IGF_II Antisense
- Known as:
- IGF_II Antisense
- Catalog number:
- 000645A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- IGF_II Antisense
Related products to: IGF_II Antisense
([125I]-Tyr)-IGF-I (24-41)([125I]-Tyr)-IGF-I (24-41)([125I]-Tyr)-IGF-I (24-41), CE-marked, Liquid([125I]-Tyr)-IGF-I (24-41), CE-marked, Liquid([125I]-Tyr)-IGF-I (24-41), CE-marked, Liquid([125I]-Tyr)-IGF-I (24-41), CE-marked, Lyophilized([125I]-Tyr)-IGF-I (24-41), CE-marked, Lyophilized([125I]-Tyr)-IGF-I (24-41), CE-marked, Lyophilized([125I]-Tyr)-IGF-I (24-41)CE-markedLiquid([125I]-Tyr)-IGF-I (24-41)CE-markedLyophilized([125I]-Tyr)-IGF-I (30-41)([125I]-Tyr)-IGF-I (30-41)([125I]-Tyr)-IGF-I (30-41), CE-marked, Liquid([125I]-Tyr)-IGF-I (30-41), CE-marked, Liquid([125I]-Tyr)-IGF-I (30-41), CE-marked, Liquid Related articles to: IGF_II Antisense
- Pathogenic variants on the paternal allele of IGF2 are linked to Silver-Russell syndrome (SRS). This report describes two unrelated individuals-a 5-year-old girl and an adult female-with de novo IGF2 missense variants, both diagnosed with SRS. While one exhibited normal development, the other had intellectual disability, highlighting phenotypic variability. A review of 20 individuals with IGF2 variants revealed that SRS features, as defined by the Netchine-Harbison Clinical Scoring System, were most common. Additional recurrent traits included delayed speech and motor development, under-masculinized male genitalia, hand/foot anomalies, and congenital heart defects. Growth faltering patterns varied, and intellectual disability was seen in some. We also demonstrated that long-read sequencing can determine the allelic origin of de novo IGF2 variants using differentially methylated regions, eliminating the need for parental samples. This approach confirms long-read sequencing as a powerful tool for identifying de novo variant origins in imprinted genes like IGF2. - Source: PubMed
Publication date: 2026/09/01
Juul Trine MaxelBoonen Susanne EriksenPedersen Katja VenborgBækgaard Caroline HeyLarsen MartinKibæk MariaIllum NielsHeideman MaleneNielsen ChristianeLester Emilie BoyeFagerberg Christina - Cranial neural crest cell (cNCC)-derived mesenchyme must precisely integrate intrinsic transcriptional programs with localized signaling cues to orchestrate craniofacial skeletogenesis. While the transcription factor Meis2 is an essential regulator of this process, the spatially defined cellular contexts and downstream effector pathways remain poorly characterized. Building upon previous single-cell transcriptomic evidence of Igf2 dysregulation, we employed spatial transcriptomics integrated with single-cell references to map the mesenchymal landscape in Meis2-deficient embryos during early ossification. This spatial mapping identified distinct chondro-osteoprogenitor niches and revealed a significant enrichment of the IGF2 signaling axis within mutant mesenchymal compartments. We validated these spatial expression patterns in vivo, confirming the localized upregulation of Igf2 in Meis2-deficient osteo-chondroprogenitors. Functional in vitro assays demonstrated that IGF signaling is a potent modulator of cNCC-derived mesenchymal differentiation. Exogenous IGF2 enhanced osteogenic potential, whereas inhibition of the IGF1 receptor (IGF1R) significantly attenuated osteogenesis as measured using ALP activity. Furthermore, the impaired bone formation in Meis2 mutants correlated with disrupted cell adhesion dynamics. Collectively, these findings establish the importance of IGF2 signaling during embryonic craniofacial ossification and provide a mechanistic link between Meis2 loss, altered cell adhesion, and dysregulated osteogenic differentiation. - Source: PubMed
Publication date: 2026/08/31
