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1                                              miR-101 expression was determined in lung tissues from p
2                                              miR-122, a pro-viral hepatitis C virus (HCV) host factor
3                                              miR-143 and miR-145 transfection decreased cervical cell
4                                              miR-146a levels are also significantly reduced in the gl
5                                              miR-155(-/-) mice developed exacerbated lung fibrosis, i
6                                              miR-18a directly targeted Smad4, Hif1a, and Rora, all ke
7                                              miR-193a interacts with major vault protein (MVP).
8                                              miR-193b also stimulated reactive oxygen species signali
9                                              miR-23 target genes, including the oncogenes Ccnd1 as we
10                                              miR-277 mimic injection partially rescued these phenotyp
11                                              miR-294 and let-7c were introduced into otherwise microR
12                                              miR-337-3p stimulates expression of cholangiocyte genes
13                                              miR-430 is crucial for the clearance of maternal mRNA du
14                                              miR-718 expression was also induced in the spleens of mi
15                                MicroRNA-122 (miR-122) is abundant in the liver and involved in lipid
16 er enhanced liver specificity (microRNA-122 [miR-122]) or provide mechanistic insights (keratin-18 [K
17 ain-enriched miRNAs miR-9/9( *) and miR-124 (miR-9/9( *)-124) trigger reconfiguration of chromatin ac
18 miR-181b-5p, miR-21-5p, miR-195-5p, miR-137, miR-346 and miR-34a-5p in PBMNCs had high diagnostic sen
19 r proinflammatory conditions, microRNA-146a (miR-146a) is transcriptionally upregulated by ligands of
20 man lung epithelial cells, the microRNA-150 (miR-150) was identified to interact with FOXD3-AS1; this
21  through the regulation of BIC/microRNA 155 (miR-155) and its target, suppressor of cytokine signalin
22                                MicroRNA-155 (miR-155) regulates antitumor immune responses.
23 ng from specific miRNA loci (e.g., miR-200c, miR-21, the miR-17/92 cluster, the miR-183/96/182 cluste
24  the normal SC niche, we found that miR-206, miR-007-3, and miR-23b individually could distinguish co
25 rcR)-284 is a potential inhibitor of miR-221/miR-222 activity.
26 nvestigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy.
27 oadly among vertebrates, whereas the miR-290/miR-371 locus is unique to eutheria, suggesting a role i
28 th endothelial-specific deletion of miR-322 (miR-424 ortholog) and miR-503 have augmented angiogenic
29        Our results suggests that miR-203-3p, miR-664-3p and miR-708-5p may be implicated in pathways
30 In this study, we show that microRNA-134-5p (miR-134) can regulate Sabin-1 replication but not Sabin-
31 response to IL-1beta, including miR-146a-5p, miR-155-5p and miR-27b-3p.
32        Validation revealed that miR-181b-5p, miR-21-5p, miR-195-5p, miR-137, miR-346 and miR-34a-5p i
33 led that miR-181b-5p, miR-21-5p, miR-195-5p, miR-137, miR-346 and miR-34a-5p in PBMNCs had high diagn
34 dation revealed that miR-181b-5p, miR-21-5p, miR-195-5p, miR-137, miR-346 and miR-34a-5p in PBMNCs ha
35              In addition, CKMT2, miR-93b-5p, miR-29b-3p were found to be positively/negatively correl
36         We demonstrate here that microRNA-9 (miR-9) modified BMSCs (pri-miR-9-BMSCs) can significantl
37                                            A miR-204 mimic (miR-204 M) decreased Cav1 in endothelial
38                                    DIAPH1, a miR-198 target, enhances directional migration through s
39              Perturbation experiments with a miR-218-5p mimic or inhibitor demonstrated a protective
40                                 In addition, miR-542-3p overexpression inhibited the morphological tr
41                                Additionally, miR-124 regulates Smed-slit-1, which encodes an axon gui
42                                Additionally, miR-150 mimics suppressed the level of FOXD3-AS1.
43 egulation of only miR-455-3p (P = 0.007) and miR-4668-5p (P = 0.016) in AD patients compared with hea
44 00HG and two embedded microRNAs, miR-100 and miR-125b, were overexpressed in the absence of known gen
45   Furthermore, we observed that miR-126* and miR-126 downregulation increased E-selectin and VCAM1, r
46 e was to determine the effect of miR-143 and miR-145 on the cervical epithelial barrier and to elucid
47 ll permeability was increased in miR-143 and miR-145 transfected cervical epithelial cells.
