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1 educed numbers of proliferative cells in the intestinal epithelium.
2 tructure and functions of AJs and TJs in the intestinal epithelium.
3 sion and neutral drift dynamics to renew the intestinal epithelium.
4 for the bacteria to adhere and colonize the intestinal epithelium.
5 s crucial for development and renewal of the intestinal epithelium.
6 ntly found to be highly expressed within the intestinal epithelium.
7 and consequently in the self-renewal of the intestinal epithelium.
8 hism that inactivates FUT2 expression on the intestinal epithelium.
9 ntial functions of the Arp2/3 complex in the intestinal epithelium.
10 differentiate into a monolayer of polarized intestinal epithelium.
11 owever, the compounds may act locally on the intestinal epithelium.
12 ich is not glycosylated) specifically in the intestinal epithelium.
13 A let-7, which has limited expression in the intestinal epithelium.
14 ck and identify compounds transported across intestinal epithelium.
15 critical roles in maintaining homeostasis of intestinal epithelium.
16 romote the innate antiviral potential of the intestinal epithelium.
17 (SHH) was overexpressed specifically in the intestinal epithelium.
18 gths and decreased lipid droplet size in the intestinal epithelium.
19 d to activate antiviral ERK signaling in the intestinal epithelium.
20 es provided by mucus and the shedding of the intestinal epithelium.
21 ells in immune responses associated with the intestinal epithelium.
22 wth regulator and tumor suppressor in normal intestinal epithelium.
23 entiation is regulated upon migration to the intestinal epithelium.
24 rating direct conversion of fibroblasts into intestinal epithelium.
25 lizes to the apical domain of differentiated intestinal epithelium.
26 lack Tgfbr2 and/or Pten specifically in the intestinal epithelium.
27 ronounced in high-turnover tissues including intestinal epithelium.
28 ts by promoting adhesion of T. foetus to the intestinal epithelium.
29 zed to the proliferative crypt region of the intestinal epithelium.
30 ces of deleting Bmi1 specifically within the intestinal epithelium.
31 gional epithelial cell identity in the adult intestinal epithelium.
32 d influence the postnatal maturation of host intestinal epithelium.
33 ctivities of these PKC family members in the intestinal epithelium.
34 as a negative regulator of cyclin D1 in the intestinal epithelium.
35 ated phosphoinositide-3 kinase (PI3K) in the intestinal epithelium.
36 n which Apc was conditionally ablated in the intestinal epithelium.
37 was also increased in GATA4-GATA6 deficient intestinal epithelium.
38 ch was needed for T cell accumulation in the intestinal epithelium.
39 elial cells and translocate Stx2a across the intestinal epithelium.
40 itate in the crypts and rejuvenate the small intestinal epithelium.
41 nd protect against bacterial invasion of the intestinal epithelium.
42 site of Ret expression in the intestine: the intestinal epithelium.
43 roviruses invade their hosts by crossing the intestinal epithelium.
44 a multilayered regenerative response in the intestinal epithelium.
45 g cell clusters, forming villi that resemble intestinal epithelium.
46 h greatly limits their absorption across the intestinal epithelium.
47 ll monolayers, an established model of human intestinal epithelium.
48 umor necrosis factor-alpha production by the intestinal epithelium.
49 in the GI lumen can significantly damage the intestinal epithelium.
50 by toxicity in Wnt-dependent tissues such as intestinal epithelium.
51 formation: the hematopoietic lineage and the intestinal epithelium.
52 A-anti-uc.173 in mice reduced renewal of the intestinal epithelium.
53 tein Clr-a as strictly associated with mouse intestinal epithelium.
54 tines to study enterovirus infections of the intestinal epithelium.
55 (IFN-lambda) controls MNV persistence in the intestinal epithelium.
56 on the regulation of tight junctions in the intestinal epithelium.
57 ct population of Notch-positive cells in the intestinal epithelium.
58 at ExPEC strain CP9 binds to and invades the intestinal epithelium.
59 l segregation between the microbiota and the intestinal epithelium.
60 eir role in maintaining the integrity of the intestinal epithelium.
61 or SATB2+ domain in developing and postnatal intestinal epithelium.
62 noma and have similar functions to the small intestinal epithelium.
63 e GALT-promoting chemokine expression in the intestinal epithelium.
64 cells was utilized to more closely mimic the intestinal epithelium.
65 Ls with immune cells that reside outside the intestinal epithelium.
66 apoptosis and promoting regeneration in the intestinal epithelium.
67 1) that are required for the invasion of the intestinal epithelium.
68 Grp78 can be conditionally deleted from the intestinal epithelium.
69 illin-TLR4 mice that overexpress TLR4 in the intestinal epithelium.
70 highly proliferative tissues, including the intestinal epithelium.
