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1 ian clock in 3D murine intestinal organoids (enteroids).
2 n Mtgr1(-/-) whole intestines and Mtgr1(-/-) enteroids.
3 pattern was also observed in differentiated enteroids.
4 response to cAMP and elevated calcium in T1D enteroids.
5 the bacterium to infect 3D bovine basal-out enteroids.
6 ently and inhibited GII.3 cellular uptake in enteroids.
7 tivation in vivo and in both mouse and human enteroids.
8 riants with high potency in human intestinal enteroids.
9 ary human airway cells and stem cell-derived enteroids.
10 n cell lines, nonhuman cell lines, and human enteroids.
11 nted HAstV infection in cell lines and human enteroids.
12 ifferentiation and maturation versus healthy enteroids.
13 of BA transporters was attenuated in NT(-/-) enteroids.
14 uration, and longevity of tubular intestinal enteroids.
15 re rhythmically expressed in mouse and human enteroids.
16 a median phase shift of 6.2 hours in murine enteroids.
17 nthetic lethality in HIF-2a-expressing tumor enteroids.
18 out cell differentiation in human intestinal enteroids.
19 man intestinal epithelial cell monolayer and enteroids.
20 of the BA-dependent strain GII.3 in jejunal enteroids.
21 functional Na+/H+ exchange activity in MVID enteroids.
22 hogenesis using human colonoids and duodenal enteroids.
23 UROG3 protein levels in BON4 cells and human enteroids.
24 d enhanced CFTR-dependent fluid secretion in enteroids.
25 control mice, and established 3-dimensional enteroids.
26 inking the circadian clock and cell cycle in enteroids.
27 observed in cell lines and human intestinal enteroids.
28 ition in undifferentiated and differentiated enteroids.
30 < .05) and conditional knockout of HDAC3 in enteroids abrogated butyrate effects on Per2 expression.
32 eta-catenin target gene expression in murine enteroids and colonoid cultures and TNF-induced beta-cat
33 encing (RNA-seq) of metabolite-exposed human enteroids and duodenal biopsies post-FMT confirmed trans
34 embryonic fibroblasts from mice, along with enteroids and human IEC lines, we found that induction o
35 on utilization of three-dimensional primary enteroids and organoids for mechanistic studies of intes
36 Using untransformed ex situ human intestinal enteroids and transformed Caco-2 cells, we report that E
37 fferocytosis, ex vivo intestinal organoids ("enteroids"), and in vivo Cre-mediated deletion of Paneth
39 inactivated by TcdB, between mouse and human enteroids, and disruption of Rac1 abolishes clock-depend
41 elopment and maintenance of upper intestinal enteroids, and these effects were rescued by acetate tre
42 milar in undifferentiated and differentiated enteroids, and was affected by known inhibitors, second
50 y askew in human small intestinal organoids (enteroids) as compared to that in paired tissue from whi
51 Utilizing primary human duodenal organoids (enteroids) as in vitro models of the functional GI epith
52 ions, efficient phagocytosis, and stabilized enteroid barrier function revealed a coordinated respons
53 ced the expression of alpha-defensin mRNA in enteroids by >100,000-fold, restoring DEFA5 and DEFA6 to
54 ndritic cells, B cells and stem-cell-derived enteroids can all support infection of certain norovirus
57 and characterized a primary human macrophage-enteroid co-culture model for in-depth studies of epithe
58 tablished the first primary human macrophage-enteroid co-culture system, defined conditions that allo
59 eltaLyz) ) mouse model and used a macrophage/enteroids coculture system to examine tissue-specific VD
60 were reproducible in human Bmal1-luciferase enteroids, colonoids, and Per2-luciferase Caco-2 cells.
61 ated intestinal crypts or stem cells (termed enteroids/colonoids) and from inducible pluripotent stem
62 In mouse and human normal and tumor-derived enteroids/colonoids, those that expressed SPDEF for 3 da
63 surement of kinetically labile iron pools in enteroids competent or blocked for iron efflux indicated
69 d showed it neutralizes noroviruses in human enteroid cultures and abrogates or reduces infection in
70 re formed in HuNoV-infected human intestinal enteroid cultures and are the sites for genome replicati
72 We infected nontransformed human intestinal enteroid cultures from multiple individuals with human r
75 colonic epithelial cells and planar colonic enteroid cultures showed a robust secretory response fol
79 human intestinal tissue-derived organoid (or enteroid) cultures, advances in structural biology techn
83 ing and replicating intracellularly in human enteroids derived from different segments of the intesti
86 Using intestinal organoids (colonoids and enteroids) derived from PWH and controls, we assessed th
89 c biopsy specimens, primary cells, and human enteroid-derived monolayers from healthy human stomach,
93 Studies in NCI-H716 cells and human jejunal enteroids engineered to make more enteroendocrine cells
94 ed studies with SKCO-15 and human intestinal enteroids established from biopsies from different intes
98 regulation of alpha-defensins, yet in human enteroids exogenous stimulation of WNT signaling appears
99 pharmacological inhibition of CFTR abrogated enteroid fluid secretion, providing proof of concept for
100 Importantly, DNAJB9 deficiency upregulated enteroids' fluid secretion in CF mice (homozygous for De
102 s demonstrate the utility of patient-derived enteroids for developing therapeutic approaches to MVID.