48                                  miR-143 and miR-145 transfection decreased cervical cell number by i
49 regulated with overexpression of miR-143 and miR-145.
50 tors of gene transcription, with miR-155 and miR-146a both implicated in macrophage activation.
51                         Elevated miR-15a and miR-16 levels down-regulated BMI1 and other polycomb gro
52         Our results suggest that miR-15a and miR-16 mediate the down-regulation of BMI1, which impede
53 redicts expression of microRNAs miR-181a and miR-181b in human brain and blood, greater nucleus accum
54         We provide evidence that miR-29a and miR-29c are increased in skeletal muscle from patients w
55 niche, we found that miR-206, miR-007-3, and miR-23b individually could distinguish colorectal cancer
56  miR-21-5p, miR-195-5p, miR-137, miR-346 and miR-34a-5p in PBMNCs had high diagnostic sensitivity and
57 retreatment plasma levels of miR-301a-3p and miR-145-5p were higher in responders (combined response
58 lts suggests that miR-203-3p, miR-664-3p and miR-708-5p may be implicated in pathways determining lif
59 embers of the miR-142 family, miR-142-5p and miR-142-3p, as inflammation-related miRNAs with potentia
60 1beta, including miR-146a-5p, miR-155-5p and miR-27b-3p.
61                      Specifically, let-7 and miR-148 antagonism modified PTH secretion in vivo and in
62 at the brain-enriched miRNAs miR-9/9( *) and miR-124 (miR-9/9( *)-124) trigger reconfiguration of chr
63 t that the FGF13 locus, comprising FGF13 and miR-504, is transcriptionally repressed by p53, defining
64  with a strong concordance between GATA2 and miR-194 levels in clinical specimens.
65                                    Menin and miR-24 expression levels were measured in the following
66 c deletion of miR-322 (miR-424 ortholog) and miR-503 have augmented angiogenic response to LPS in a M
67 ates in the induction of IL-13 receptors and miR-126a expressed on/in the MDSCs.
68      Treatment with locked nucleic acid anti-miR-29a significantly improved survival in a mouse model
69       Weekly treatments of mice with MN-anti-miR-10b and low-dose doxorubicin resulted in complete re
70                    Systemic delivery of anti-miR-181b in angiotensin II-infused Apoe(-/-) and Ldlr(-/
71 e enriched with proangiogenic miRNAs such as miR-126-3p.
72 ed a significant inverse correlation between miR-375 expression and RUNX1, vimentin, and L-plastin RN
73 interactions remain to be elucidated between miR-17-92 and as-of-yet unidentified molecules important
74 ated by a bi-directional interaction between miR-574-3p, a CA-rich microRNA, and hnRNP L.
75   Inverse correlations were observed between miR-218 levels and Slug/ZEB2 levels in cancer tissue sam
76 ays, functional interaction occurred between miR-18a-5p and the microRNA recognition element of miR-1
77  CD69 as a nonredundant key regulator of BIC/miR-155-dependent Treg cell development and homeostasis.
78               Whereas down-regulation of bta-miR-23a by its inhibitors increased lipid accumulation a
79 K1/2 signaling pathway inversely affected by miR-519d or EphA4 expression.
80 vator ICP0, inhibition of ICP0 expression by miR-H2 has been a major hypothesis to help explain the r
81 ing obesogenic diet on IRS-1 are mediated by miR-126 independent mechanisms, including increased IRS-
82  We find that PIM3 repression is mediated by miR-33, an intronic microRNA encoded within the SREBP lo
83 duction pathway, and that can be overcome by miR-7 overexpression.
84 ty acid oxidation is negatively regulated by miR-29 overexpression, potentially through the regulatio
85 ansduction rescues metastasis suppression by miR-452.
