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11 publications mentioning mmu-mir-488

Open access articles that are associated with the species Mus musculus and mention the gene name mir-488. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 105
The double-staining of POMC-Tau-Topaz GFP mice brain sections with the fluorescein-labeled probes and an antibody against GFP revealed that a high proportion of POMC neurons express mir-383, mir-384-3p, and mir-488, suggesting that these miRNAs target the expression of protein-coding genes that are distributed in this neuronal population. [score:7]
It was observed that mir-383, mir-384-3p, and mir-488 were up-regulated in ob/ob and db/db mice and mir-488 was down-regulated in leptin -treated mice. [score:7]
Quantitative analysis of double-labeled neurons showed that, in the whole arcuate nucleus, 80.7 ± 3.4% of the GFP -positive neurons expressed mir-383 miRNAs, 39.8 ± 2.5% of the GFP -positive cells expressed mir-384-3p miRNAs and 64.9 ± 3.2% of the GFP- immunoreactive cells contained mir-488 miRNAs (Figures 2D–F). [score:5]
Surprisingly, i. c. v administration of leptin in mice only decreased the expression of mir-488 in the hypothalamus suggesting that the expression of mir-488 is under the control of leptin. [score:5]
Considering these expression patterns, we focused our work on mir-383, mir-384-3p as mir-488 which are expressed in the hypothalamus. [score:5]
Relative expression levels of mir-383, mir-384-3p, mir-471-3p, and mir-488 are expressed in fold change of the normalized level obtained in the hypothalamus. [score:5]
The above data suggest that leptin may be involved in the regulation of the expression of mir-383, mir-384-3p, and mir-488 miRNAs in the hypothalamus. [score:4]
This data provides the first evidence that the expressions of mir-383, mir-384-3p, and mir-488 are associated with an impaired leptin signaling pathway. [score:3]
In one hand, we identified three conserved miRNAS (mir-383, mir-384-3p, and mir-488) with targetscan. [score:3]
The expression of mir-488 is decreased in the hypothalamus of C57BL/6 mice after central leptin administrationBecause leptin exhibits a large range of effect at peripheral level (Margetic et al., 2002), we next investigated the effect of a daily i. c. v leptin administration (5 μg/mice) during 4 days on hypothalamic expression of mir-383, mir-384-3p, and mir-488 miRNAs. [score:3]
The expression of mir-488 is decreased in the hypothalamus of C57BL/6 mice after central leptin administration. [score:3]
Firstly, we studied the pattern of expression of miRNAs, i. e., mir-383, mir-384-3p, and mir-488, in the CNS. [score:3]
The expression profiles of mir-383, mir-384-3p, and mir-488 miRNAs presented many similarities, but also major differences. [score:3]
White arrowheads point to POMC neurons expressing miR-383, miR-384-3p or miR-488 miRNA. [score:3]
For instance, mir-488 could modulate the expression of STAT3. [score:3]
The highest amounts of mir-384-3p miRNAs were found in the brainstem, cerebellum, and olfactory bulb while mir-488 miRNAs were wi dely expressed throughout the structures studied. [score:3]
The mir-488 miRNAs were wi dely expressed throughout the CNS with the same intensity (Figure 1B). [score:3]
Figure 2 Expression of mir-383, mir-384-3p, and mir-488 in POMC neurons of the arcuate nucleus. [score:3]
To evaluate whether leptin signaling in hypothalamus is essential for the expression of mir-383, mir-384-3p, or mir-488 miRNAs, we analyzed the expression of these miRNAs among groups of leptin -deficient (ob/ob) mice and C57BL/6 controls. [score:3]
We observed an up-regulation of mir-383, mir-384-3p, and mir-488 miRNAs in 12-week-old ob/ob animals treated with vehicle compared to C57BL/6 control mice (+42, +32%; P < 0.05 and +137%; P < 0.01, respectively) (Figure 4). [score:3]
Similarly, double staining of brain sections with the GFP antibody and mir-384-3p or mir-488 probes showed that a large proportion of GFP neurons expressed mir-384-3p or mir-488 miRNAs (Figures 2B,C). [score:3]
In accordance with this hypothesis, we observed in the databases that mir-488 can also target PC1 3′UTR. [score:3]
