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1 tive intracellular pathogen that invades the intestinal epithelium.
2 formation: the hematopoietic lineage and the intestinal epithelium.
3 or SATB2+ domain in developing and postnatal intestinal epithelium.
4 Ls with immune cells that reside outside the intestinal epithelium.
5 Grp78 can be conditionally deleted from the intestinal epithelium.
6 for the bacteria to adhere and colonize the intestinal epithelium.
7 differentiate into a monolayer of polarized intestinal epithelium.
8 t is also involved in the normal turnover of intestinal epithelium.
9 ronounced in high-turnover tissues including intestinal epithelium.
10 site of Ret expression in the intestine: the intestinal epithelium.
11 h greatly limits their absorption across the intestinal epithelium.
12 te contents of the intestinal lumen from the intestinal epithelium.
13 A-anti-uc.173 in mice reduced renewal of the intestinal epithelium.
14 tein Clr-a as strictly associated with mouse intestinal epithelium.
15 tines to study enterovirus infections of the intestinal epithelium.
16 (IFN-lambda) controls MNV persistence in the intestinal epithelium.
17 on the regulation of tight junctions in the intestinal epithelium.
18 ct population of Notch-positive cells in the intestinal epithelium.
19 ivation affects ISCs and regeneration of the intestinal epithelium.
20 at ExPEC strain CP9 binds to and invades the intestinal epithelium.
21 l segregation between the microbiota and the intestinal epithelium.
22 eir role in maintaining the integrity of the intestinal epithelium.
23 noma and have similar functions to the small intestinal epithelium.
24 e GALT-promoting chemokine expression in the intestinal epithelium.
25 cells was utilized to more closely mimic the intestinal epithelium.
26 nder factors to enhance the radiotoxicity of intestinal epithelium.
27 apoptosis and promoting regeneration in the intestinal epithelium.
28 1) that are required for the invasion of the intestinal epithelium.
29 rom intestinal progenitors to differentiated intestinal epithelium.
30 illin-TLR4 mice that overexpress TLR4 in the intestinal epithelium.
31 highly proliferative tissues, including the intestinal epithelium.
32 in the gut can influence the homeostasis of intestinal epithelium.
33 DNA methylation and genomic integrity in the intestinal epithelium.
34 ealed unexpected and unique roles within the intestinal epithelium.
35 educed numbers of proliferative cells in the intestinal epithelium.
36 tructure and functions of AJs and TJs in the intestinal epithelium.
37 sion and neutral drift dynamics to renew the intestinal epithelium.
38 hich translocate enteric bacteria across the intestinal epithelium.
39 s crucial for development and renewal of the intestinal epithelium.
40 ntly found to be highly expressed within the intestinal epithelium.
41 and consequently in the self-renewal of the intestinal epithelium.
42 hism that inactivates FUT2 expression on the intestinal epithelium.
43 ntial functions of the Arp2/3 complex in the intestinal epithelium.
44 (ISCs) maintain regenerative capacity of the intestinal epithelium.
45 owever, the compounds may act locally on the intestinal epithelium.
46 ich is not glycosylated) specifically in the intestinal epithelium.
47 A let-7, which has limited expression in the intestinal epithelium.
48 ck and identify compounds transported across intestinal epithelium.
49 critical roles in maintaining homeostasis of intestinal epithelium.
50 romote the innate antiviral potential of the intestinal epithelium.
51 (SHH) was overexpressed specifically in the intestinal epithelium.
52 gths and decreased lipid droplet size in the intestinal epithelium.
53 measured their transport across a polarized intestinal epithelium.
54 d to activate antiviral ERK signaling in the intestinal epithelium.
55 es provided by mucus and the shedding of the intestinal epithelium.
56 ells in immune responses associated with the intestinal epithelium.
57 wth regulator and tumor suppressor in normal intestinal epithelium.
58 ation via interaction with circPABPN1 in the intestinal epithelium.
59 rol of autophagy-related genes (ATGs) in the intestinal epithelium.
60 cus specifically on the role of IL-22 in the intestinal epithelium.
61 eria or bacterial products through the small intestinal epithelium.
62 of nutrients and drug molecules towards the intestinal epithelium.
63 ells that fuel the continuous renewal of the intestinal epithelium.
64 4G were expressed in ISCs and throughout the intestinal epithelium.
65 reflects the characteristics of the in vivo intestinal epithelium.
66 irects the flow of water absorbed across the intestinal epithelium.
67 ironment to the bacteria as the normal human intestinal epithelium.
68 Hippo pathway that promotes regeneration of intestinal epithelium.
69 indoleamine 2,3-dioxygenase 1 (IDO1) in the intestinal epithelium.