86   We proved that it was directly targeted by miR-124-3p with a luciferase reporter assay.
87                          In addition, CKMT2, miR-93b-5p, miR-29b-3p were found to be positively/negat
88 cells transfected with miR-negative control, miR-143 or miR-145 were used in cell permeability and fl
89  of DCC and suggest that, by regulating DCC, miR-218 may be a switch of susceptibility versus resilie
90 ee signals explained late-onset degradation: miR-430 seeds, AU-rich sequences, and Pumilio recognitio
91 rthermore, we investigate that BMSCs deliver miR-9 to the injured pancreas or peripheral blood mononu
92 rticles capable of simultaneously delivering miR-34a mimic and targeting dysregulated polyamine metab
93 y restored expression of several derepressed miR-155 targets in tumor-infiltrating, miR-155-deficient
94 otch pathway inhibitor, as a critical direct miR-279/996 target.
95                                     Elevated miR-15a and miR-16 levels down-regulated BMI1 and other
96               We found that gammaSI enhanced miR-34a-dependent anti-tumor effects by activating the e
97 zation in microglia, and microglial exosomal miR-124-3p inhibited neuronal inflammation in scratch-in
98 udy demonstrated circulating plasma exosomal miR-125a-3p is readily accessible as diagnosis biomarker
99 ed two mature members of the miR-142 family, miR-142-5p and miR-142-3p, as inflammation-related miRNA
100  here for the first time a critical role for miR-424 in the regulation of HPV replication.
101 her, these data suggest a potential role for miR-7 as an RNA-based therapeutic to treat refractory an
102                        We propose a role for miR-718 in controlling TLR4 signaling and inflammatory c
103       Introduction of expression vectors for miR-424 reduced both the levels of HPV genomes in undiff
104  act as intercellular carriers of functional miR-4443, which might exert heterotypic regulation of PT
105 tRFs arising from specific miRNA loci (e.g., miR-200c, miR-21, the miR-17/92 cluster, the miR-183/96/
106                           Moreover, both gga-miR-219b and BCL11B influenced the expression of Meq gen
107 ere in accordance with that triggered by gga-miR-219b overexpression, suggesting that BCL11B was a st
108 erase reporter assays demonstrated that high miR-375 expression reduced vimentin promoter activity, s
109 trol (n = 15) and STOPP (n = 42), but higher miR-9-3p than STOPP.
110 hlighted correlation of hsa-miR-642a-3p, hsa-miR-4459 and hsa-miR-135a-3p expression with inosine in
111 RRMS patients versus HC: hsa-miR-122-5p, hsa-miR-196b-5p, hsa-miR-301a-3p, and hsa-miR-532-5p.
112 sus HC: hsa-miR-122-5p, hsa-miR-196b-5p, hsa-miR-301a-3p, and hsa-miR-532-5p.
113 ion of hsa-miR-642a-3p, hsa-miR-4459 and hsa-miR-135a-3p expression with inosine in the vein tissue,
114 p, hsa-miR-196b-5p, hsa-miR-301a-3p, and hsa-miR-532-5p.
115 ations in delivering hsa-miR-199a-3p and hsa-miR-590-3p both in primary neonatal mouse cardiomyocytes
116         Extracellular vesicle-associated hsa-miR-483-5p thus appears to be a promising minimally inva
117 fferent lipid formulations in delivering hsa-miR-199a-3p and hsa-miR-590-3p both in primary neonatal
118 ly expressed in RRMS patients versus HC: hsa-miR-122-5p, hsa-miR-196b-5p, hsa-miR-301a-3p, and hsa-mi
119 pression of cel-mir-237 and its homolog, hsa-miR-125b, functions as sensitizers to gamma-irradiation
120 ation testing highlighted correlation of hsa-miR-642a-3p, hsa-miR-4459 and hsa-miR-135a-3p expression
121  silico and experimental analyses identified miR-141-3p as a direct target of circRNA_100338.
122  the KRas downstream pathway, and identified miR-193a-3p, which directly targets KRas.
123 r post-transcriptional regulators identified miR-495 as a novel regulator of multiple ARGs that have
124                   Thus, our study identifies miR-146a as an important molecular brake that blocks the
125 ion analysis in clinical samples to identify miR-125b-5p down-regulated in gallbladder cancer.
