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9 publications mentioning bta-mir-499

Open access articles that are associated with the species Bos taurus and mention the gene name mir-499. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 319
Lin28B protein expression was strongly suppressed by overexpression of bta-miR-499, whereas inhibition of bta-miR-499 enhanced Lin28B expression (Fig.   5d). [score:11]
Collectively, placental exosome-derived bta-miR-499, Lin28B, and bta-let-7 miRNAs constitute a loop that negatively regulates NF-κB p65 activation, contributing to the pro/anti-inflammatory balance at the maternal-fetal interface during early pregnancy in cattleIn addition, NF-κB activation upregulated the expression of Lin28B (Fig.   6d), and inhibition of NF-κB activation led to a decrease in the expression of Lin28B (Fig.   7f). [score:11]
bta-miR-499 upregulated bta-let-7 microRNAs by targeting Lin28B, and subsequent upregulation of bta-let-7 microRNAs inhibited the NF-κB pathway 61, 62. [score:11]
Collectively, placental exosome-derived bta-miR-499, Lin28B, and bta-let-7 miRNAs constitute a loop that negatively regulates NF-κB p65 activation, contributing to the pro/anti-inflammatory balance at the maternal-fetal interface during early pregnancy in cattle In addition, NF-κB activation upregulated the expression of Lin28B (Fig.   6d), and inhibition of NF-κB activation led to a decrease in the expression of Lin28B (Fig.   7f). [score:11]
Taken together, these results indicated that exosome-derived bta-miR-499 inhibits the expression of Lin28B, thereby increasing intracellular bta-let-7 miRNAs levels and impairing the activation of NF-κB, leading to downregulation of proinflammatory cytokine expression. [score:10]
During early pregnancy, the proinflammatory uterine immune microenvironment leads to the activation of NF-κB and promotes the transcriptional expression of downstream proinflammatory cytokines, such as TNF-α and IL-6. However, to maintain an appropriate, proinflammatory environment, placental exosomes target the Lin28B/let-7-ras signaling axis through miR-499 to directly or indirectly inhibit NF-κB activation and attenuate transcriptional regulation of downstream proinflammatory cytokines, resulting in a mild proinflammatory environment. [score:10]
To determine whether bta-miR-499 inhibits activation of NF-κB by upregulating the bta-let-7 family via targeting Lin28B, we determined the effects of bta-miR-499 on the expression of the bta-let-7 family. [score:10]
However, no direct target gene of bta-miR-499 in the NF-κB pathway was found, suggesting that bta-miR-499 might inhibit NF-κB signaling by indirectly targeting other genes. [score:9]
miRNAs are ~22-nucleotide (nt) non-coding RNAs that regulate the expression of complementary messenger RNAs (mRNAs) involved in a broad spectrum of biological processes, including the inflammatory immune response 14, 15. miR-499 is conserved across species and acts as an inflammation “suppressor” by targeting genes to ameliorate the inflammatory damage to endothelial cells [16]. [score:8]
In conclusion, bta-miR-499 regulates Lin28B expression in BEND cells by directly targeting the 3′-UTR of Lin28B mRNA. [score:7]
b Following intervention with synthetic antagomiR-499, uterine miR-499 expression was determined by qPCR, and the expression of the mmu-miR-499 target Lin28B at both mRNA (c) and protein levels (d) was also detected. [score:7]
As shown in Fig.   8b, intervention with synthetic antagomiR-499 produced a significant decrease in uterine miR-499 expression on day 8.5 and increased the expression of the mmu-miR-499 target Lin28B at both mRNA and protein levels (Fig.   8c, d). [score:7]