71 in the gut can influence the homeostasis of intestinal epithelium.
72 DNA methylation and genomic integrity in the intestinal epithelium.
73 ealed unexpected and unique roles within the intestinal epithelium.
74 -exposed mice had decreased CFTR activity in intestinal epithelium (84.3 and 45%, after 5 and 17 wk,
77 icate Tfr1 in homeostatic maintenance of the intestinal epithelium, acting through a role that is ind
79 e not revealed homeostatic phenotypes in the intestinal epithelium-an archetypal canonical, Wnt pathw
80 , that also is specifically expressed by the intestinal epithelium and acts as a ligand of the inhibi
81 use "TEM-17" cells to be enriched within the intestinal epithelium and among lamina propria lymphocyt
82 proliferative Lgr5+ stem cells maintain the intestinal epithelium and are thought to be largely homo
83 Y294002, the difference in disruption of the intestinal epithelium and bacterial translocation was no
84 ulatory pathways to promote growth of normal intestinal epithelium and crypt regeneration after irrad
85 ed histone 3 lysine 27 profiles from primary intestinal epithelium and cultured organoids, which we h
86 critical synergistic interactions within the intestinal epithelium and especially Paneth cells that a
88 ng DNA regulatory regions that are active in intestinal epithelium and immune cells are potentially i
89 standing of complex interactions between the intestinal epithelium and immune cells, with a focus on
90 g pathway controls stem cell identity in the intestinal epithelium and in many other adult organs.
92 of 10 Gy irradiation was used to injure the intestinal epithelium and induce subsequent crypt regene
93 se to elevated TLR4 signaling in the newborn intestinal epithelium and is characterized by TLR4-media
94 estinal stem cells were able to colonize the intestinal epithelium and many underwent oncogenic trans
95 mice that express human DAF specifically on intestinal epithelium and measured their susceptibility
96 he A33 antigen, which is highly expressed in intestinal epithelium and more than 95% of human colon c
97 1beta (PGC-1beta) is highly expressed in the intestinal epithelium and possesses dual activity, stimu
98 such as tumor necrosis factor-alpha, in the intestinal epithelium and promotes development of coliti
100 thogens to prevent microbial invasion of the intestinal epithelium and subsequent dissemination.
101 sms of pathogenicity of T. foetus toward the intestinal epithelium and support further investigation
102 the mechanical properties of the developing intestinal epithelium and surrounding smooth muscle fold
103 ggest that TleA promotes colonization of the intestinal epithelium and that it may modulate the host
104 lly distinct cell types of the mouse jejunal intestinal epithelium and that miRNAs respond to microbi
106 imit direct contact between bacteria and the intestinal epithelium and thus promote tolerance to the
107 tive intracellular pathogen that infects the intestinal epithelium and utilizes actin-based motility
109 e secreted from enteroendocrine cells in the intestinal epithelium, and help to coordinate metabolic
110 ls, decreased protein levels of GLP-1 in the intestinal epithelium, and reduced number of L cells in
111 ateral recycling endosomes in the C. elegans intestinal epithelium, and sdpn-1 deletion mutants displ
112 the NF-kappaB inhibitor IkappaBalpha in the intestinal epithelium, and systemically decreased serum
113 brium linking the intestinal microbiota, the intestinal epithelium, and the host immune system establ
114 athogenicity on adhesion of T. foetus to the intestinal epithelium, and the identity of mediators res
115 EC) mice, which do not express VEGFR2 in the intestinal epithelium, and VEGFR2(fl/fl) mice (controls)
116 gic shock requires activation of TLR4 in the intestinal epithelium, and we sought to determine the me
119 many ways in which critical functions of the intestinal epithelium are regulated under physiological
120 roliferation and cell migration rates in the intestinal epithelium are related under healthy, damaged
121 are epithelial cell type in the steady-state intestinal epithelium, are responsible for initiating ty
122 we have used the adult Drosophila and mouse intestinal epithelium as paradigms to define a role for
123 by inhibiting NF-kappaB specifically in the intestinal epithelium as well as by decreasing systemic
124 both CD4(+)CD8(+) and CD4(+) T cells in the intestinal epithelium, as well as CD8(+) T cells in the
125 ely deleted the autophagy gene ATG7 from the intestinal epithelium (ATG7(DeltaIEC)), the induction of
128 glia are not required for maintenance of the intestinal epithelium, but are required for regulation o
129 potent trophic effects on normal or injured intestinal epithelium, but specific effects on intestina
130 strate that exposure to acrolein affects the intestinal epithelium by decrease/redistribution of tigh
131 a monocytogenes achieve dissemination in the intestinal epithelium by displaying actin-based motility
132 racellular pathogen that disseminates in the intestinal epithelium by displaying actin-based motility
133 ist that stimulates water secretion from the intestinal epithelium by promoting chloride and bicarbon