126                         Overall, we identify miR-500a-5p as an oxidative stress response miRNA whose
127 lds on previous studies that have implicated miR-17-92 in the regulation of important molecular compo
128       Focusing on the RNA editing hotspot in miR-200b, a key tumor metastasis suppressor, we found th
129 Denervation resulted in a marked increase in miR-206 and reduced expression of miRs 1, 133a, and 133b
130 pithelial cell permeability was increased in miR-143 and miR-145 transfected cervical epithelial cell
131 he miRISC in response to IL-1beta, including miR-146a-5p, miR-155-5p and miR-27b-3p.
132          CXCR4 overexpression also increased miR-15a/16-1, shifting their oncogenic dependency from t
133      Maternal diet-induced obesity increased miR-126 expression however levels of this miR were not i
134 S. aureus inhibits wound closure and induces miR-15b-5p in acute human and porcine wound models and i
135 essed miR-155 targets in tumor-infiltrating, miR-155-deficient CD8(+) T cells, suggesting that miR-15
136 AD3 to bind to the miR-140 locus and inhibit miR-140 transcription.
137 t of OEPCs is improved in vivo by inhibiting miR-17.
138 more, transplantation of WT bone marrow into miR-155KO mice mitigated this phenotype.
139 n, our data show that by reducing CD82, KSHV miR-K6-5p expedites cell invasion and angiogenesis by ac
140                   Consequently, mice lacking miR-34/449 display infertility as well as severe chronic
141 g carotid endarterectomy revealed that local miR-100 expression was inversely correlated with inflamm
142 shows that mutation of a single miRNA locus (miR-iab4/iab8) affects the capacity of the larva to corr
143 e adjusted risk ratios per one-SD higher log miR-122 were 1.60 (95% CI 1.30-1.96; P < 0.001) for meta
144 in PCa clinical tissues established that low miR-383 expression is associated with poor prognosis.
145 cise, START (n = 22) had significantly lower miR-22-3p than control (n = 15) and STOPP (n = 42), but
146 nally, we demonstrate that OA induces mature miR-7 production in HeLa cells.
147                             Mechanistically, miR-520f inhibited tumor cell invasion by directly targe
148 uction of either the anti-migratory microRNA miR-198 or the pro-migratory follistatin-like 1 (FSTL1)
149                                    MicroRNA (miR)-155 has recently been described to regulate adaptiv
150  cargo includes proteins, mRNA and microRNA (miR) that can be transferred to recipient cells and regu
151     We examined HCV entry in HepG2/microRNA (miR) 122/CD81 cells, which support entry and replication
152  glycolysis through suppression of microRNA (miR)-455-3p.
153 -46 levels also restored perturbed microRNA (miR-2) function in smn-1(lf) animals.
154 of rs322931 predicts expression of microRNAs miR-181a and miR-181b in human brain and blood, greater
155 essential for functional immunity.MicroRNAs (miR) are important regulators of gene transcription, wit
156 jury, dysregulation of non-coding microRNAs (miRs) occurs in dorsal root ganglia (DRG) sensory neuron
157                               How microRNAs (miRs) regulate IOP and glaucoma in vivo is largely unkno
158  characterize the contribution of microRNAs (miRs) delivered by microvesicles to MC activation.
159 the study was to explore specific microRNAs (miRs) in rectal cancer that would predict response to ra
160 ing RNA MIR100HG and two embedded microRNAs, miR-100 and miR-125b, were overexpressed in the absence
161                             A miR-204 mimic (miR-204 M) decreased Cav1 in endothelial cells.
162  Here we show that the brain-enriched miRNAs miR-9/9( *) and miR-124 (miR-9/9( *)-124) trigger reconf
163                                    Moreover, miR-146a-deficient mice do not resolve inflammation afte
164  Mechanistically, acid-induced epithelial MV miR-17/221 promoted beta1 integrin recycling and present
165 ued by bone marrow exosomes from WT, but not miR-155(-/-), cells, suggesting that uptake of miR-155-c
166   Whole-genome RNA sequencing uncovers novel miR-141-regulated molecular targets in PCa cells includi
167 aimed at investigating whether alteration of miR-194-dependent MMPs and PARP-1 causes renal fibrosis
168                       Expression analyses of miR-383 in PCa clinical tissues established that low miR
169                         Finally, analysis of miR-100 expression in >70 samples obtained during caroti
170                               Application of miR-146b combined with stem cell therapy could enhance r
171 d region, phenocopied the characteristics of miR-223(-/y) mice.