70 nal lumen and increased proliferation of the intestinal epithelium.
71 acteria prevent rotavirus from infecting the intestinal epithelium.
74 higher affinity for bacteria than simulated intestinal epithelium, a valuable activity at therapeuti
75 icate Tfr1 in homeostatic maintenance of the intestinal epithelium, acting through a role that is ind
77 e not revealed homeostatic phenotypes in the intestinal epithelium-an archetypal canonical, Wnt pathw
78 orial, but inflammatory signaling within the intestinal epithelium and a subsequent failure of the in
79 , that also is specifically expressed by the intestinal epithelium and acts as a ligand of the inhibi
80 use "TEM-17" cells to be enriched within the intestinal epithelium and among lamina propria lymphocyt
81 proliferative Lgr5+ stem cells maintain the intestinal epithelium and are thought to be largely homo
82 ulatory pathways to promote growth of normal intestinal epithelium and crypt regeneration after irrad
83 critical synergistic interactions within the intestinal epithelium and especially Paneth cells that a
84 are specialised sensory cells located in the intestinal epithelium and generate signals in response t
85 the antiviral mechanisms at play within the intestinal epithelium and how these responses are shaped
87 standing of complex interactions between the intestinal epithelium and immune cells, with a focus on
88 g pathway controls stem cell identity in the intestinal epithelium and in many other adult organs.
90 of 10 Gy irradiation was used to injure the intestinal epithelium and induce subsequent crypt regene
93 mice that express human DAF specifically on intestinal epithelium and measured their susceptibility
96 sms of pathogenicity of T. foetus toward the intestinal epithelium and support further investigation
97 ggest that TleA promotes colonization of the intestinal epithelium and that it may modulate the host
98 lly distinct cell types of the mouse jejunal intestinal epithelium and that miRNAs respond to microbi
99 ion between symbiotic microorganisms and the intestinal epithelium and the effective killing of penet
101 l cycle arrest inhibits proliferation of the intestinal epithelium and ultimately results in compromi
103 nating PPAR-regulated lipid oxidation in the intestinal epithelium, and identify intestinal HDAC3 as
104 ateral recycling endosomes in the C. elegans intestinal epithelium, and sdpn-1 deletion mutants displ
105 brium linking the intestinal microbiota, the intestinal epithelium, and the host immune system establ
106 EC) mice, which do not express VEGFR2 in the intestinal epithelium, and VEGFR2(fl/fl) mice (controls)
107 rams that guide the cell-fate transitions of intestinal epithelium, and we identify an inhibitor of t
108 gic shock requires activation of TLR4 in the intestinal epithelium, and we sought to determine the me
109 lammatory responses in human macrophages and intestinal epithelium; and ii) directly cleared pro-infl
111 eviously showed that mice lacking FAK in the intestinal epithelium are phenotypically normal under ho
112 many ways in which critical functions of the intestinal epithelium are regulated under physiological
113 roliferation and cell migration rates in the intestinal epithelium are related under healthy, damaged
114 are epithelial cell type in the steady-state intestinal epithelium, are responsible for initiating ty
116 n, the loss of TMIGD1 significantly impaired intestinal epithelium brush border membrane, junctional
118 glia are not required for maintenance of the intestinal epithelium, but are required for regulation o
120 potent trophic effects on normal or injured intestinal epithelium, but specific effects on intestina
121 strate that exposure to acrolein affects the intestinal epithelium by decrease/redistribution of tigh
122 a monocytogenes achieve dissemination in the intestinal epithelium by displaying actin-based motility
124 model in which various cell types within the intestinal epithelium can de-differentiate and function
127 we found that IGF2BP1 ablation in the adult intestinal epithelium causes mild active colitis and mil
128 animals age, the cellular composition of the intestinal epithelium changes, resulting in a decreased
129 mice, but not in mice that lack TLR4 in the intestinal epithelium, confirming the importance of inte
130 suggest that a depletion of PGC1alpha in the intestinal epithelium contributes to inflammatory change
132 and KRIT1 knockdown in differentiated Caco-2 intestinal epithelium decreases epithelial barrier funct
133 ells mediate immunity and maintain the small intestinal epithelium; defects in activities of these ce
134 Here we show that deletion of Znhit1 in intestinal epithelium depletes Lgr5+ stem cells thus dis
135 in vivo, as mice with loss of Ptger4 in the intestinal epithelium did not produce WAE cells and exhi
136 he regenerative potential of human and mouse intestinal epithelium diminishes with age owing to defec
137 d that FGF2 cooperates with IL-17 to protect intestinal epithelium during dextran sodium sulfate (DSS