137 of two frequently used protocols to isolate intestinal epithelium cells (IECs) from 6 healthy indivi
139 sruption of the gene encoding cFlip from the intestinal epithelium (cFlip(fl/fl) VillinCre(+) mice) r
140 -/-) mice depended on increased apoptosis of intestinal epithelium, changed gut microflora, and eleva
141 nuclear leukocyte (PMN) migration across the intestinal epithelium closely parallels disease symptoms
142 mice, but not in mice that lack TLR4 in the intestinal epithelium, confirming the importance of inte
144 suggest that a depletion of PGC1alpha in the intestinal epithelium contributes to inflammatory change
145 ells mediate immunity and maintain the small intestinal epithelium; defects in activities of these ce
147 onstrate that MyD88 and autophagy within the intestinal epithelium detect invasive bacteria and preve
148 in vivo, as mice with loss of Ptger4 in the intestinal epithelium did not produce WAE cells and exhi
150 d that FGF2 cooperates with IL-17 to protect intestinal epithelium during dextran sodium sulfate (DSS
151 illin-Cre, which deletes specifically in the intestinal epithelium during the period of villus develo
152 disruption in Lgr5(+) stem cells or in whole intestinal epithelium eliminated H3K79me2 from the respe
153 To cause disease, Salmonella must invade the intestinal epithelium employing genes encoded within Sal
154 Specifically, upon loss of NDR1/2 in the intestinal epithelium, endogenous S127 phosphorylation i
155 inal epithelial cell types that comprise the intestinal epithelium (enterocytes and goblet, enteroend
156 utrophil infiltration, IL-17 expression, and intestinal epithelium erosion were observed in JAK3 knoc
157 ptake of mercury in Caco-2 cells, a model of intestinal epithelium, exposed to Hg(II) and CH3Hg stand
159 Following conditional deletion of Snai1, the intestinal epithelium fails to produce a proliferative r
162 rived organoids are a promising model of the intestinal epithelium for assessing interactions with en
163 Ps can effectively be transported across the intestinal epithelium for oral insulin delivery, leading
168 mediated NOX4 downregulation may protect the intestinal epithelium from oxidative stress-induced dama
170 rly separate the effects of radiation on the intestinal epithelium from those on the BM and endotheli
172 ria invade the small intestine, crossing the intestinal epithelium from where they are transported to
175 nt carbohydrates and host glycans lining the intestinal epithelium, gut bacteria produce a wide range
176 his allowed visualization of areas where the intestinal epithelium had been compromised and demonstra
178 and is a stem cell marker in the stomach and intestinal epithelium, hair follicles, and ovarian surfa
183 yers of Caco-2 cells, used as a model of the intestinal epithelium, has been characterised by HPLC an
184 ish a similar stem cell hierarchy within the intestinal epithelium have yielded conflicting results,
185 asmic reticulum (ER) stress is implicated in intestinal epithelium homeostasis and inflammatory bowel
186 uclear receptor-4alpha (HNF-4alpha) controls intestinal epithelium homeostasis and intestinal absorpt
187 from the interactions between the pathogen, intestinal epithelium, host immune system, and gastroint
191 olling the proliferation and function of the intestinal epithelium in the context of beta-catenin act
192 effect of TLR4-induced autophagy within the intestinal epithelium in the pathogenesis of NEC and ide
195 nversely, ectopic expression of Snai1 in the intestinal epithelium in vivo results in the expansion o
197 ng PGRP-SC2 expression in enterocytes of the intestinal epithelium, in turn, prevents dysbiosis, prom
198 istics associated with normal differentiated intestinal epithelium, including brush border enzymes, p
204 icrobial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a
208 nt a method in which genetic labeling in the intestinal epithelium is acquired as a mutation-induced
212 Ablation of both Dnmt1 and Dnmt3b in the intestinal epithelium is lethal, while deletion of eithe
213 on of mouse colonic intestinal stem cells to intestinal epithelium is not associated with major chang
214 te that the absence of an apical receptor on intestinal epithelium is not the major barrier to infect
219 nt on Caco-2 monolayers and on primary human intestinal epithelium markedly induces the expression of
220 by bacteria that have already colonized the intestinal epithelium may recruit E. coli and other ente
221 hway-driven proliferation and renewal of the intestinal epithelium must be tightly controlled to prev
222 ock-out approach to knock out Nedd4L in mice intestinal epithelium (Nedd4L(f/f) ;Vil-Cre(ERT2) ) we s
223 rica serovar Typhimurium colonization in the intestinal epithelium of caspase-11-deficient mice, but
224 1 light chain 3beta (Map1lc3b or LC3) in the intestinal epithelium of control mice but not in Atg16l1
225 n both the ovarian follicular epithelium and intestinal epithelium of Drosophila, apical Spectrins an
226 The translocation of bacteria across the intestinal epithelium of immunocompromised patients can
227 regulation of TNF-induced cell death in the intestinal epithelium of mice and intestinal organoids.