172 t mice with endothelial-specific deletion of miR-322 (miR-424 ortholog) and miR-503 have augmented an
173                          Ectopic delivery of miR-194 stimulated migration, invasion, and epithelial-m
174  genosensor was applied for determination of miR-221 in total RNA extracted from human lung and breas
175 udy objective was to determine the effect of miR-143 and miR-145 on the cervical epithelial barrier a
176 o screen downstream targets and effectors of miR-32, we identified RAC2 as a potential, and clinicall
177 odel to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy.
178 a-5p and the microRNA recognition element of miR-18a-5p in the 3'-untranslated region of hPXR mRNA.
179     This work presents the first evidence of miR control of HCN4 and heart rate.
180                                Expression of miR-193b in liposarcoma cells was downregulated by promo
181                           High expression of miR-30a or miR-200c was associated with significantly be
182                                Expression of miR-487b-3p is decreased in colon adenocarcinomas and in
183 LR4, but not TLR3, induced the expression of miR-718 in macrophages.
184 p to activate MYC signaling via induction of miR-33b.
185                                Inhibition of miR-142-3p could be neuroprotective in MS.
186                                Inhibition of miR-204 protects against tunicamycin-induced vascular/en
187  RNA (circR)-284 is a potential inhibitor of miR-221/miR-222 activity.
188 ansfection of MCs with mimic or inhibitor of miR-4443 resulted in decreased or enhanced PTPRJ express
189 re observed with spatiotemporal knockdown of miR-8 and luciferase assays.
190 RS-1 are associated with increased levels of miR-126 and consequently reduced translation of Irs1 mRN
191                Pretreatment plasma levels of miR-301a-3p and miR-145-5p were higher in responders (co
192  as an efficient small-molecule modulator of miR-34a to reverse chemoresistance and further enhance t
193 expression of miR-183, the human ortholog of miR-263a, can also directly target the expressions of al
194                            Overexpression of miR-10b increased Ki-67 staining in human organ-cultured
195 1, were downregulated with overexpression of miR-143 and miR-145.
196 , we provide evidence that overexpression of miR-183, the human ortholog of miR-263a, can also direct
197 cer cell lines, and stable overexpression of miR-194 enhanced metastasis of intravenous and intrapros
198                 Lentiviral overexpression of miR-26a in ZOS and 143B osteosarcoma cells decreases the
199                Conversely, overexpression of miR-31-3p ameliorated the severity of DSS-induced coliti
200 of iPSC generation and impedes processing of miR-125b, leading to Rybp upregulation and suppression o
201 nuclease 1 is required for the processing of miR-221/222 in regulating expression of the tumor suppre
202 nt study demonstrate that down-regulation of miR-214 may reverse acquired resistance to erlotinib in
203 t time, the transcriptional up-regulation of miR-34c-5p in response to TCR stimulation in naive CD4 T
204 r was identified as an upstream regulator of miR-194, consistent with a strong concordance between GA
205  We suggest that upregulation and release of miR-21 contribute to sensory neuron-macrophage communica
206                               Restoration of miR-874 expression impeded S phase progression, suppress
207 ely, these results reveal a critical role of miR-122 in acetaminophen detoxification and implicate it
208 im of this study was to evaluate the role of miR-125a-5p in VSMCs phenotypic switch.
209  findings demonstrate the functional role of miR-146b in the chondrogenic differentiation of human bo
210   In this study, we investigated the role of miR-155 specifically within T cells during the immune re
211  inhibitor demonstrated a protective role of miR-218-5p in cigarette smoke-induced inflammation and C
212  vivo and required, in part, MV shuttling of miR-17 and/or miR-221.
