Mouse pre-microRNA Expression Construct mir-23b
- Known as:
- Mouse pre-microRNA Expression Construct mir-23b
- Catalog number:
- mmir-23b-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-23b
Related genes to: Mouse pre-microRNA Expression Construct mir-23b
- Gene:
- MIR23B NIH gene
- Name:
- microRNA 23b
- Previous symbol:
- MIRN23B
- Synonyms:
- hsa-mir-23b
- Chromosome:
- 9q22.32
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-24
Related products to: Mouse pre-microRNA Expression Construct mir-23b
Related articles to: Mouse pre-microRNA Expression Construct mir-23b
- Persistent infection with high-risk human papillomavirus type 16 (HPV16) is a major cause of cervical cancer and is associated with viral oncoproteins that disrupt tumor suppressor pathways and influence cellular microRNA (miRNA) expression. Given increasing interest in phytochemicals as potential anticancer agents, this study evaluated the effects of chrysin, a natural flavonoid, on cell viability, selected cancer-related miRNAs, and HPV16 E6 protein levels in HPV16-positive CaSki cervical cancer cells. CaSki cells and normal human dermal fibroblasts (HDF) were treated with chrysin (31.5-500 µg/ml) for 24 and 48 h. Cell viability was assessed by MTT assay. Expression of miR-34a, miR-218, miR-20a, miR-195, and miR-23b was quantified by qRT-PCR (2 method), and E6 protein levels were analyzed by Western blot. Chrysin selectively reduced CaSki cell viability with minimal toxicity toward HDF cells, resulting in a high selectivity index. Treatment was associated with increased expression of miR-34a (10.05-fold, P < 0.0001) and miR-218 (5.64-fold, P < 0.01), a moderate increase in miR-20a (1.7-fold, P < 0.05), decreased miR-195 expression (0.18-fold, P < 0.01), and no significant change in miR-23b. A significant reduction in E6 protein levels was also observed (0.64 ± 0.01 vs. control, P < 0.001). These findings indicate that chrysin treatment is associated with selective cytotoxicity and concurrent modulation of HPV16 E6 protein levels and several cancer-related miRNAs in CaSki cells. Further studies in additional cellular models and mechanistic systems are required to clarify the underlying pathways. - Source: PubMed
Publication date: 2026/08/29
Gholami Fashkhami MahdisHabibollahi HadiShafighi Seyedeh Tooba - Blood-brain barrier (BBB) disruption drives stroke and other CNS disorders pathology, yet restoring its integrity remains challenging. Using an unbiased anti-miR lentiviral screen, miR-23b was identified as a critical negative regulator of BBB integrity in brain endothelial cells (BECs). Targeted inhibition of miR-23b using anti-miR-23b, validated by Wnt-reporter, Wnt-rescue, and eCLIP analysis, demonstrates that BEC miR-23b silencing, enhances junctional protein expression and strengthens barrier function while suppressing transcellular transport. Global multi-omics analysis reveals that miR-23b acts as a robust driver of angiogenesis-specific genes and proteins. Conversely, anti-miR-23b induces the expression of factors essential for BBB stabilization and repair. Notably, anti-miR-23b enhances these protective barrier properties through a multi-faceted regulation of Wnt/β-catenin, TGF-β, Notch, and VEGF signaling mechanisms. Using a 3D microfluidic platform, anti-miR-23b was shown to foster BBB repair by accelerating vessel maturation and enhancing resilience against ischemic injury. Proof-of-concept studies show that BEC-specific AAVBR1-anti-miR-23b gene therapy reinforces BBB tight junctions, reduces BBB leakage, and improves outcome measures in a transient middle cerebral artery occlusion (t-MCAO) stroke model. Thus, miR-23b is a critical regulator of cerebrovascular integrity, positioning anti-miR-23b as a promising RNA-based therapy to enhance BBB stability and repair in stroke and other CNS disorders. - Source: PubMed