Two-tailed Student’s t-test, * P < 0.05; ** P < 0.01 Table 2 Enriched pathways (top 10) of differentially expressed miRNA predicted target genes in exosomes isolated from cows plasma at gestational day 0 and 60 KEGG pathway ID P-value Lysosome bta04142 0.017449658 Ras signaling pathway bta04014 0.029067512 MAPK signaling pathway bta04015 0.03076703 TNF signaling pathway bta00564 0.032438895 NF-kappa B signaling pathway bta04010 0.033583162 Fc gamma R -mediated phagocytosis bta04666 0.039375185 Rap1 signaling pathway bta04668 0.041994059 Glycerophospholipid metabolism bta04064 0.063277411 Adherens junction bta04520 0.06419703 Endocytosis bta04144 0.066272413 G_D0 and G_D60 represent exosomes isolated from cows plasma at gestational day 0 and 60, respectively TNF-α and IL-6 levels were first detected by immunohistochemical staining and real-time polymerase chain reaction (qPCR) to confirm whether placental exosome-derived bta-miR-499 is involved in the regulation of uterine inflammation to support a balance between anti- and proinflammation during early pregnancy. [score:6]
However, inhibition of miR-499 enhances NF-κB activation, leading to the upregulation of inflammatory cytokines. [score:6]
These results indicate that bta-miR-499 upregulates the bta-let-7 family via targeting Lin28B. [score:6]
Bta-miR-499 upregulates bta-let-7 miRNAs via targeting Lin28B. [score:6]
Inhibition of mmu-miR-499 expression in vivo during early pregnancy increases the risk of pregnancy failure. [score:5]
Luciferase activity was markedly reduced in cells overexpressing bta-miR-499 but was relatively enhanced by inhibition of bta-miR-499 (Fig.   5c). [score:5]
However, activation of NF-κB also promotes Lin28B expression, which counters the continued inhibition of miR-499. [score:5]
We provided the first evidence that exosome-derived bta-miR-499 attenuates the expression of proinflammatory cytokines by inhibiting NF-κB signaling. [score:5]
These results suggested that exosome-derived bta-miR-499 attenuates the expression of proinflammatory cytokines through inhibition of NF-κB signaling. [score:5]
The above results suggest that the upregulation of bta-let-7 miRNAs in BEND cells partly originates from exosomes and combines with exosome-derived bta-miR-499 to regulate the activation of NF-κB signaling. [score:5]
Inhibition of mmu-miR-499 expression in vivo during early pregnancy increases the risk of pregnancy failure: embryo loss and fetal growth restriction. [score:5]
To assess whether placental exosome-derived bta-miR-499 decreases LPS -induced expression of proinflammatory cytokines by inhibiting the activation of the NF-κB pathway, we detected nuclear translocation of NF-κB. [score:5]
The above results strongly suggested that placental exosome-derived bta-miR-499 inhibits LPS -induced expression of proinflammatory cytokines. [score:5]
Placental exosome-derived bta-miR-499 inhibits LPS -induced expression of proinflammatory cytokines. [score:5]
BEND cells were then transfected with Lin28B siRNA and exposed to LPS to determine whether bta-miR-499 inhibits the activation of NF-κB signaling via targeting Lin28B. [score:5]
Among all targets predicted by bioinformatics methods, Lin28B was identified as a potential target of miR-499. [score:5]
Bta-miR-499 inhibits the activation of NF-κB signaling via targeting Lin28B. [score:5]
These results indicate that bta-miR-499 inhibits activation of NF-κB signaling via targeting Lin28B. [score:5]
Bta-miR-499 inhibits activation of NF-κB signaling via targeting Lin28B. [score:5]
Compared with the control (NC) + LPS, overexpression of bta-miR-499 led to significantly decreased expression of TNF-α and IL-6 (Fig.   3g, h), whereas antagomiR-499 increased these values (Fig.   3h) in accordance with the results of treatment with exosomes. [score:4]
Zhang YH He K Shi G Effects of MicroRNA-499 on the inflammatory damage of endothelial cells during coronary artery disease via the targeting of PDCD4 through the NF-Κβ/TNF-α signaling pathwayCell Physiol. [score:4]
In vitro, placental exosome-derived bta-miR-499 inhibited the activation of NF-κB via the Lin28B/let-7 axis, thus repressing LPS -induced inflammation in BEND cells. [score:3]
In addition, miR-499 or let-7 may be potential therapeutic agents for pregnancy disorders caused by early uterine inflammation or provide references for the treatment of other inflammatory diseases. [score:3]
These results indicated that NF-κB activation occurs during early pregnancy and that inhibition of miR-499 may induce its activation. [score:3]
