Human Amphiregulin ELISA , AREG
- Known as:
- Human Amphiregulin Enzyme-linked immunosorbent assay test , AREG
- Catalog number:
- E01A0616
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Amphiregulin ELISA AREG
Related genes to: Human Amphiregulin ELISA , AREG
- Gene:
- AREG NIH gene
- Name:
- amphiregulin
- Previous symbol:
- SDGF, AREGB
- Synonyms:
- -
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2015-08-24
Related products to: Human Amphiregulin ELISA , AREG
Related articles to: Human Amphiregulin ELISA , AREG
- Despite the extensive use of in vitro embryo production (IVP) in cattle, its efficiency remains variable, mainly due to suboptimal conditions during oocyte in vitro maturation (IVM). Oocyte developmental competence is influenced by the local signaling environment, particularly by interactions between the oocyte and cumulus cells. Among the mediators involved in this process, amphiregulin (AREG) was identified as an important regulator of oocyte maturation. This study evaluated the effect of supplementing maturation media with AREG during bovine IVM on oocyte maturation, meiotic spindle organization, and subsequent embryo development. Oocytes were matured under three conditions: control (0 ng/mL AREG), A50 (50 ng/mL AREG), and A100 (100 ng/mL AREG). Supplementation with A100 significantly increased cumulus expansion compared with the control and A50 groups (P < 0.05). The A100 group also showed higher rates of progression to metaphase II (>89%) and a lower proportion of oocytes arrested at the germinal vesicle breakdown stage (P < 0.05). In addition, A100 supplementation reduced severe chromosome misalignment and spindle multipolarity and α-tubulin volume (P < 0.05). Embryo development was improved in the A100 group, as evidenced by higher cleavage rates on D3 (>80%), increased proportions of embryos reaching the ≥ 8-cell stage, and greater blastocyst and hatching rates on D7 compared with the control and A50 groups (P < 0.05). No differences among treatments were detected in blastocyst global 5 methylcytosine levels (P > 0.05). In summary, 100 ng/mL AREG supplementation during bovine IVM improves oocyte quality and embryo developmental competence without altering global DNA methylation. - Source: PubMed
Publication date: 2026/07/11
de Oliveira Lhara Ricarliany MedeirosLatorraca Lais BarbosaPereira Alexsandra FernandesFair Trudee - Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with limited therapeutic options. Although macrophage heterogeneity has been implicated in pathogenesis, the contribution of transitional macrophage states remains poorly understood. - Source: PubMed
Publication date: 2026/07/02
Lin CenshanWu MingyueZhang ZiyingZheng MuxuLi HuiqinWang YufangDu ZhanxinWu LinxiangDai JunjieYu YuDu XuhangWu YehuiXu JieWang ZhongxingXiang Fu-Li - Psoriasis is a chronic autoimmune skin disorder marked by IL-17 producing gamma delta T cell (γδT17) and pruritus, but immunoregulatory roles of itch-inducing neurons in this context remain unclear. This study addressed whether non-peptidergic (NP) afferents bearing the Mas-related G protein-coupled receptor D (MrgprD/NP1) and MrgprA3/NP2 subsets had differential effects on psoriasiform immunopathology. Data show human NP1 and NP2 neurons basally expressed an array of pattern recognition and cytokine receptor genes and psoriatic human skin had a profound dysregulation of neuropeptides and their receptors. In mice, imiquimod (IMQ) application reduced the density of MrgprD+ skin afferents, whereas NP1 neuron ablation exacerbated IMQ-induced disease. Strikingly, NP1 activation using either optogenetics or β-alanine before IMQ exposure significantly reduced epidermal thickness, psoriatic clinical score and γδT17 cell accumulation. In stark contrast, NP2 activation increased the numbers of γδT17 cells that co-expressed amphiregulin (Areg) and exacerbated IMQ-driven skin pathology. Instead, pre-emptive NP1 stimulation shifted γδ T cell profiles away from being IL-17 and Areg dominant to IL-13+ γδ T cells expressing the transcription factor GATA3 accompanied by IL-10 secretion. Importantly, IL-10 signaling blockade reversed NP1-mediated suppression of IMQ-induced dermatitis. These data show that inflammatory skin disease can be distinctly modulated by sensory neuron subsets. - Source: PubMed
Publication date: 2026/07/09
Inclan-Rico Juan MNapuri Camila MStephenson AdrianaRossi Heather LFemoe Ulrich MMusaigwa FungaiHung Li-YinYu HuashengLuo WenqinHerbert De'Broski R - Progression from differentiated thyroid cancer to anaplastic thyroid cancer (ATC) involves profound epithelial plasticity and remodeling of the tumor microenvironment (TME), but how BRAF and RAS driver mutations shape these processes remains unclear. Here, we integrated single-nucleus RNA-seq, spatial transcriptomics, and bulk RNA-seq across BRAF- and RAS-driven thyroid tumors to delineate mutation-specific progression trajectories. BRAF-driven tumors exhibited a gradual dedifferentiation trajectory with immune pathway activation, whereas RAS-driven tumors displayed abrupt transitions characterized by aneuploidy, epithelial-mesenchymal transition, hypoxia, and extracellular matrix remodeling. Cancer-associated fibroblasts (CAFs) emerged as key regulators, with mutation-specific ligand-receptor interactions: integrin-based signaling predominated in BRAF-mutant ATCs, while PLAU-PLAUR, TNFSF10-TNFRSF10B, and AREG-EGFR were additionally enriched in RAS-driven ATCs. These CAF-epithelial circuits were spatially validated and associated with poor prognosis. Together, our findings reveal mutation-dependent epithelial and TME dynamics associated with thyroid cancer dedifferentiation and highlight the potential importance of molecular-tailored approaches in the management of advanced thyroid cancer. - Source: PubMed
Publication date: 2026/07/16
Joo Eun HyeSong Young ShinLee Han SaiJung GyeongseoChung Eun-JaeKim Su-JinKim Yoo HyungCho Sun WookChoi HongyoonWon Jae-KyungPark Woong-YangPark Young Joo - Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) that results from oligodendrocyte loss and multifocal demyelination of the CNS white matter. Current therapies can suppress the progression of CNS inflammation but do not actively promote tissue repair. Nanoparticles (NPs) coated with CNS-specific peptide-major histocompatibility complex class II (pMHCII) molecules can alleviate disability in mice with experimental autoimmune encephalomyelitis (EAE) by triggering the formation, expansion, and recruitment of antigen-specific type 1 regulatory CD4 T cells (Tr1 cells). By investigating the effects of pMHCII-NP therapy on focal demyelinated lesions in the spinal cord induced by lysolecithin and sustained by chronic autoimmune encephalitogenic insults, here, we show that CNS antigen-specific Tr1 cells promote oligodendrogenesis, the preservation of axon caliber, and remyelination. Cell-specific deletion of () in T cells or of the () in oligodendrocytes abrogated these therapeutic outcomes. Oligodendrocyte-specific deletion of did not impair the pharmacodynamic or anti-inflammatory effects of pMHCII-NP treatment. These findings indicate that the oligodendrocyte-mediated therapeutic effects of pMHCII-NP treatment are dissociated from the anti-inflammatory properties of Tr1 cells; instead, they involve Tr1 cell-derived Areg to activate oligodendrocytes in an EGFR-dependent manner. Together, these results indicate that antigen-specific regulatory T cells can promote oligodendrogenesis and highlight the amphiregulin-oligodendrocyte EGFR pathway as a target for therapeutic intervention in MS. - Source: PubMed
Publication date: 2026/07/15
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