Mouse pre-microRNA Expression Construct mir-148a
- Known as:
- Mouse pre-microRNA Expression Construct mir-148a
- Catalog number:
- mmir-148a-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-148a
Related genes to: Mouse pre-microRNA Expression Construct mir-148a
- Gene:
- MIR148A NIH gene
- Name:
- microRNA 148a
- Previous symbol:
- MIRN148, MIRN148A
- Synonyms:
- hsa-mir-148, hsa-mir-148a
- Chromosome:
- 7p15.2
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-30
Related products to: Mouse pre-microRNA Expression Construct mir-148a
Related articles to: Mouse pre-microRNA Expression Construct mir-148a
- Targeted delivery and controlled expression of mRNA encapsulated by lipid nanoparticles (mRNA-LNPs) are critical for the development of safe and effective mRNA medicines. However, efficient post-delivery regulation of mRNA-LNP expression remains challenging, and conventional approaches largely rely on modifying the 3' UTR at the expense of other regulatory elements. In this study, we engineered segmented poly(A) tail variants that function as gene-specific regulatory elements for synthetic mRNAs, providing an alternative regulatory module that preserves UTR integrity. Insertion of miR-122 or miR-142 target sites (MTSs) at various positions within the poly(A) tail suppressed luciferase expression in non-target cells and in a position-dependent manner. Furthermore, by incorporating triple-MTS sequences for miR-142, miR-126, and miR-148a in all possible combinations at the 5' end of the poly(A) tail, we identified specific arrangements that simultaneously reduced luciferase activity in three non-target hepatic cell types while preserving robust expression in hepatocytes. MTS insertion order proved critical for optimal silencing, highlighting a design parameter not observed in dual-MTS constructs. These findings establish the poly(A) tail as a programmable platform for cell-type-selective regulation, complementing tissue-tropic LNPs and expanding the toolbox for mRNA therapeutic design. - Source: PubMed
Publication date: 2026/09/08
Qi RuiChen HuaChen RuiBao HuiSun YingXu RuiwenHan LuXu YingmeiLi JuanLi NaLi QiangZhang TingtingLv KaiDong YijieCen ShanZhang Weiguo - Milk-derived extracellular vesicles (EVs) carry proteins and microRNAs that mediate immune communication between mother and offspring, yet which inflammation-related cargo is conserved-and which is species specific-across mammals remains poorly defined. We assembled MetaMilkDB, a provenance-tracked database integrating proteomic, transcriptomic, metabolomic and pathway-level evidence for milk-EVs across four species (, , , ), combining curated studies with in-house EV proteomics (265,009 measurements). Of 4958 EV protein families, 570 (11.5%) formed a conserved core containing five inflammation markers (HP, LTF, MUC1, MUC15, TLR2), four re-detected in our in-house proteomes. This core was an innate scaffold and was not itself enriched for inflammation; instead, inflammation cargo concentrated in the species-specific fraction, overwhelmingly in human milk (45/966 vs. 6/1222 shared; odds ratio 9.9; q = 1.6 × 10), forming a secretory-immunoglobulin and complement module absent from ruminant cargo. A parallel layer of inflammation-annotated EV-microRNAs showed heterogeneous conservation across species and converged on TLR/NF-κB-related immune regulation. Milk-EV immunity is organized on two axes-a conserved innate scaffold shared across species and a divergent, largely human adaptive-immune fraction-clarifying which cargo is a candidate cross-species biomarker and which may underlie species-specific immune transfer. - Source: PubMed
Publication date: 2026/09/12
Papakonstantinou EleniChrousos George PVlachakis Dimitrios - Subsequently to the publication of the above article, an interested reader drew to the Editor's attention that, in Fig. 2C and D on p. 2921 showing the methylation status of the miR‑148a promoter, the centrally placed 'M' and 'U' lanes in these figure parts apparently showed the same data, albeit with horizonal stretching of the bands in question. Furthermore, in Fig. 6B on p. 2923, which showed the results of cell migration and invasion assay experiments, the 'Mimics‑NC/Migration' and 'Blank/Invasion' data panels apparently showed the same data, albeit with different sizing of the panels, such that these were derived from the same orginal source. Finally, the reader noted that one of the antibodies the authors had used in their study was apparently selected inappropriately: The antibody (cat. no. ab51243) that the authors reported to have used is specific for the protein known as p16‑ARC (or ARPC5), not the apoptosis‑associated protein p16‑INK4a, as was intended. The authors were asked to investigate these various matters, and have fully responded to the reader's queries. Concerning the antibody, after thoroughly examining the original reagent purchase records and raw experimental data, the authors can confirm that the correct anti‑CDKN2A/p16 antibody (cat. no. ab108349; Abcam) was in fact used in this study: As the catalogue number of antibody was not stated in the initial manuscript submission and this information was requested during the editing stage of the paper, the authors inadvertently entered the incorrect catalogue number into the text of the paper (they also provided a copy of the original purchase form to the Editorial Office for our inspection). Therefore, the sentence commencing on p. 2918, left‑hand column, line 20, in the '' subsection of the Materials and methods section should have read as follows: 'The primary antibodies used were as follows: DNMT1 (1:500, cat. no. ab188453; Abcam), p16 (1:200, cat. no. ab108349; Abcam)...'.Concerning Figs. 2 and 6, the authors were able to examine their original data, and realized that errors had inadvertently been made when assembling these figures. Corrected versions of Figs. 2 and 6, now showing data from one of the repeated sets of experiments for Fig. 2A‑D and the correct data for the 'Blank/Invasion' data panel in Fig. 6B, are shown on the next two pages. The authors wish to emphasize that the errors made in assembling the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused; they also thank the reader of the article for drawing these matters to their attention. [Oncology Reports 40: 2916‑2925, 2018; DOI: 10.3892/or.2018.6700]. - Source: PubMed