213 otential, and clinically relevant, target of miR-32.
214 sting that vimentin is an indirect target of miR-375.
215  direct and functionally relevant targets of miR-141.
216 nd 8 (ilp7 and ilp8) are putative targets of miR-277; RNA immunoprecipitation and a luciferase report
217 , Notch2, and Jagged 1, as direct targets of miR-34a.
218 w that the levels of two putative targets of miR-424 that function in DNA damage repair, CHK1 and Wee
219 nd we subsequently validated upregulation of miR-139-5p in two independent clinical cohorts, wherein
220 mice, promotes ER stress via upregulation of miR-204, whereas overexpression of Sirt1 in endothelial
221 R-155(-/-), cells, suggesting that uptake of miR-155-containing exosomes is important for a proper LP
222 ncrease in miR-206 and reduced expression of miRs 1, 133a, and 133b in myofiber-derived exosomes.
223                  Here we show that oncogenic miR-182 is a strong regulator of C/EBPalpha.
224 -PCR showed significant upregulation of only miR-455-3p (P = 0.007) and miR-4668-5p (P = 0.016) in AD
225 fected with miR-negative control, miR-143 or miR-145 were used in cell permeability and flow cytometr
226                High expression of miR-30a or miR-200c was associated with significantly better overal
227 ired, in part, MV shuttling of miR-17 and/or miR-221.
228 steoblasts, but in aggressive osteosarcomas, miR-874 is down-regulated, leading to elevated CCNE1 exp
229  Drosophila Larval fly hearts overexpressing miR-1 have profound defects in actin filament organizati
230                         Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell
231                        Analyses of potential miR-1 targets revealed that miR-1 directly regulates the
232 lated with decreased expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-
233  that microRNA-9 (miR-9) modified BMSCs (pri-miR-9-BMSCs) can significantly reduce the pancreatic ede
234 ed virus 8 vector that expressed the primary miR-122 transcript (pri-MIR122, to overexpress MIR122 in
235                                   We propose miR-142-3p as a molecular mediator of the IL-1beta-depen
236 ime that a microRNA component of this region-miR-383-is frequently downregulated in prostate cancer,
237   We previously determined that low relative miR-375 expression was associated with poor patient prog
238 g the type I IFN-induced antiviral response, miR-BART16 provides a means to facilitate the establishm
239 NA profiling in the human brain has revealed miR-132 as one of the most severely down-regulated miRNA
240  of Tyr359-phosphorylated hnRNP L sequesters miR-574-3p, overcoming its decoy activity and seed seque
241 ics approach, the authors identified several miR-7a2 target genes and pathways that have not been pre
242                                   Ever since miR-H2's discovery as a viral microRNA bearing complete
243  abrogates KIT signaling cascade through Sp1/miR-29b network.
244 al oncogene that regulates TOP2A by sponging miR-411-5p in glioma.
245                                  In summary, miR-193b not only functions as a tumor suppressor in lip
246 ion of Sirt1 in endothelial cells suppresses miR-204-induced ER stress.
247 in upregulating NF-kappaB signaling and that miR-19a has roles in inflammation and CAC.