Overexpression of miR-499 significantly decreased the phosphorylation level of NF-κB p65 induced by LPS (Fig.   4d). [score:3]
The effect of placental exosome-derived bta-miR-499 on LPS -induced expression of proinflammatory cytokines. [score:3]
The delivery of miR-499 inhibitors (antagomiR-499) disrupts the balance of uterine local inflammatory immune response and increases the risk of pregnancy failure, such as embryo loss and FGR, indicating that the uterine local immune microenvironment may be an important cause of early pregnancy failure. [score:3]
Prediction of bta-miR-499/mRNAs by TargetScan (http://www. [score:3]
Exosome-derived miR-499 inhibits NF-κB signaling pathway activation. [score:3]
Mmu-miR-499 was more highly expressed in early pregnancy exosomes than in non-pregnant exosomes (Fig.   8a). [score:3]
Subsequently, inhibition of mmu-miR-499 led to an impaired balance of inflammation at the maternal-fetal interface in vivo, resulting in an increased risk of pregnancy failure. [score:3]
The lower panel shows the alignment of miR-499 and its target site in the 3′-UTR of Lin28B. [score:3]
Overall, our research provides new possibilities for the regulation of immune tolerance in the maternal-fetal interface in dairy cows and other mammals during early pregnancy, with a role of placental exosomal miR-499 in the regulation of the uterine immune inflammatory response. [score:3]
d The effect of overexpression of miR-499 on the phosphorylation level of NF-κB p65 induced by LPS; total protein (NF-κB p65) was used as a control. [score:3]
Therefore, we suggest that inhibiting mmu-miR-499 triggers a risk of embryo loss. [score:3]
b Conservation of the miR-499 target sequence in Lin28B among different species (upper panel) and conservation of the sequence of miR-499 among different species (lower panel). [score:3]
Lin-28 homolog B (Lin28B), an RNA -binding protein, promotes degradation of the let-7 family of miRNAs (let-7 miRNAs) [17] and was identified as a target of miR-499 in this study. [score:3]
The inhibitory effects of bta-miR-499 on luciferase activity were clearly lost when binding sites were absent (Fig.   5c). [score:3]
BEND cells were transfected with bta-miR-499agomiRs, followed by detection of TNF-α and IL-6 mRNA by qPCR to explore the effects of differential loading of bta-miR-499 in exosomes on LPS -induced expression of proinflammatory cytokines. [score:3]
Collectively, these data confirmed a critical role of miR-499 in maintaining an appropriate local immune microenvironment during early pregnancy by targeting the Lin28B/let-7 axis. [score:3]
These results suggest that exosome-derived bta-let-7 miRNAs cooperate with bta-miR-499 to participate in the regulation of NF-κB signaling. [score:2]
Further analysis of these differential miRNAs revealed that bta-miR-499, a highly conserved miRNA among species, is associated with pregnancy loss, preeclampsia and idiopathic recurrent spontaneous abortion 55, 56, suggesting a crucial role of bta-miR-499 in immune regulation in the uterus during early pregnancy in dairy cows. [score:2]
Based on these results, bta-miR-499 with the Lin28B/let-7 axis constitutes the key regulatory mechanism in the immune inflammatory response during early pregnancy in cattle. [score:2]
Consistent with this hypothesis, miR-499 is reportedly involved in the immune inflammatory process [25], suggesting that miR-499 may play a crucial role in maternal immune regulation during early pregnancy in dairy cows. [score:2]
Two-tailed Student’s t-test, * P < 0.05; ** P < 0.01 To provide direct evidence of the interaction between bta-miR-499 and Lin28B, we used a luciferase reporter plasmid containing either the wild type or mutant 3′-UTR of Lin28B mRNA; the binding sites of bta-miR-499, which are conserved across species, are shown in Fig.   5b. [score:2]
We hypothesized that placental exosomes can regulate the balance of inflammation in the uterus through bta-miR-499. [score:2]