The present study shows that leptin peripheral treatment rescues the expression of mir-383, mir-384-3p, and mir-488 in ob/ob mice. [score:3]
To directly test this hypothesis, ob/ob mice were i. p. injected with leptin at dose of 5 mg/kg and the hypothalamic expression of mir-383, mir-384-3p, and mir-488 miRNAs was evaluated by qRT-PCR 4 h later. [score:2]
As expected, leptin treatment significantly reduced hypothalamic expression of mir-383, mir-384-3p, and mir-488 miRNAs in 12-week-old ob/ob animals treated with leptin compared to vehicle -treated ob/ob mice (−25, −21%; P < 0.05 and −58%; P < 0.01, respectively) (Figure 4). [score:2]
As shown in Figure 3B, the mir-383, mir-384-3p, and mir-488 miRNAs levels were over-expressed in 16-week-old db/db mice compared to C57BL/6 animals (+25, +32 and +110%, respectively; P < 0.001). [score:2]
Based on bioinformatic predictions of their involvement in POMC-signaling pathway and their conservation among vertebrates, the expression of mir-383, mir-384-3p, and mir-488 were investigated in mo dels of obesity characterized by a decrease of POMC mRNA expression and leptin insufficiency (ob/ob) or leptin insensitivity (db/db) (Mizuno et al., 1998). [score:1]
In contrast, leptin significantly decreased mir-488 miRNA contents in the hypothalamus after treatment (−60%; P < 0.01) (Figure 5D). [score:1]
In many brain regions, mir-383, mir-384-3p, and mir-488 miRNAs distribution patterns did not match each other suggesting that the three miRNAs also exert specific roles. [score:1]
Absence of leptin resulted in a significant increase in mir-383, mir-384-3p, and mir-488 miRNAs (+400%, +101%; P < 0.05 and +605%; P < 0.001, respectively) (Figure 3A). [score:1]
The proportion of GFP neurons that exhibited mir-383, mir-384-3p, or mir-488 miRNAs were not different in the anterior and posterior subdivisions of the arcuate nucleus (Figures 2D,F). [score:1]
For the first time, we found that the miRNAs encoding the mir-383, mir-384-3p, and mir-488 miRNAs are abundant in the arcuate nucleus. [score:1]
These observations suggest that, mir-383, mir-384-3p, and mir-488 in the arcuate nucleus are involved in a complex network controlling the sensitivity of POMC neurons to peripheral signals. [score:1]
org are mir-384-3p, mir-371-3p, and mir-488 (Figure 1A). [score:1]
Because leptin exhibits a large range of effect at peripheral level (Margetic et al., 2002), we next investigated the effect of a daily i. c. v leptin administration (5 μg/mice) during 4 days on hypothalamic expression of mir-383, mir-384-3p, and mir-488 miRNAs. [score:1]
We used the antisense probes 5′-AGCCACAGTCACCTTCTGATCTTT-3′-6FAM for mir-383; 5′-TTACATTGCCTAGGAATTGTTTACATA-3′-6FAM for mir-384-3p; 5′-AAAACTCTCACGATAATAGACCCTT-3′-6FAM for mir-488. [score:1]
Although mir-383, mir-384-3p, and mir-488 miRNAs were evenly distributed along the rostro-caudal axis of the arcuate nucleus, the proportion of double labeled GFP/ mir-383, GFP/ mir-384-3p, and GFP/ mir-488 neurons did not reflect each other in terms of the proportion of their distribution. [score:1]
The levels of mir-383, mir-384-3p, and mir-488 miRNAs in the hypothalamus of 16-week-old ob/ob and C57BL/6 mice were determined by qRT-PCR. [score:1]
Because the lack of circulating leptin was associated with a significant increase in the miRNAs of interest, we measured the expression of mir-383, mir-384-3p, and mir-488 miRNAs in the hypothalamus of db/db mice, a mo del that exhibits a non-functional leptin receptor leading to impaired leptin signaling. [score:1]
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2
[+] score: 45
Similarly, at E17.5 in Pkd1 [-/- ]animals, the up-regulation of Fgfr3 and Fgf10 (components of MAPK signaling) and down-regulation of their target miRNAs- miR-488 and miR-126-5p respectively, may stimulate MAPK signaling and cell proliferation in Pkd1 [-/- ]samples. [score:9]
Similarly, down-regulation of miR-10a, miR-126-5p, miR-204, and miR-488 at E17.5 were inversely correlated with up-regulation of Ltbp1, Edil3, P2rx7, and Fgfr3 respectively (Additional file 21). [score:7]
miR-204 and miR-488 (A) were down-regulated in Pkd1 [-/- ]kidneys whereas miR10a, miR-30a, miR-96, miR-126-5p, miR-182, miR-200a and miR-429 (B) were up-regulated in Pkd1 [-/- ]kidneys. [score:7]