228 We selectively deleted PGC1alpha from the intestinal epithelium of mice by breeding a PGC1alpha(lo
229 that Ret is also expressed by the developing intestinal epithelium of mice, where its expression is m
231 dentified several abnormalities in the small-intestinal epithelium of Nod2(-/-) mice including inflam
235 response to regenerative stimuli, SCs in the intestinal epithelium of the fly and in the tracheal epi
238 This culture system recapitulates the human intestinal epithelium, permits human host-pathogen studi
239 he apical junction orientation, and impaired intestinal epithelium polarity, which can contribute to
241 Rapid induction of Il25 expression in the intestinal epithelium preceded onset of the anaphylactic
242 ramatically increase the surface area of the intestinal epithelium, preparing the gut for the neonata
243 ential regulatory regions that are active in intestinal epithelium (primary intestinal crypts and cul
244 tion of the tyrosine phosphatase Shp2 in the intestinal epithelium reduced MAPK signaling and led to
248 Significantly, ablation of NDR1/2 from the intestinal epithelium renders mice exquisitely sensitive
250 pporting the concept that maintenance of the intestinal epithelium requires enteric glia can be attri
252 clearly distinguish Clr-a from the likewise intestinal epithelium-restricted Clr-f, pointing to a no
253 te that conditional knockout of Snai1 in the intestinal epithelium results in apoptotic loss of crypt
257 with disruption of Sirt1 specifically in the intestinal epithelium (SIRT1 iKO, villin-Cre+, Sirt1(flo
258 ression of Epas1 (Epas1(LSL/LSL)), mice with intestinal epithelium-specific deletion of Epas1 (Epas1(
261 l aspect of PPARgamma function, we submitted intestinal epithelium-specific PPARgamma knockout mice (
263 ed Campylobacter must translocate across the intestinal epithelium, spread systemically in the circul
264 e with a conditional deletion of Tfeb in the intestinal epithelium (Tfeb (DeltaIEC)) to examine its i
265 tricate nature of ETEC interactions with the intestinal epithelium that have potential implications f
266 results indicate a novel role for Crh in the intestinal epithelium that involves regulation of autoph
267 ss of adaptive cellular reprogramming of the intestinal epithelium that occurs to ensure proper repai
268 se in transepithelial resistance and a leaky intestinal epithelium that was determined by in vivo tra
271 ll populations in aging tissues, such as the intestinal epithelium, the hematopoietic system, and the
272 we review advancements in understanding the intestinal epithelium, the mucosal immune system, and th
273 s not required for the survival of the adult intestinal epithelium, the only rapidly dividing somatic
274 h to model feline T. foetus infection of the intestinal epithelium, these studies demonstrate that T.
275 llular pathogen that disseminates within the intestinal epithelium through acquisition of actin-based
276 F2 and IL-17 cooperate to repair the damaged intestinal epithelium through Act1-mediated direct signa
277 regulator of growth factor signaling in the intestinal epithelium through activation of PTP1B and su
278 -beta as a novel mRNA stability regulator in intestinal epithelium through its ability to promote TTP
279 s activation of the LPS receptor TLR4 on the intestinal epithelium, through its effects on modulating
280 atment increased the barrier function of the intestinal epithelium, thus preventing the translocation
281 sence of an endogenous mechanism used by the intestinal epithelium to dynamically regulate its parace
282 or understanding the genetic response of the intestinal epithelium to maintain whole-body iron homeos
283 teria-secreted particles (ET-BSPs) stimulate intestinal epithelium to produce IDENs (intestinal mucos
285 . monocytogenes that efficiently invades the intestinal epithelium to show that Vgamma4(+) memory gam
286 he permeability and inflammatory response of intestinal epithelium under normal, inflammatory, and hy
287 titutive active form of LXRalpha only in the intestinal epithelium, under the control of villin promo
288 pathologies is particularly important as the intestinal epithelium undergoes self-renewal every 4-7 d
289 n complex 1 (mTORC1), was acutely deleted in intestinal epithelium via Tamoxifen injection in Tritric
295 fter trauma, and mice that lack HMGB1 in the intestinal epithelium were protected from the developmen
296 that NOX1 regulates DUOX2 expression in the intestinal epithelium, which magnified the epithelial RO
298 ls (MC) are immune cells located next to the intestinal epithelium with regulatory function in mainta
299 nd highlight a critical role of IL-10 in the intestinal epithelium, with broad implications for disea
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