Collectively, placental exosome-derived bta-miR-499, Lin28B, and bta-let-7 miRNAs constitute a loop that negatively regulates NF-κB p65 activation, contributing to the pro/anti-inflammatory balance at the maternal-fetal interface during early pregnancy in cattle To further validate the selective sorting of miR-499 into exosomes during early pregnancy, we isolated exosomes from peripheral blood plasma from Institute of Cancer Research (ICR) mice on day 8.5 of pregnancy (day 0.5 = vaginal plug), and mmu-miR-499 was detected by qPCR. [score:2]
Two-tailed Student’s t-test, * P < 0.05; ** P < 0.01To provide direct evidence of the interaction between bta-miR-499 and Lin28B, we used a luciferase reporter plasmid containing either the wild type or mutant 3′-UTR of Lin28B mRNA; the binding sites of bta-miR-499, which are conserved across species, are shown in Fig.   5b. [score:2]
These results demonstrated that placental exosome-derived bta-miR-499, Lin28B, and bta-let-7 miRNAs constitute a loop that negatively regulates NF-κB p65 activation (Fig.   7g). [score:2]
Therefore, we hypothesized that placental exosome- delivered miR-499 mediates the inflammatory balance at the maternal-fetal interface by regulating the NF-κB signaling pathway through the Lin28B/let-7 axis, thereby forming an immune-tolerant microenvironment in the uterus that is beneficial for pregnancy maintenance in the first trimester. [score:2]
Two-tailed Student’s t-test, * P < 0.05; ** P < 0.01 TNF-α and IL-6 levels were first detected by immunohistochemical staining and real-time polymerase chain reaction (qPCR) to confirm whether placental exosome-derived bta-miR-499 is involved in the regulation of uterine inflammation to support a balance between anti- and proinflammation during early pregnancy. [score:2]
Therefore, in the early gestation of dairy cows and other mammals, placental exosomes may be involved in the regulation of inflammation balance at the maternal-fetal interface by carrying some significant molecules, such as miR-499. [score:2]
a Mmu-miR-499 levels were analyzed by qPCR in exosomes isolated from peripheral blood plasma in ICR mice on day 8.5 of pregnancy (day 0.5 = vaginal plug). [score:1]
Therefore, LPS, an NF-κB activator, was used in BEND cells, a bovine endometrial epithelial cell line, to explore the potential mechanism of exosomal bta-miR-499 in early pregnancy. [score:1]
To further validate the selective sorting of miR-499 into exosomes during early pregnancy, we isolated exosomes from peripheral blood plasma from Institute of Cancer Research (ICR) mice on day 8.5 of pregnancy (day 0.5 = vaginal plug), and mmu-miR-499 was detected by qPCR. [score:1]
In this study, we demonstrated that placenta-specific exosomes are abundant in the peripheral blood of dairy cows during early pregnancy, these exosomes selectively load miRNAs, such as bta-miR-499. [score:1]
Placental exosomes in early pregnancy selectively load bta-miR-499. [score:1]
Bta-miR-499 is highly enriched in placenta-specific exosomes. [score:1]
These results indicated that bta-miR-499 was selectively loaded in placental exosomes and might play a crucial role in the immune inflammatory process during early pregnancy in dairy cows. [score:1]
c The levels of bta-miR-499 in peripheral blood, early embryo and uterus during early pregnancy (G_D. [score:1]
Co-transfection of bta-miR-499 and pCDNA. [score:1]
Bta-miR-499 was significantly enriched in early pregnancy exosomes (Fig.   2b). [score:1]
In addition, we examined the levels of bta-miR-499 in peripheral blood, early embryo and uterus; the most significant accumulation of bta-miR-499 occurred in exosomes, followed by the uterus, fetus, and peripheral blood (Fig.   2c). [score:1]
miR-499 and let-7 miRNAs both belong to broadly conserved miRNA families that have unique cross-species advantages. [score:1]
c Schematic diagram showing dual-luciferase reporter constructs harboring the 3′-UTR of Lin28B with the putative miR-499 binding site. [score:1]
BEND cells were transfected with agomiR-499for 24 h, followed by 1 h of exposure to LPS to further confirm the role of placental exosome-derived miR-499 in this process. [score:1]
f Bta-miR-499 levels in cells cultured with placental exosomes (p-EXO) or non-pregnant cow exosomes (n-EXO). [score:1]