138 why Giardia trophozoites adhere to the small intestinal epithelium during human and animal infections
139 ial cells, their contribution was studied in intestinal epithelium dysfunction using coculture of pri
140 Specifically, upon loss of NDR1/2 in the intestinal epithelium, endogenous S127 phosphorylation i
141 inal epithelial cell types that comprise the intestinal epithelium (enterocytes and goblet, enteroend
142 Moreover, NEUROG3 was highly unstable in the intestinal epithelium, explaining the enhanced sensitivi
143 ptake of mercury in Caco-2 cells, a model of intestinal epithelium, exposed to Hg(II) and CH3Hg stand
145 Following conditional deletion of Snai1, the intestinal epithelium fails to produce a proliferative r
146 l expression of genes in mammalian liver and intestinal epithelium, fly and zebrafish embryos, sectio
147 injury and pro-tumorigenic responses in the intestinal epithelium following AOM/DSS treatment, and t
150 nate immune responses that are active in the intestinal epithelium following viral infection, but our
151 rived organoids are a promising model of the intestinal epithelium for assessing interactions with en
152 Ps can effectively be transported across the intestinal epithelium for oral insulin delivery, leading
156 mediated NOX4 downregulation may protect the intestinal epithelium from oxidative stress-induced dama
159 ria invade the small intestine, crossing the intestinal epithelium from where they are transported to
162 cattered cells found along the length of the intestinal epithelium, gut hormones generate signals rel
163 his allowed visualization of areas where the intestinal epithelium had been compromised and demonstra
165 stinal stem cells (ISCs) expressing Lgr5 The intestinal epithelium has to cope with continuous stress
166 ish a similar stem cell hierarchy within the intestinal epithelium have yielded conflicting results,
167 rine cells, which are relatively rare in the intestinal epithelium, have evolved to sense and respond
168 asmic reticulum (ER) stress is implicated in intestinal epithelium homeostasis and inflammatory bowel
169 uclear receptor-4alpha (HNF-4alpha) controls intestinal epithelium homeostasis and intestinal absorpt
170 from the interactions between the pathogen, intestinal epithelium, host immune system, and gastroint
174 accumulation and promotes repair of damaged intestinal epithelium in inflamed colon, serves as a pot
176 This work highlights the importance of the intestinal epithelium in the colitis response and the po
177 olling the proliferation and function of the intestinal epithelium in the context of beta-catenin act
178 ous enteropathogen Shigella in breaching the intestinal epithelium in vitro and in vivo Whether and h
180 nversely, ectopic expression of Snai1 in the intestinal epithelium in vivo results in the expansion o
181 Forced expression of Neurod1 throughout intestinal epithelium increased the number of EECs as we
182 n colon after DMOG treatment associates with intestinal epithelium integrity and reduced damage cause
183 efines the ability to study microbiome:human intestinal epithelium interactions in the laboratory.
184 logical response of the local RAS within the intestinal epithelium involves mechanisms distinct from
185 transplantation, that all cells of the mouse intestinal epithelium-irrespective of their location and
191 icrobial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a
197 he probability of mutant fixation within the intestinal epithelium is dictated by a combination of st
199 Ablation of both Dnmt1 and Dnmt3b in the intestinal epithelium is lethal, while deletion of eithe
201 on of mouse colonic intestinal stem cells to intestinal epithelium is not associated with major chang
202 te that the absence of an apical receptor on intestinal epithelium is not the major barrier to infect
210 microbiome restores barrier function of the intestinal epithelium, leading to a reestablishment of h
211 Specific deletion of Smarcad1 in the mouse intestinal epithelium leads to colitis resistance and su
212 activation of NOTCH1 signaling in the murine intestinal epithelium leads to highly penetrant metastas
213 nt on Caco-2 monolayers and on primary human intestinal epithelium markedly induces the expression of
214 evaluated by cell viability tests with human intestinal epithelium model cells (Caco-2) have shown th
215 hway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prev
216 ock-out approach to knock out Nedd4L in mice intestinal epithelium (Nedd4L(f/f) ;Vil-Cre(ERT2) ) we s
217 n both the ovarian follicular epithelium and intestinal epithelium of Drosophila, apical Spectrins an
219 ctive CaMKIV was highly expressed within the intestinal epithelium of humans with ulcerative colitis
220 The translocation of bacteria across the intestinal epithelium of immunocompromised patients can
221 regulation of TNF-induced cell death in the intestinal epithelium of mice and intestinal organoids.
