GHP_21 Mouse IGF_I (in preparation) _
- Known as:
- GHP_21 Mouse IGF_I (in preparation) _
- Catalog number:
- GHP-21
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- PLR
- Gene target:
- GHP_21 Mouse IGF_I ( preparation) _
Related genes to: GHP_21 Mouse IGF_I (in preparation) _
- Gene:
- IGF1 NIH gene
- Name:
- insulin like growth factor 1
- Previous symbol:
- -
- Synonyms:
- IGF1A, IGFI, IGF-I, IGF
- Chromosome:
- 12q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-06-04
- Gene:
- IGF1R NIH gene
- Name:
- insulin like growth factor 1 receptor
- Previous symbol:
- -
- Synonyms:
- JTK13, CD221, IGFIR, MGC18216, IGFR
- Chromosome:
- 15q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-07
- Date modifiied:
- 2019-04-23
Related products to: GHP_21 Mouse IGF_I (in preparation) _
Related articles to: GHP_21 Mouse IGF_I (in preparation) _
- Osteoarthritis (OA) is a leading cause of pain and disability, yet the biological mechanisms linking structural disease and pain remain incompletely understood. Insulin-like growth factors (IGFs) are involved in cartilage homeostasis, inflammation, and pain signaling and may serve as biomarkers or therapeutic targets in OA. This exploratory cross-sectional study examined associations between circulating levels and peripheral blood DNA methylation of with chronic knee OA pain phenotypes in 158 adults aged 45-85 years with and without symptomatic knee OA. Participants were classified into five radiographic OA (ROA)-pain phenotypes based on pain impact and Kellgren-Lawrence grade: no pain/no ROA, pain/no ROA, pain/late ROA, high-impact pain/early ROA, and low-impact pain/early ROA. In adjusted analyses, ROA-pain phenotypes were associated with circulating IGF-1 and IGF-2 levels in a sex-dependent manner. Females with low-impact pain and early ROA had higher IGF-1 levels than males in the same phenotype. For IGF-2, males with no ROA, with and without pain, had higher levels than males with high-impact pain and early ROA, and males with no pain/no ROA also had higher IGF-2 levels than females. Mean DNA methylation levels of and showed limited associations after covariate adjustment, and no probe-level findings survived multiple-testing correction. These findings identify sex-dependent associations between circulating IGF-1 and IGF-2 and knee OA pain phenotypes, most notably lower IGF-2 in males with high-impact pain and early radiographic disease. The largely null peripheral methylation results suggest that tissue-level epigenetic regulation of IGF pathways, beyond what the buffy coat captures, warrants further investigation in larger cohorts. - Source: PubMed
Publication date: 2026/09/07
Abbas MuhammadTamargo Javier AZhang YutaoCruz Carlos JGilliam JohnWohlgemuth StephanieWu KevinStaud RolandChen LiGoodin Burel RFillingim Roger BLeeuwenburgh ChristiaanCruz-Almeida Yenisel - How mammalian organ size is precisely regulated remains incompletely understood. This process depends on the coordinated balance between cell proliferation, differentiation, and apoptosis. In the heart, the epicardium plays a central role in embryonic cardiac growth as a source of multiple cardiac progenitor lineages. The transcription factor is essential for epicardial development and maturation, and its loss disrupts epicardial maintenance and the generation of epicardial-derived cells (EPDCs). In addition, the epicardium produces mitogenic factors required for cardiomyocyte (CM) proliferation, including those of the insulin-like growth factor () signaling pathway. Consistently, functional inactivation of or in mice results in severe prenatal growth reduction, with mutant embryos ∼60% smaller than controls, underscoring the roles of these genes in organ and fetal growth. We recently identified the cardiac lymphatic vasculature as an unexpected regulator of heart size during embryonic development. Here, by combining single-cell RNA sequencing with loss-of-function mouse models, we uncover a critical regulatory network linking cardiac lymphatics, the epicardium, , and signaling that controls the final stages of embryonic cardiac growth. Our findings suggest that cardiac lymphatics act as a physiological quality control system for heart growth. Furthermore, using gain-of-function approaches in human epicardial organoids, we demonstrate that Reelin promotes epicardial fate, suggesting that the beneficial roles of lymphatics in adult cardiac repair are likely mediated through Reelin-dependent epicardial reactivation. - Source: PubMed
Publication date: 2026/09/11
Zhou YaluEl Bobakry Sara PascualRoy ArpitaTorroja CarlosDorn TatjanaZengerle SophieVidal-Cruchez OliviaKahn SamanLiang XiaoyanQuaggin Susan EMoretti AlessandraBen-Sahra IssamThomson Benjamin RSosa-Pineda BeatrizOliver Guillermo - To determine features of physical development and hormonal status in preschool- and school-age children born to mothers with obesity. - Source: PubMed
Publication date: 2026/09/11
Firsova LiudmilaNovikova ValeriaEvdokimova NinaGurina OlgaBlinov AleksandrVarlamova OlgaKarelov DmitryPetrenko YuriyIvanov Dmitry - 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