Fig. 8 a Mmu-miR-499 levels were analyzed by qPCR in exosomes isolated from peripheral blood plasma in ICR mice on day 8.5 of pregnancy (day 0.5 = vaginal plug). [score:1]
b Bta-miR-499 levels were analyzed in exosomes isolated from the plasma of non-pregnant (G_D. [score:1]
In addition, bta-miR-499 levels in cells increased significantly when the cells were cultured with placental exosomes (Fig.   3f, p < 0.05, vs the CG and the non-pregnant group). [score:1]
Toraih EA Structure and functional impact of seed region variant in MIR-499 gene family in bronchial asthmaRespir. [score:1]
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Essential amino acids increase microRNA-499, -208b, and -23a and downregulate myostatin and myocyte enhancer factor 2C mRNA expression in human skeletal muscle. [score:6]
In the present study, among the 231 exosomal miRNAs detected in the cattle plasma, muscle-enriched miR-486 and a trace of miR133b were detected, but miR-1, miR-133a, miR-206, miR-208b, and miR-499 were not detected. [score:1]
On the other hand, these muscle-specific miRNAs and miR-499 are present at a very low level in the serum of healthy humans who have not just exercised [30, 39]. [score:1]
Muscle-specific miRNAs such as miR-1, miR-133a, miR-206, miR-208b, and miR-499 were not significantly detected in the plasma exosomes across all samples (i. e., grazing and housed during experiment) except for miR-486 (0.18%) and a trace of miR-133b (< 0.001%). [score:1]
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Other miRNAs from this paper: ssc-mir-122, ssc-mir-125b-2, ssc-mir-181b-2, ssc-mir-20a, ssc-mir-23a, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-107, ssc-mir-21, ssc-mir-29c, ssc-mir-30c-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-20a, bta-mir-21, bta-mir-26b, bta-mir-30d, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-199a-1, bta-mir-30b, bta-mir-107, bta-mir-10a, bta-mir-127, bta-mir-142, bta-mir-181b-2, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-132, bta-mir-138-2, bta-mir-17, bta-mir-181c, bta-mir-192, bta-mir-199b, bta-mir-200a, bta-mir-200c, bta-mir-214, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-455, bta-let-7g, bta-mir-10b, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-mir-30c, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-99b, ssc-mir-99b, ssc-mir-17, ssc-mir-30b, ssc-mir-199b, bta-mir-1-2, bta-mir-1-1, bta-mir-129-1, bta-mir-129-2, bta-mir-133a-2, bta-mir-133a-1, bta-mir-133b, bta-mir-135b, bta-mir-138-1, bta-mir-143, bta-mir-144, bta-mir-146b, bta-mir-146a, bta-mir-181d, bta-mir-190a, bta-mir-199a-2, bta-mir-202, bta-mir-206, bta-mir-211, bta-mir-212, bta-mir-223, bta-mir-26a-1, bta-mir-29d, bta-mir-30f, bta-mir-338, bta-mir-33a, bta-mir-33b, bta-mir-375, bta-mir-429, bta-mir-451, bta-mir-92a-1, bta-mir-92b, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-133a-1, ssc-mir-1, ssc-mir-146b, ssc-mir-181a-1, ssc-mir-30a, bta-mir-199c, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-133b, ssc-mir-29a, ssc-mir-30d, ssc-mir-30e, ssc-mir-199a-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-10b, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-99a, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-192, ssc-mir-142, ssc-mir-127, ssc-mir-202, ssc-mir-129a, ssc-mir-455, ssc-mir-125b-1, ssc-mir-338, ssc-mir-133a-2, ssc-mir-146a, bta-mir-26c, ssc-mir-30c-1, ssc-mir-126, ssc-mir-199a-1, ssc-mir-451, ssc-let-7a-2, ssc-mir-129b, ssc-mir-429, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-132, ssc-mir-138, ssc-mir-144, ssc-mir-190a, ssc-mir-212, bta-mir-133c, ssc-mir-26b, ssc-mir-200b, ssc-mir-223, ssc-mir-375, ssc-mir-33b
MicroRNA-499 expression distinctively correlates to target genes sox6 and rod1 profiles to resolve the skeletal muscle phenotype in Nile tilapia. [score:4]
Duran et al. (2015) analyzed the impact of the miRNA-target interactions of miR-1/ hdac4, miR-133-a/b/ srf, miR-206/ pax7, and miR-499/ sox6 in fast- and slow-twitch skeletal muscles during growth. [score:3]
MiR-1, miR-133a, miR-133b, miR-206, and miR-499 have been shown to be involved in the control of genes related to myoblast proliferation and differentiation. [score:1]