Publication date: 2026/07/30
Martinez Victor AnthonyPresby Rose ENakanishi SaraGaur PallaviAkcan UgurDaugaard Krog JohannesDaugaard Krog IbenDas LipiJohnson David SJamoul DannyJury DouglasLawson BrianKörbelin JacobBrown Lewis MMenon VilasAgalliu DritanMunk Pedersen Irene - Myotonic dystrophy type 1 (DM1) is a severe neuromuscular disorder caused by CTG repeat expansions in the DMPK gene, leading to the formation of toxic RNA foci that sequester essential splicing regulators MBNL1/2. Beyond muscle impairment, DM1 affects also the brain, leading to significant cognitive deficits, behavioral abnormalities, and intellectual disabilities. This study evaluates the therapeutic potential of the lipid-conjugated antimiR-23b, X82108, designed to promote MBNL1/2 upregulation through inhibition of miR-23b. Systemic administration of X82108 in mice and non-human primates efficiently crosses the blood-brain barrier, increasing MBNL1 in the brain. In DMSXL transgenic mice, treatment increases Mbnl1/2, reduces toxic DMPK, and restores normal splicing patterns across all brain regions. These molecular improvements correlate with improved behavioral outcomes, including reduced impulsivity and normalized exploratory activity. Collectively, the findings highlight X82108 as a promising systemic therapy for DM1, targeting not only muscular features as we have previously shown but also DM1-related CNS alterations. - Source: PubMed
Publication date: 2026/07/22
Piqueras-Losilla DiegoGarcia-Rey AndreaHuguet-Lachon AlineMayoral-Olmos ArgimiroCampillo IsabelNufer MelanieChakraborty MouliDíaz-Maqueda AnaBarquero NuriaGonzalez-Barriga AnchelMartinez-Hernandez Joséde Garnica García María GraciaGourdon GenevièveArtero RubenLlamusí BeatrizCerro-Herreros Estefanía - Sjögren's syndrome (SS) is a systemic autoimmune disorder characterized by chronic inflammation, oxidative stress, and progressive salivary gland dysfunction. Current therapies remain limited in efficacy. - Source: PubMed
Publication date: 2026/06/08
Cai YanWang XianzhenFeng JingE Changyong - Blood-brain barrier (BBB) disruption drives stroke and other CNS disorders pathology, yet restoring its integrity remains challenging. Using an unbiased anti-miR lentiviral screen, miR-23b was identified as a critical negative regulator of BBB integrity in brain endothelial cells (BECs). Targeted inhibition of miR-23b using anti-miR-23b, validated by Wnt-reporter, Wnt-rescue, and eCLIP analysis, demonstrates that BEC miR-23b silencing in BECs, enhances junctional protein expression and strengthens barrier function while suppressing transcellular transport. Global multi-omics analysis reveals that miR-23b acts as a robust driver of angiogenesis-specific genes and proteins. Conversely, anti-miR-23b induces the expression of factors essential for BBB stabilization and repair. Notably, anti-miR-23b enhances these protective barrier properties through the multi-faceted regulation of Wnt/β-catenin, TGF-β, Notch, and VEGF signaling mechanisms. Using a 3D microfluidic platform, anti-miR-23b was shown to foster BBB repair by accelerating vessel maturation and enhancing resilience against ischemic injury. Proof-of-concept studies show that BEC specific AAVBR1-anti-miR-23b gene therapy reinforces BBB tight junctions, reduces BBB leakage, and improves outcome measures in a transient middle cerebral artery occlusion (t-MCAO) stroke model. Thus, miR-23b is a critical regulator of cerebrovascular integrity, positioning anti-miR-23b as a promising RNA-based therapy to enhance BBB stability and repair in stroke and other CNS disorders. - Source: PubMed
Publication date: 2026/05/28
Martinez Victor AnthonyPresby RoseNakanishi SaraGaur PallaviAkcan UgurKrog Johannes DaugaardKrog Iben DaugaardDas LipiJohnson David SJamoul DannyJury DouglasLawson BrianKörbelin JacobBrown Lewis MMenon VilasAgalliu DritanPedersen Irene Munk