222 We selectively deleted PGC1alpha from the intestinal epithelium of mice by breeding a PGC1alpha(lo
223 that Ret is also expressed by the developing intestinal epithelium of mice, where its expression is m
227 response to regenerative stimuli, SCs in the intestinal epithelium of the fly and in the tracheal epi
229 nificant delay in recovery and repair of the intestinal epithelium of up to 2 wk post the infection p
230 dysfunction, telomerase reactivation in the intestinal epithelium or pharmacological inhibition of A
231 This culture system recapitulates the human intestinal epithelium, permits human host-pathogen studi
234 Rapid induction of Il25 expression in the intestinal epithelium preceded onset of the anaphylactic
235 ramatically increase the surface area of the intestinal epithelium, preparing the gut for the neonata
242 Significantly, ablation of NDR1/2 from the intestinal epithelium renders mice exquisitely sensitive
245 pporting the concept that maintenance of the intestinal epithelium requires enteric glia can be attri
247 clearly distinguish Clr-a from the likewise intestinal epithelium-restricted Clr-f, pointing to a no
248 removal compromises barrier function of the intestinal epithelium, resulting from altered protein ex
249 te that conditional knockout of Snai1 in the intestinal epithelium results in apoptotic loss of crypt
251 Our findings provide insight into how the intestinal epithelium senses dietary vitamin A status to
256 with disruption of Sirt1 specifically in the intestinal epithelium (SIRT1 iKO, villin-Cre+, Sirt1(flo
257 showed it to efficiently cross healthy human intestinal epithelium (SMI-100) by a vesicular transcyto
259 l aspect of PPARgamma function, we submitted intestinal epithelium-specific PPARgamma knockout mice (
260 ed Campylobacter must translocate across the intestinal epithelium, spread systemically in the circul
262 e with a conditional deletion of Tfeb in the intestinal epithelium (Tfeb (DeltaIEC)) to examine its i
263 tricate nature of ETEC interactions with the intestinal epithelium that have potential implications f
264 results indicate a novel role for Crh in the intestinal epithelium that involves regulation of autoph
265 ncer (CRC) is a heterogeneous disease of the intestinal epithelium that is characterized by the accum
266 ss of adaptive cellular reprogramming of the intestinal epithelium that occurs to ensure proper repai
267 (EECs) are specialized sensory cells in the intestinal epithelium that sense and transduce nutrient
270 ll populations in aging tissues, such as the intestinal epithelium, the hematopoietic system, and the
271 we review advancements in understanding the intestinal epithelium, the mucosal immune system, and th
272 s not required for the survival of the adult intestinal epithelium, the only rapidly dividing somatic
273 viding insights into chemical uptake via the intestinal epithelium, this system can easily be transfe
274 llular pathogen that disseminates within the intestinal epithelium through acquisition of actin-based
275 F2 and IL-17 cooperate to repair the damaged intestinal epithelium through Act1-mediated direct signa
276 s activation of the LPS receptor TLR4 on the intestinal epithelium, through its effects on modulating
277 atment increased the barrier function of the intestinal epithelium, thus preventing the translocation
278 sence of an endogenous mechanism used by the intestinal epithelium to dynamically regulate its parace
279 teria-secreted particles (ET-BSPs) stimulate intestinal epithelium to produce IDENs (intestinal mucos
281 . monocytogenes that efficiently invades the intestinal epithelium to show that Vgamma4(+) memory gam
282 overexpress fluorescence-tagged IDO1 in the intestinal epithelium under control of the villin promot
283 he permeability and inflammatory response of intestinal epithelium under normal, inflammatory, and hy
285 pathologies is particularly important as the intestinal epithelium undergoes self-renewal every 4-7 d
287 n complex 1 (mTORC1), was acutely deleted in intestinal epithelium via Tamoxifen injection in Tritric
289 d in the stem and proliferative zones of the intestinal epithelium, we explore its role in this tissu
290 on residual F508del-Cftr function in murine intestinal epithelium, we were prompted to determine whe
293 fter trauma, and mice that lack HMGB1 in the intestinal epithelium were protected from the developmen
294 moted in vivo Salmonella pathogenesis in the intestinal epithelium where Salmonella initiates infecti
295 that NOX1 regulates DUOX2 expression in the intestinal epithelium, which magnified the epithelial RO
296 ls (MC) are immune cells located next to the intestinal epithelium with regulatory function in mainta
297 show the extended coculture of living human intestinal epithelium with stable communities of aerobic
298 nd highlight a critical role of IL-10 in the intestinal epithelium, with broad implications for disea
300 derivatives retinol and retinoic acid by the intestinal epithelium, yet little is known about how epi