Finally, miR-499 may promote differentiation of slow-twitch muscle fibers, which corroborates previous findings in Nile tilapia (Nachtigall et al., 2015). [score:1]
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It has been reported that muscle-specific miRNAs, miR-206 and miR-499, are upregulated and miR-1, miR-133a, and miR-133b are downregulated in extraocular muscles compared to limb muscle, concluding that a miRNA network contributes to the extraocular muscles by regulating posttranscriptional expression of genes involved in structure, signaling, metabolism, angiogenesis, myogenesis, and regeneration in extraocular muscles [7]. [score:9]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-31, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-181a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-184, hsa-mir-186, hsa-mir-193a, hsa-mir-194-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-219a-2, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-374a, hsa-mir-148b, hsa-mir-423, hsa-mir-486-1, hsa-mir-499a, hsa-mir-532, hsa-mir-590, bta-mir-26a-2, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-221, bta-mir-222, bta-mir-27a, bta-mir-125b-1, bta-mir-181a-2, bta-mir-205, bta-mir-27b, bta-mir-30b, bta-mir-31, bta-mir-193a, bta-let-7d, bta-mir-148b, bta-mir-186, bta-mir-191, bta-mir-192, bta-mir-200a, bta-mir-214, bta-mir-22, bta-mir-23a, bta-mir-29c, bta-mir-423, bta-let-7g, bta-mir-24-2, bta-let-7a-1, bta-mir-532, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-365-1, bta-mir-374a, bta-mir-99b, hsa-mir-374b, hsa-mir-664a, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-1915, bta-mir-146a, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-194-2, bta-mir-219-1, bta-mir-223, bta-mir-26a-1, bta-mir-365-2, bta-mir-374b, bta-mir-486, bta-mir-763, bta-mir-9-1, bta-mir-9-2, bta-mir-181a-1, bta-mir-2284i, bta-mir-2284s, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2339, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-664a, bta-mir-2284e, bta-mir-1388, bta-mir-194-1, bta-mir-193a-2, bta-mir-2284w, bta-mir-2284x, bta-mir-148c, hsa-mir-374c, hsa-mir-219b, hsa-mir-499b, hsa-mir-664b, bta-mir-2284y-1, bta-mir-2284y-2, bta-mir-2284y-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2284y-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2284z-4, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2284z-2, hsa-mir-486-2, hsa-mir-6516, bta-mir-2284ab, bta-mir-664b, bta-mir-6516, bta-mir-219-2, bta-mir-2284ac, bta-mir-219b, bta-mir-374c, bta-mir-148d
Furthermore, the differential expression pattern of five miRNAs (bta-miR184, miR-24-3p, miR-148, miR-486 and bta-let-7a-5p) were unique to E. coli while four (bta-miR-2339, miR-499, miR-23a and miR-99b) were unique to S. aureus. [score:3]
Five differentially expressed miRNAs (bta-miR-184, miR-24-3p, miR-148, miR-486 and let-7a-5p) were unique to E. coli while four (bta-miR-2339, miR-499, miR-23a and miR-99b) were unique to S. aureus. [score:3]
Interestingly, our study shows that a different set of five miRNAs (miR-184, miR-24-3p, miR-148, miR-486 and let-7a-5p) were unique to E. coli bacteria while another set of four (miR-2339, miR-499, miR-23a and miR-99b) were unique to S. aureus bacteria. [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181a-1, hsa-mir-215, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-mir-15b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-141, hsa-mir-143, hsa-mir-152, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-184, hsa-mir-200c, hsa-mir-155, hsa-mir-29c, hsa-mir-200a, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-342, hsa-mir-148b, hsa-mir-451a, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-15b, ssc-mir-184, ssc-mir-224, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-let-7f-1, ssc-mir-103-1, ssc-mir-21, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-671, hsa-mir-378d-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-16b, bta-mir-21, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-27b, bta-mir-31, bta-mir-15b, bta-mir-215, bta-mir-30e, bta-mir-148b