248        METHODS AND Here, we demonstrate that miR-181b was overexpressed in symptomatic human atherosc
249          These new findings demonstrate that miR-19a has a direct role in upregulating NF-kappaB sign
250                          We demonstrate that miR-21-5p is released in the exosomal fraction of cultur
251              Herein, it is demonstrated that miR-194 is a driver of prostate cancer metastasis.
252      Together, our results demonstrated that miR-19a carried through the exosomes from HCV-infected h
253 Results of miRNA profiling demonstrated that miR-30a was markedly downregulated in diabetic cataract
254                     We provide evidence that miR-29a and miR-29c are increased in skeletal muscle fro
255                                We found that miR-124-3p promoted the anti-inflamed M2 polarization in
256                  Consequently, we found that miR-155 expression by T cells is necessary for proper tu
257 ature for the normal SC niche, we found that miR-206, miR-007-3, and miR-23b individually could disti
258                           We identified that miR-195 was packaged in the extracellular vesicles from
259                     Our study indicates that miR-96 might be a potential target for therapy of pediat
260                Furthermore, we observed that miR-126* and miR-126 downregulation increased E-selectin
261                             We observed that miR-874 inhibits CCNE1 expression in primary osteoblasts
262                              We propose that miR-26a delivery might not be a viable therapeutic strat
263             Altogether, our data reveal that miR-155 collaborates with FLT3-ITD to promote myeloid ce
264 ses of potential miR-1 targets revealed that miR-1 directly regulates the 3'UTR of the E3 ubiquitin l
265                     Validation revealed that miR-181b-5p, miR-21-5p, miR-195-5p, miR-137, miR-346 and
266                           Here, we show that miR-29 promotes pathologic hypertrophy of cardiac myocyt
267 uman clinical specimens, we also showed that miR-152 expression levels were negatively correlated wit
268                     Our results suggest that miR-15a and miR-16 mediate the down-regulation of BMI1,
269                        Our data suggest that miR-323-3p acts in a negative feedback loop to control t
270 55-deficient CD8(+) T cells, suggesting that miR-155 and ICB regulate overlapping pathways to promote
271                    Our results suggests that miR-203-3p, miR-664-3p and miR-708-5p may be implicated
272                                          The miR-302 locus is found broadly among vertebrates, wherea
273 ific miRNA loci (e.g., miR-200c, miR-21, the miR-17/92 cluster, the miR-183/96/182 cluster) and from
274 miR-200c, miR-21, the miR-17/92 cluster, the miR-183/96/182 cluster) and from specific tRNA loci (e.g
275 ociation of a functional polymorphism in the miR-146a precursor (rs2910164).
276 llergen papain, mice selectively lacking the miR-17 approximately 92 cluster in ILC2s displayed reduc
277 viously identified two mature members of the miR-142 family, miR-142-5p and miR-142-3p, as inflammati
278 rophages, contributed by deregulation of the miR-155 target gene the liver X receptor (LXR)alpha in l
279                        Overexpression of the miR-183 cluster reduced zinc transporter and intracellul
280  of a novel mouse line, with deletion of the miR-223 binding site in the NLRP3 3' untranslated region
281 al interaction studies, we revealed that the miR-144-3p target, PTEN, colocalized with miR-144-3p in
282 mor metastasis suppressor, we found that the miR-200b editing level correlates with patient prognosis
283 naling, causing phospho-SMAD3 to bind to the miR-140 locus and inhibit miR-140 transcription.
284 found broadly among vertebrates, whereas the miR-290/miR-371 locus is unique to eutheria, suggesting
285 ion by hCMEC/D3 cells, suggesting that these miRs regulate leukocyte adhesion by modulating the expre
286 ed miR-126 expression however levels of this miR were not influenced by a post-weaning obesogenic die
287 lin signaling is up-regulated in response to miR-277 depletion.
288 NA with 3G ('22-3G') comprised <63% of total miR-122 in human liver, whereas other variants (23-3A, 2
289  1 (FSTL1) protein from a single transcript; miR-198 expression in healthy skin is down-regulated in
290 te to the pattern observed for the wild-type miR-200b expression.
291                     In addition, we verified miR-449b could regulate the expression levels of CDK6, c
292 t differentiation of myoblast cells, whereas miR-30c targets the 3'-UTR of Tnrc6a mRNA to weaken its
293  growth is controlled by miRNAs, among which miR-352 is a novel candidate that negatively regulates a
294 ed E-selectin and VCAM1, respectively, while miR-126 overexpression reduced VCAM1 and CCL2 expression
295 ssion with inosine in the vein tissue, while miR-216a-5p, conversely, was correlated with phosphatidy
296 eature during the initiation of colitis with miR-223 deficiency.
297 he miR-144-3p target, PTEN, colocalized with miR-144-3p in the basolateral amygdala and showed functi
298 l maturation of the mouse visual cortex with miR-132/212 family being one of the top upregulated miRN
299 rtant regulators of gene transcription, with miR-155 and miR-146a both implicated in macrophage activ
300 ical and endocervical cells transfected with miR-negative control, miR-143 or miR-145 were used in ce

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