxA receptor on airway M cells.

5 ich facilitate adherence of S Typhimurium to M cells.

6 ired for preferential accumulation of GUS in M cells.

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

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

9 llometry compared with the earlier-generated M cells.

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

11 Virus particles have been observed within M cells.

12 ylate cyclase AC3 underlies PDF signaling in M cells.

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

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

15 t marks epithelial transdifferentiation into M cells.

16 primary gene that dictates directionality in M cells.

17 cells and inhibited in Exoc5-KD and EXOC5CTS-m cells.

18 when enteroids are differentiated to include M cells.

19 7 GBS crosses the intestinal barrier through M cells.

20 med that S Typhi also preferentially targets M cells.

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

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

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

24 sociates with spindle-associated proteins in mES cells.

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

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

27 n and spindle pole integrity specifically in mES cells.

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

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

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

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

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

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

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

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

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 eptide (CGRP), a neuropeptide that modulates M cells and SFB levels to protect against Salmonella inf

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

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

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 likelihood of spatial proximity of hybrid E/M cells, and (iii) expand the fraction of CSCs.

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

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

51 M cells are specialized epithelial cells mediating immun

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

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

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

55 pulation of hybrid epithelial/mesenchymal (E/M) cells are required to recapitulate CTC size distribut

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

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

58 Microfold cells (M-cells) are specialized cells of the intestine that sam

59 ties of a patient-derived tumor (with ~0.5-2 M cells) at single-cell resolution within 2 h.

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

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

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

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

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

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

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

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

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

73 ly induced apoptosis, differentiation and G2/M cell cycle arrest and caused less undesirable stabiliz

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

75 the ERR-beta2 isoform to play a role in G(2)/M cell cycle arrest and induction of apoptosis, in contr

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

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

78 75 and B16F10 cell proliferation, induced G2/M cell cycle arrest and led to apoptosis and cell death.

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

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

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

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

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

84 o abrogate radiation therapy (RT)-induced G2/M cell cycle arrest in multiple cell lines and, we find

85 s also widely accepted that Vif induces G(2)/M cell cycle arrest in several different cell types.

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

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

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

89 We show that G(2)/M cell cycle arrest strongly enhances the replication of

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

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

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

93 the proliferation of these cells, induced G2/M cell cycle arrest, and led to apoptosis.

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

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

96 4-HNE induced G(2)-M cell cycle arrest, led to formation gammaH2AX foci, an

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

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

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

100 ecessary and sufficient for Vif-dependent G2/M cell cycle arrest.

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

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

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

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

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

106 essory protein is also known to trigger G(2)/M cell cycle arrest.

107 y the phosphorylation of H2AX and induced G2/M cell cycle arrest.

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

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

110 ts of the conventional DNA damage-induced G2/M cell cycle checkpoint and the spindle assembly checkpo

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

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

113 o small-molecule inhibitors targeting the G2/M cell cycle checkpoint kinase, CHK1, in a variety of no

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

115 described as important regulators of the G2-M cell cycle checkpoint.

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

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

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

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

120 X-351 activates CHK1 as well as the S and G2/M cell cycle checkpoints.

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

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

123 inhibited proteins controlling G(1) and G(2)/M cell cycle phases during the differentiation of human

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

125 e (Cdk)1, one of the master regulators of G2/M cell cycle progression in U. maydis, interacts and con

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

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

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

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

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

131 hances HIV-1 gene expression and induces (G2/M) cell cycle arrest.

132 d proliferation, clonogenicity, induced G(2)/M cell-cycle arrest and caspase-mediated-apoptosis of CR

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

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

135 < 0.0001), corresponding with a prolonged G2-M cell-cycle arrest and increased apoptosis following ra

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

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

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

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

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

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

142 ry and longevity by minimizing apoptosis, G2/M cell-cycle arrest, and subsequent fibrosis.