, bta-mir-192, bta-mir-200a, bta-mir-200c, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-10b, bta-mir-24-2, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-mir-342, bta-let-7f-1, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-125b-2, bta-mir-15a, bta-mir-99b, hsa-mir-664a, ssc-mir-99b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, bta-mir-141, bta-mir-143, bta-mir-146a, bta-mir-152, bta-mir-155, bta-mir-16a, bta-mir-184, bta-mir-24-1, bta-mir-223, bta-mir-224, bta-mir-26a-1, bta-mir-296, bta-mir-29d, bta-mir-378-1, bta-mir-451, bta-mir-486, bta-mir-671, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, ssc-mir-181a-1, ssc-mir-215, ssc-mir-30a, bta-mir-2318, bta-mir-2339, bta-mir-2430, bta-mir-664a, bta-mir-378-2, ssc-let-7a-1, ssc-mir-378-1, ssc-mir-29a, ssc-mir-30e, ssc-mir-499, ssc-mir-143, ssc-mir-10b, ssc-mir-486-1, ssc-mir-152, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-99a, ssc-mir-148b, ssc-mir-664, ssc-mir-192, ssc-mir-342, ssc-mir-125b-1, oar-mir-21, oar-mir-29a, oar-mir-125b, oar-mir-181a-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-296, ssc-mir-155, ssc-mir-146a, bta-mir-148c, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-664b, hsa-mir-378j, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-31, ssc-mir-671, bta-mir-378b, bta-mir-378c, hsa-mir-486-2, oar-let-7a, oar-let-7f, oar-mir-103, oar-mir-10b, oar-mir-143, oar-mir-148a, oar-mir-152, oar-mir-16b, oar-mir-181a-2, oar-mir-200a, oar-mir-200b, oar-mir-200c, oar-mir-23a, oar-mir-26a, oar-mir-29b-1, oar-mir-30a, oar-mir-99a, bta-mir-664b, chi-let-7a, chi-let-7f, chi-mir-103, chi-mir-10b, chi-mir-125b, chi-mir-126, chi-mir-141, chi-mir-143, chi-mir-146a, chi-mir-148a, chi-mir-148b, chi-mir-155, chi-mir-15a, chi-mir-15b, chi-mir-16a, chi-mir-16b, chi-mir-184, chi-mir-192, chi-mir-200a, chi-mir-200b, chi-mir-200c, chi-mir-215, chi-mir-21, chi-mir-223, chi-mir-224, chi-mir-2318, chi-mir-23a, chi-mir-24, chi-mir-26a, chi-mir-27b, chi-mir-296, chi-mir-29a, chi-mir-29b, chi-mir-29c, chi-mir-30a, chi-mir-30e, chi-mir-342, chi-mir-378, chi-mir-451, chi-mir-499, chi-mir-671, chi-mir-99a, chi-mir-99b, bta-mir-378d, ssc-mir-378b, oar-mir-29b-2, ssc-mir-141, ssc-mir-200b, ssc-mir-223, bta-mir-148d
Similarly, Jin et al. (2014a) demonstrated a differential expression of nine miRNAs (bta-miR-184, miR-24-3p, miR-148, miR-486, and let-7a-5p, miR-2339, miR-499, miR-23a, and miR-99b) upon challenge of MACT-cells (bovine mammary epithelia cell line) with heat inactivated E. coli and S. aureus bacteria. [score:3]
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[+] score: 2
We also conducted qPCR of miRNAs that are enriched in muscle or plasma (miR-21-5p, miR-30d-5p, miR-103, miR-206, miR-208b, miR-451, miR-486, miR-499, miR-2412, and miR-2478), some of which are abundant in bovine skeletal muscles [4]. [score:1]
Our previous studies revealed that skeletal muscle-specific miRNAs, namely miR-1, miR-133a/b, miR-206, miR-208a/b, miR-496, and miR-499, were abundant in the muscles of JB cattle [4], whereas none of them was detected in the plasma profiles except for a modest miR-486 content [24]. [score:1]
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[+] score: 1
Bta-miR-184, miR-24-3p, miR-148, miR-486 and let-7a-5p were unique to E. coli, whereas bta-miR-2339, miR-499, miR-23a and miR-99b were specific to S. aureus in an in-vitro study with bovine mammary epithelial cells 32. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-130a, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-211, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-455, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, mmu-mir-455, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Among the seven other conserved intragenic precursors in human, mouse and cow, mir-1249 in the host gene KIAA0930 and mir-499 in the host gene MYH7B (Myosin heavy chain 7B cardiac muscle beta) were not retrieved either in the goat protein-coding genes available, suggesting once again that these genes have yet to be described in the goat genome. [score:1]
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