Among the 9 miRNAs tested at E14.5, only two miRNAs, miR-488 and miR-204, were down-regulated in Pkd1 [-/- ]kidneys compared to WT, miR-96 did not change, and the remaining 6 miRNAs were up-regulated in Pkd1 [-/- ]kidneys compared to WT (Figure 7). [score:5]
For example, miR-30a-5p may be involved in histone deactylase inhibitor pathways, apoptosis, calcium and Wnt signaling (Figure 9); miR-10a may be involved in TGF-β and hedgehog signaling; miR-204 may be involved in calcium signaling while miR-488 may be involved in MAPK signaling by targeting Fgfr3 (Figure 9). [score:5]
Expression of 9 miRNAs (miR-204, miR-488, miR10a, miR-30a, miR-96, miR-126-5p, miR-182, miR-200a and miR-429), predicted to target significantly regulated genes at E14.5 was assayed using miRNA-qPCR. [score:5]
Expression of 9 miRNAs (miR-10a, miR-126-5p, miR-200a, miR-204, miR-429, miR-488, miR-96, miR-182 and miR-30a-5p), predicted to target significantly regulated genes at E17.5 was evaluated using miRNA-qPCR assays. [score:3]
We tested this hypothesis by determining the differential expression of 9 miRNAs (mmu-miR-10a, mmu-miR-30a-5p, mmu-miR-96, mmu-miR-126-5p, mmu-miR-182, mmu-miR-200a, mmu-miR-204, mmu-miR-429, and mmu-miR-488) between WT and Pkd1 [-/- ]genotypes at E14.5 and E17.5 (Figures 7 and 8). [score:3]
We observed that miRNAs: miRs-10a, -30a-5p, -96, -126-5p, -182, -200a, -204, -429, and -488; and the such as miR-126-5p-Fgf10, miR-488-Fgfr3, miR-182-Hdac9, miR-204-P2rx7 and miR-96-Sox6 (as shown in Table 6) have not been previously reported in ADPKD. [score:1]
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3
[+] score: 4
Other miRNAs from this paper: hsa-mir-488, hsa-mir-622
We also noticed that several potential PtpA -targeted ncRNA genes (such as miR-488, CASC2, and miR-622) are involved in tumor progression through regulating cell apoptosis, proliferation, and migration 55– 57. [score:4]
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4
[+] score: 4
On the other hand, up-regulated miR-384-5p in CTX and miR-488-3p in MB were among the miRNAs with the highest positive correlations with protein modules associated with the EoC trait. [score:4]
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5
[+] score: 3
miR-431, miR-714, miR-744, miR-877, miR-130b, miR-21, miR-323-3p, miR-325, miR-409-3p, miR-154*, and miR-681 were significantly increased 4 days post-sciatic nerve crush in pre-conditioned DRGs, while miR-190, miR-1, miR-33, miR-32, miR-153, miR-335-5p, miR-193, and miR-488 showed significantly decreased expression. [score:3]
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6
[+] score: 3
Target sites of two miRNA families, miR-488 and miR-329, are also very well conserved across both species. [score:3]
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7
[+] score: 3
They suggested miR-22 and miR-125 as possible master regulators, and miR-344-5p/484 and miR-488 as possible master coregulators that may influence the genes involved in one-carbon metabolism. [score:3]
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8
[+] score: 3
Genomic mapping of HTR2C transcripts (NM_000868, NM_001256760 and NM_001256761) and their six intragenic miRNAs (miR-1912, miR-764, miR-1264, miR-1298, miR-1911 and miR-488) as well as the expression correlation between HTR2C and these miRNAs. [score:3]
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9
[+] score: 3
Examples of such miRNAs include those that show enriched expression in brain tissue such as miR-451 and miR-488 (see [32]) and miRNAs that have been implicated in the etiology of other tumor types, such as miR-346 in follicular thyroid carcinoma [36]. [score:3]
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10
[+] score: 1
Other miRNAs from this paper: hsa-mir-488
We found that rs17737058, located in the 3′UTR of NCOA1 gene, causes the disruption of the binding with the hsa-miR-488* miRNA. [score:1]
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11
[+] score: 1
Additionally, seven miRNAs exhibited a consistent pattern of no amplification in TEC from infected animals (miR-144, miR-208b, miR-291b-3p, miR-295, miR-302a, miR-488, and miR-654-3p, Figure S4 in). [score:1]
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