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

144 th delay, DNA double-strand breaks, and G(2)-M cell-cycle arrest, which led to ATR-dependent phosphor

145 on and slowed proliferation by inducing G(2)-M cell-cycle arrest, while upregulating DNA damage pathw

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

147 It also induced G(2)/M cell-cycle arrest.

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

149 eplication fork recovery, and enforcing a G2/M cell-cycle arrest.

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

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

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

153 iated tissue, and through deactivation of G2/M cell-cycle checkpoint allows the cell-cycle progressio

154 ancer cells to override the p53-dependent G2/M cell-cycle checkpoint.

155 r caspase-8 to override the p53-dependent G2/M cell-cycle checkpoint.

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

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

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

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

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

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

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

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

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

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

166 d by E2-P4 C(7) concentrations which promote M cell differentiation and CC17 GBS invasiveness.

167 y to inflammatory injury by inducing ectopic M-cell differentiation and a chronic increase of IL-17A.

168 Intestinal NIK signaling modulates M-cell differentiation and elicits both local and system

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

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

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

172 However, the mechanistic basis for M cell entry remains undefined.

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

174 22, and Il26) in CCR6(+), but not CCR6(-), T(M) cells, even in CCR6(+) cells lacking IL-17 expression

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

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

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

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

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

180 (2) and C(4) Neurachne species; width of the MS cells; frequency of plasmodesmata in the MS cell wall

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

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

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

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

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

186 M-cells have been proposed as evolutionary ancestors of

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

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

189 for Mtb binding to and translocation across M cells in mouse and human tissue.

190 Though the host M cells in Peyer's patch and the bacterial invasion prot

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

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

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

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

195 ciceptors regulate the density of microfold (M) cells in ileum Peyer's patch (PP) follicle-associated

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

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

198 important function of non-canonical NFkB and M-cells in immune homeostasis, inflammation and polymicr

199 The function of M-cells in systemic inflammatory responses are still unc

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

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

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

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

204 82 expressed genes; 14,972 were expressed in M cells, including 53 M-enriched transcription factor (T

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

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

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

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

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

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

211 The giant Mauthner (M) cell is the largest neuron known in the vertebrate br

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

213 Only 1 wedge had M-cell islands.

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

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

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

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

218 1A3 cell lines and the human HT1080 and HeLa-M cell lines, in which both the TLR3 and the STING pathw

219 000 individual haploid mouse embryonic stem (mES) cell lines targeting 16,970 genes with genetically

220 inal lymphoid follicles, and is required for M-cell maintenance.

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

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

223 s to directly test the survival value of the M cell-mediated escapes and to show that the absence of

224 isingly unclear: An actual survival value of M cell-mediated escapes has never been supported experim

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

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

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

228 Downstream of M cells, nociceptors maintain levels of segmentous filam

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

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

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

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

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

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

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

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

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

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

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

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

241 ions between epithelial (E) and mesenchymal (M) cell phenotypes are essential in many biological proc

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

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

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

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

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

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

248 al invasion and identify SR-B1 as the airway M cell receptor for Mtb.

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

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

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

252 Although M cells represent a small proportion of the specialized

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

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

255 ransferred MYHCA614-629-specific CD4+ T (TCR-M) cells selectively accumulated in the myocardium and m

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

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

258 he essential regulatory elements for driving M-cell-specific expression in rice leaves.

259 ne from three C(4) grass species could drive M-cell-specific expression of a reporter gene in rice.

260 upstream element(s) is required for driving M-cell-specific expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 Here, we show that M cell transcytosis depends on the Mtb Type VII secretio

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

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

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

287 MS cells; frequency of plasmodesmata in the MS cell walls adjoining the parenchymatous bundle sheath

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

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

290 ects in Palb2 knockout mouse embryonic stem (mES) cells, we identify various VUS in PALB2 that impair

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

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

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

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

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

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

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

298 an increase in organelle and GLDP content in MS cells, which generated a sink for photorespired CO(2)

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

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