Publication date: 2026/09/18
Hong LeSun GenPeng LongTu YiWan ZhenXiong HaiweiLi YongXiao Weidong - Gestational diabetes mellitus (GDM) is linked to poor infant metabolic outcomes, potentially via altered human milk (HM) hormones and microRNAs. Since their specific roles remain unclear, this study synthesizes current evidence on HM adipose tissue-derived hormones (particularly adiponectin, leptin, and resistin) and microRNA modifications during gestational diabetes. Firstly, a systematic review following PRISMA 2020 guidelines was conducted (PROSPERO: CRD42024612813). Searches in major databases identified studies comparing HM adiponectin, leptin, or resistin concentrations and/or miRNA profiles between GDM and normoglycemic mothers. Secondly, bioinformatics analysis using miRWalk 3.0, functional enrichment, and network topology mapping examined miRNA interactions with , and genes. Twelve studies were included. Adiponectin showed the most consistent GDM-associated reductions, though findings were context-dependent. Leptin was primarily associated with maternal adiposity rather than GDM status. Resistin evidence was insufficient. Three miRNA studies revealed stage-dependent dysregulation in GDM, with , and linked to infant growth outcomes during the first 6 months. Bioinformatics identified and as targeting all three adipokine genes, with enrichment in glucose homeostasis and insulin resistance pathways. Network analysis highlighted , and as central nodes. GDM is associated with selective alterations in HM adipokines and miRNAs, with adiponectin and specific miRNAs showing the strongest signals. These findings support a conceptual model where GDM shapes HM's molecular composition through interacting endocrine and posttranscriptional mechanisms, potentially influencing infant metabolic programming. Larger longitudinal studies are needed to validate these observations and determine clinical relevance. - Source: PubMed
Publication date: 2026/08/31
Zhang ZhijunDavoudi MaryamGhafourian AmirrezaDehghan ParmidaAhmadi MojdeAyyoubzadeh Seyed MohammadMiao XiaoleiChoobineh HamidAfrisham Reza - Milk-derived extracellular vesicles (EVs) transport microRNAs (miRNAs) that are unusually stable and have been proposed to survive digestion and modulate gene expression in the consumer, although their dietary bioavailability and physiological relevance remain debated. How the predicted regulatory potential of these miRNAs differs among the milks of different animals most relevant to human nutrition has not been systematically compared. Here, we performed an integrative in silico analysis of publicly available small-RNA sequencing data from 29 milk and milk-cell samples of human, cow, goat, and donkey origin. miRNAs were quantified against human (hsa) miRBase references-thereby restricting the analysis to evolutionarily conserved miRNAs with human orthologs-and their predicted effect on the human transcriptome was modeled by integrating predicted (mirDIP database) and experimentally supported (TarBase v9 database) miRNA-target interactions into a per-gene, per-species weighted targeting score. Because miRNAs act predominantly as repressors, this score is read as a prediction of which genes would be post-transcriptionally down-regulated in a recipient. miR-148a-3p dominated the exosomal spectrum of all four species (human, cow, goat, and donkey; ≈21.5% of pooled abundance), and the twenty most abundant miRNAs accounted for roughly three quarters of the signal. Of 4577 robustly targeted genes, a 1809-gene conserved "pan-milk" core showed the highest cross-species targeting and was enriched for transcriptional regulation, PI3K-Akt, MAPK, and TGF-β/SMAD signaling, autophagy and-strikingly-the components of the RNA-interference machinery itself. Species-restricted gene sets recapitulated biologically plausible programs, including a human-biased neuronal/axon-guidance and chromatin module, a donkey-biased transcriptional, epithelial, and immune () module, and a ruminant lipid/cholesterol and insulin-mTOR module. Across categories, we observed a reproducible confidence-exclusivity trade-off. We emphasize that these results are computational predictions that assume dietary miRNA uptake and do not constitute experimental validation. We provide the complete targetome as a hypothesis-generating resource to prioritize candidate genes, pathways, and milk types for future functional, nutritional, and epigenetic investigation. Across the 29 samples from the four species, miRNA composition segregated by species (silhouette width = 0.82, a cluster-separation measure ranging from -1 to 1, with values near 1 indicating well-separated groups) and the category structure exceeded a permutation null, indicating that the between-species signal is robust to differences in dataset origin and milk state. - Source: PubMed
Publication date: 2026/08/02
Zoziuk MaksymDjibagaou Abel DafogoTerrinoni AlessandroKoroliouk DimitriColizzi Vittorio