Hudacova ErikaZucha DanielKaplan Mehmet MahsumMachon Ondrej - Corneal fibrosis is a major cause of visual impairment worldwide and is characterized by persistent stromal scarring that disrupts corneal transparency. Although transforming growth factor-β (TGF-β)-mediated myofibroblast differentiation is well established, the mechanisms that sustain myofibroblast survival and persistence remain poorly understood. In this study, we investigated the role of the insulin-like growth factor (IGF) signaling axis in corneal myofibroblast survival and evaluated the therapeutic potential of linsitinib, a dual IGF-1 receptor (IGF-1R)/insulin receptor (INSR) inhibitor. Primary corneal myofibroblasts were exposed to pro-apoptotic conditions and treated with IGF ligands in the presence or absence of linsitinib. The effects of IGF pathway inhibition were further examined in a mouse model of corneal fibrosis. IGF-1 and IGF-2 promoted myofibroblast survival under pro-apoptotic conditions, whereas pharmacologic inhibition of IGF-1R/INSR signaling with linsitinib blocked these pro-survival effects. In vivo, linsitinib treatment reduced myofibroblast persistence and attenuated corneal fibrosis. These findings identify the IGF axis as a critical regulator of corneal myofibroblast survival and suggest that persistent fibrosis is maintained, in part, by IGF-dependent resistance to apoptosis. Targeting survival pathways rather than myofibroblast differentiation may represent a novel therapeutic strategy for the treatment of corneal fibrosis. - Source: PubMed
Publication date: 2026/08/16
Hwang YunjeongSon Kyung-NoChaudhary ManojLee EunbeeKim MinhyungYou SungyongSmith Terry JAakalu Vinay KumarHan Kyu-Yeon - To recover endangered green peafowl () populations, China has implemented ex situ conservation programs centered on captive breeding. However, captive-bred individuals frequently suffer from skeletal deformities, creating a critical bottleneck that compromises future wild reintroductions. - Source: PubMed
Publication date: 2026/08/11
Pan DengSun ShengjiaChen YanqiuTu WenjiLiu BoZhu XiaomingZhang YingShu XianghuaSong ChunlianLi FangLu Lin - This study evaluated the potential of synergistically degraded low-molecular-weight chitosan (LMW-CS) as a functional feed additive to promote growth, antioxidant capacity, innate immunity, and disease resistance in Pacific white shrimp (). High-molecular-weight chitosan (HMW-CS, approximately 85 kDa) was degraded using γ-irradiation in combination with HO to produce LMW-CS with improved functional properties. Shrimp were fed five experimental diets for 4 weeks: a control diet, HMW-CS0.4 (0.4% /), LMW-CS0.1 (0.1% /), LMW-CS0.2 (0.2% /), and LMW-CS0.4 (0.4% /). Growth performance, oxidative stress markers, antioxidant enzyme activities, lysozyme activity, immune-related gene expression, bacterial load, and survival after challenge were evaluated. The results indicate that dietary LMW-CS supplementation improved growth performance and feed utilization, with LMW-CS0.2 showing significantly higher final weight, total weight gain, and average daily gain than the control group ( < 0.05). Antioxidant assays showed that LMW-CS reduced malondialdehyde levels and increased reduced glutathione, nitric oxide, glutathione reductase, catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase activities in both plasma and hepatopancreas ( < 0.05). Lysozyme activity was significantly enhanced, particularly in the LMW-CS0.4 and HMW-CS0.4 groups ( < 0.05). Gene expression analysis revealed upregulation of genes associated with growth regulation, antimicrobial defense, pathogen recognition, and prophenoloxidase activation, including , , , , and . Gut microbiota profiling showed that chitosan supplementation altered bacterial community composition, reduced the relative abundance of some -associated taxa, and descriptively lowered predicted pathogenic and stress-tolerant bacterial phenotypes. Following the challenge, shrimp fed LMW-CS0.4 showed the lowest bacterial load and highest survival rate, indicating improved disease resistance ( < 0.05). Overall, synergistically degraded LMW-CS enhanced growth, redox balance, innate immune competence, gut microbial structure, and resistance to , supporting its potential as an antibiotic-free functional feed additive for sustainable shrimp aquaculture. - Source: PubMed
Publication date: 2026/08/04
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