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
- Rupture of carotid atherosclerotic plaques is a significant cause of stroke. We have previously analyzed 21 plaques by mass spectrometry and reported differing proteomic profiles between morphologically unstable (rupture-prone) and stable plaques. This expanded dataset includes additional carotid plaques as well as non-atherosclerotic arteries, allowing comparison with control tissue. Additionally, the role of insulin-like growth factor 1 (IGF-1) signaling in plaque stability was investigated with ex vivo cultured plaques. - Source: PubMed
Publication date: 2026/04/14
Jørgensen Sara MYang-Jensen Karen CYeung KarinKhare Harshvardhan ADawoodi Ida MKjær AndreasResch Timothy AEiberg Jonas PDavies Michael JLorentzen Lasse G - While soybean meal (SBM) is a cost-effective protein source for Nile tilapia, its anti-nutritional factors require dietary interventions such as the supplementation of organic acid salts to maintain health and gut functions. Therefore, this study evaluated the dietary effects of organic acid salts as sodium propionate (PR), sodium butyrate (BT), and their mixture (PR + BT) on the growth, digestive enzymes, hepatic antioxidant responses and intestinal histomorphology of Nile tilapia fed a high SBM diet. Fingerlings (average initial weight ~ 19.65 ± 0.1 g) were assigned to five triplicate diets for 12 weeks: a negative control (CNT, contains 350 g/kg SBM), a high SBM diet (SB, contains 550 g/kg SBM), SB + PR (2.0 g/kg), SB + BT (6.25 g/kg), and their mixture (SB + PR + BT). Results revealed that fish fed solely on SB diet had significantly reduced growth, feed efficiency, and digestive enzyme activities, alongside higher levels of oxidative stress markers (MDA malondialdehyde levels) and intestinal inflammatory lesions (enteritis). Supplementation with PR, BT, or their mixture improved final body weight, weight gain, and feed conversion ratio. Digestive enzyme activities (lipase, amylase, protease) and antioxidant defenses (T-AOC, SOD, CAT, and GPx) were improved, while lipid peroxidation (MDA) was reduced in the treated groups. The histological examination confirmed that organic acid salts supplementation, especially PR + BT, alleviated SB-induced enteritis. Gene expression analysis revealed enhanced growth (IGF-2, GHR1, IGF-1, and GHR2) and immune-related markers (TLR2, and IFN-γ) and suppression of inflammatory (IL-1β, TNF-α, and caspase-3) related genes in the treated groups. In conclusion, PR and BT supplementation, especially in combination, effectively counteracted the negative impacts of high SB diets, supporting growth, alleviating inflammation, mitigating oxidative stress, and improving intestinal health of fish. These effects underscore the fascinating roles of organic acid salts in the improvement of aquafeed for tilapia culture. - Source: PubMed
Publication date: 2026/04/17
Awad AbeerGhetas Hanan AKhallaf Mohamed AShukry MustafaSoliman Ali AGewaily Mahmoud SAmer Asem AShehata Akram IsmaelAbdel-Latif Hany M R - Genomic imprinting is a crucial epigenetic mechanism directing parent-of-origin-specific gene expression in mammals, and it is regulated by allele-specific DNA methylation at imprinting control regions (ICRs). In this canonical imprinting mechanism, maintenance factors preserve germline-derived DNA methylation at ICRs during genome-wide demethylation after fertilization. However, our studies of the Igf2/H19 locus reveal that allele-specific de novo DNA methylation after fertilization, termed 'post-fertilization imprinted methylation,' also contributes to imprint maintenance. In this process, epigenetic imprints other than DNA methylation are thought to guide the recognition of parental alleles by de novo methyltransferases in the next generation, acting in concert with maintenance factors to ensure stable DNA methylation at canonical imprinted loci. Recently identified non-canonical imprinting, in contrast, relies on non-DNA methylation marks that are converted into DNA methylation only after implantation. Despite differences in the timing of this conversion, post-fertilization imprinted methylation may share similarities with non-canonical imprinting. Collectively, these findings suggest that the robustness of canonical imprinting is supported by a two-tiered regulatory system. - Source: PubMed
Publication date: 2026/04/17
Matsuzaki HitomiIshihara TeruhitoTanimoto Keiji - Stem cells proliferate after injury to repair damaged tissue, and chronic injury can promote cancer. However, the injury-activated signals and regulatory mechanisms, and their relationship to cancer, are poorly understood. Here, we identified insulin-like growth factor 2 (Igf2) as an injury-activated mitogen for lung neuroendocrine stem cells, which are facultative airway progenitors and a cell of origin of small-cell lung cancer in mice. Igf2 was constitutively produced by the stem cells but sequestered in the niche by coexpressed Igf binding proteins (Igfbps). Airway injury released Igf2 and induced proliferation by transiently activating Igf2 receptors and repressing retinoblastoma (Rb) tumor suppressor. Permanent pathway activation by deletion initiated continuous stem cell division. Thus, beyond their classical hormonal roles in physiology, growth, and aging, Igf proteins operate locally and rapidly with Igfbp and Rb to control injury-induced stem cell proliferation and tumor initiation. - Source: PubMed
Publication date: 2026/04/16
Zhang YueOuadah YoucefLiu YinKumar Maya EMorck Makenna MKrasnow Mark A - Endometriosis is a benign gynaecological disorder characterised by the presence of endometrial-like tissue outside the uterus. Proliferation of endometrial tissue and neoangiogenesis are essential factors in the development of endometriosis. Vascular endothelial growth factor () and insulin-like growth factors (, ) can be effective in neoangiogenesis and cell proliferation. Imprinted long non-coding RNA (lncRNA) H19 is involved in endometriosis pathogenesis through the regulation of cellular proliferation and differentiation. Curcumin has antiangiogenic, anti-proliferative, and anti-invasive properties for various diseases, and it is hypothesised that it may have therapeutic effects on endometriosis. This study aimed to evaluate the effects of curcumin on the expression of , , , and lncRNA, as well as on cell migration and proliferation in endometrial stromal cells isolated from women with endometriosis. - Source: PubMed
Publication date: 2026/04/13
Kamrani SedighehHayaei Tehrani Reyhaneh SadatEsfandiari FereshtehGhaffari FirouzehAmirchaghmaghi ElhamGhaedi KamranShahhoseini Maryam