104 icantly higher LGR5 expression (p < .01) and enteroid forming efficiency (p < .0001) compared with LG
105 patients and compared them with aged-matched enteroids from healthy subjects (HS) using bulk RNA sequ
106 ocked fluid secretion in primary cultures of enteroids from human small intestine and anion current i
108 f the intestinal epithelium but establishing enteroids from individuals with long-standing T1D has pr
110 However, intestinal tissues and derived enteroids from MYO5B(P663L) piglets maintained CFTR on a
111 cretion by group 2 innate lymphoid cells and enteroid gene expression consistent with goblet cell dif
112 ock-controlled genes in both mouse and human enteroids governing organism-specific, circadian phase-d
115 vitro, cultured ErbB4(-/-) ileal epithelial enteroids had reduced Paneth cell markers and were highl
116 urable cytokine response of human intestinal enteroids has been limited following exposure to host or
117 lopment of animal models and patient-derived enteroids, has provided critical insights into the enter
119 Since the development of human intestinal enteroid (HIE) cell culture systems, significant advance
120 rovirus replication using a human intestinal enteroid (HIE) culture system and/or could block norovir
122 CRISPR-Cas9 modification of human intestinal enteroid (HIE) cultures, and functional studies with two
123 emiology and infectivity in human intestinal enteroid (HIE) monolayers and clinical characteristics o
124 The development of the human intestinal enteroid (HIE) system has revolutionized norovirus resea
125 infection in biopsy-derived human intestinal enteroids (HIE) has been described: 3D-HIE are first dis
129 ion of two HuSaV strains in human intestinal enteroids (HIEs) known to support the replication of HuN
130 fected cells and DGAT1(-/-) human intestinal enteroids (HIEs) show a decrease in expression of nutrie
131 we generated cell lines and human intestinal enteroids (HIEs) stably expressing cytosolic and/or ER-t
132 Here, using nontransformed human jejunal enteroids (HIEs) that recapitulate the physiology of the
133 w enable the cultivation of human intestinal enteroids (HIEs), which are derived from human intestina
134 the replication of HuSaV in human intestinal enteroids (HIEs), which are nontransformed cultures orig
137 ve to epithelial cytokine responses by human enteroids, HIEs can facilitate exploration of many exper
139 induce goblet cell differentiation in murine enteroids; however, IL-13, a cytokine induced by IL-33,
140 es and 55 (49 stool and six human intestinal enteroids) HuNoV positive samples encompassing major sub
141 L-33-induced Muc2 expression is dependent on enteroid Il4ra expression, demonstrating a requirement f
144 4/Sydney/2012-like virus in human intestinal enteroids in samples collected before and 4 weeks after
146 e, we reveal that mouse and human intestinal enteroids in three-dimensional ex vivo cultures express
147 ntestinal crypts from C57BL/6 mice, cultured enteroids, incubated these with TNF (50 ng/mL, 24 hours)
148 RNA sequence (RNA-seq) analysis of human enteroids indicated that the effects of 1,25(OH)(2)D(3)
149 ary to an immortalized intestinal cell line, enteroids induced antiviral and inflammatory signaling p
151 denosine monophosphate with forskolin caused enteroid intracellular acidification in HCO3(-)-free buf
153 ation quantified simultaneously in scores of enteroid lumens, recapitulating ETEC-induced intestinal
162 ing a high-throughput approach that combines enteroid monolayers and quantitative imaging, we identif
163 es enhanced barrier function and maturity of enteroid monolayers as indicated by increased transepith
165 ctions with human intestinal epithelia using enteroid monolayers on permeable supports (such as Trans
166 IEC (Caco-2BBe/HT-29.cl19a cells) and mouse enteroid monolayers were cocultured with human macrophag
167 bility in cocultures with human IEC or mouse enteroid monolayers, which were restored by anti-IL6.
170 to mice and patient-derived human intestinal enteroids possess circadian rhythms and demonstrate circ
173 ke, and differentiated or villus-like, human enteroids represent distinct points along the crypt-vill
174 neutralization assay using human intestinal enteroids reveal that the GII-specific mAb NORO-320, med
180 gfbeta signaling in cultured mouse and human enteroids supports further the in vivo data and reveals
181 d HuNoV infectivity via the human intestinal enteroid system and HuNoV persistence via reverse transc
182 robust alternative model of infection in 3D enteroids that undergoes differentiation and spontaneous
183 in epithelial cell lines and murine colonic enteroids through mechanisms possibly involving histone
184 ly the same methods to patient-derived ileal enteroids to explore the utility of using this experimen
188 In vitro cleavage assays and studies of enteroids verified that HMGB1 protects beclin 1 and ATG5
189 knockdown gene and miRNA expression ex vivo enteroids, we demonstrate that we can knock down gene ex
191 formed in human cell lines and human-derived enteroids, we show that IL-22 signaling regulates expres
192 formed in human cell lines and human-derived enteroids, we show that IL-22 signaling regulates expres
193 m tissues were collected from mice; IECs and enteroids were cultured and analyzed by histology, immun
194 thogenic intestinal bacterium, human jejunal enteroids were cultured as monolayers in microengineered
201 h to engineer vascularized, perfusable human enteroids, which can be used to model innate immune resp
206 mice with TNF or incubation of crypt-derived enteroids with TNF reduced their expression of DRA messe
208 crine, and tuft cells, compared with control enteroids, with a concomitant decrease in markers of abs
209 duced the number of intestinal crypt-forming enteroids without affecting their structure, ASM induced
210 affected by the presence of fungi in jejunal enteroids, yet the immune landscape in white adipose tis