Ask about this productRelated genes to: NRG1 antibody
- Gene:
- NRG1 NIH gene
- Name:
- neuregulin 1
- Previous symbol:
- HGL, NRG1-IT2
- Synonyms:
- HRG, NDF, GGF
- Chromosome:
- 8p12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-19
- Date modifiied:
- 2015-01-28
Related products to: NRG1 antibody
Related articles to: NRG1 antibody
- The co-occurrence of plastic-derived particles and plastic-associated chemicals represents an emerging toxicological concern, yet their combined neurotoxicity remains insufficiently understood. Here, we evaluated whether repeated oral concurrent exposure to polyethylene nanoplastics (PE-NPs) and butyl benzyl phthalate (BBP) aggravates neurotoxic outcomes and characterized associated cell-type-resolved brain responses. In HT-22 neuronal cells, concentration-response matrix analysis revealed a positive interaction pattern between PE-NPs and BBP. A 90-day oral exposure model was then established in mice using pristine 50 nm PE-NPs, BBP, and their combination. Compared with single exposures, concurrent exposure caused more pronounced impairment in locomotor/exploratory behavior and spatial learning, accompanied by aggravated hippocampal neuronal and synaptic injury, neurotransmitter disturbance, enhanced glial reactivity, and reduced tight-junction-associated markers. Whole-brain single-nucleus RNA sequencing of control and co-exposure groups identified co-exposure-associated transcriptional alterations across neuronal, glial, and endothelial populations, involving synaptic organization, mitochondrial bioenergetics, glial/complement responses, and neurovascular barrier-related processes. Cell-cell communication analysis further suggested contraction of neuronal adhesion/trophic and vascular-associated signaling networks under the co-exposure condition. Targeted qRT-PCR validation using all four exposure groups supported representative snRNA-seq-derived candidates, including decreased Rbfox3, Rims1, Erbb4, Nrg1, Ptprm, and Cldn5 and increased Apoe and C1qa, with significant PE-NP × BBP interactions detected for Apoe, C1qa, and Cldn5. Overall, these findings show that concurrent PE-NP and BBP exposure aggravated neurotoxic outcomes and highlight the need to consider mixed plastic-derived contaminants in neurotoxicity assessment. - Source: PubMed
Publication date: 2026/08/12
Lu YitongRen HoudaoLv ZhongtingZhang TiehuaZhang JieRen Li - HER-positive cancers comprise a heterogeneous group of malignancies driven by dysregulated activation of the human epidermal growth factor receptor (HER/ERBB) family. While chimeric antigen receptor (CAR) T-cell therapies targeting HER2 have demonstrated potent anti-tumor capabilities, their clinical translation remains hampered by safety hurdles and antigen escape. We developed a modular "Targeted Chimeric Artificial Reporter" (TcAR) system using the natural epidermal growth factor (EGF)-like binding domains of neuregulin-1 (NRG1) isoforms to decode complex HER dimerization profiles. Leveraging the superior targeting plasticity of the β-isoform, we engineered NRG1β-based CAR-T and CAR-natural killer (NK) cells. Our study demonstrates that NRG1β-directed therapy overcomes therapeutic antigen escape in HER2-depleted models and exerts potent anti-tumor activity within complex three-dimensional (3D) tissue microenvironments ex vivo, exhibiting a significantly safer, muted inflammatory profile compared to clinical standards. - Source: PubMed
Publication date: 2026/07/29
Novikov AlexNaumchik AlonBanerji RajashriGreenshpan YarivWaidha KamranBhattacharya BaisaliElkabets MosheRadinsky OlgaPorgador Angel - Biliary tract cancers (BTC), including cholangiocarcinoma, gallbladder cancer, and ampullary cancer, remain poor-prognosis tumours. Chemo-immunotherapy is now established as the first-line standard of care. In parallel, precision medicine is now well established in the form of targeted therapies. These have transformed outcomes for defined subgroups, particularly intrahepatic cholangiocarcinoma with FGFR2 fusions/rearrangements, where pemigatinib and futibatinib provide meaningful response rates and durable disease control. On top of this, next-generation FGFR inhibitors aim to address secondary resistance. IDH1-mutant cholangiocarcinoma benefits from ivosidenib, with multiple combination strategies currently under investigation. HER2-directed therapies, including zanidatamab and trastuzumab deruxtecan, have shown promising efficacy in HER2-amplified or strongly overexpressing BTC, with ongoing clinical trials in the first-line setting. Tumour-agnostic targets (BRAF V600E, MSI-H/dMMR, RET/NTRK/NRG1 fusions) and other emerging therapies are further broadening therapeutic opportunities. However, key barriers to implementation include heterogeneous biomarker testing, limited tissue availability, the need for DNA/RNA hybrid-capture sequencing, and evolving resistance biology, underscoring the importance of optimised diagnostics and innovative trial designs to realise personalised care in BTC. This review provides detailed insights on these therapies, and most importantly a view to what the future may hold. - Source: PubMed
Publication date: 2026/06/08
Lamarca AngelaHarding James JOh Do Youn - How fungal pathogens coordinate genotoxic stress responses with membrane homeostasis to sustain cellular signaling remains poorly understood. In this study, we characterize Mrv6, a MARVEL domain-containing membrane protein that is prominently induced by genotoxic stress. Intriguingly, rather than functioning as a canonical DNA repair factor, Mrv6 acts as a critical biophysical adjuster governing membrane lipid homeostasis. Deletion of MRV6 triggers a global transcriptional activation of the ergosterol biosynthetic pathway, resulting in aberrant cellular ergosterol accumulation. We demonstrate that this lipid imbalance fundamentally alters plasma membrane homeostasis, resulting in a less permeable architecture. Paradoxically, while this structural alteration inadvertently shields the fungus from exogenous genotoxins, conferring unexpected resistance to methyl methanesulfonate, it simultaneously hinders the intracellular transduction of environmental morphogenetic signals under hypoxic conditions. Consequently, the major hyphal repressor NRG1 remains aberrantly expressed, leading to an attenuated signaling response that significantly impairs virulence. Crucially, targeted genetic suppression of either the lipid biosynthetic node (ERG1) or the downstream signaling node (NRG1) effectively mitigates this biophysical constraint, rescuing both morphogenetic switching and pathogenicity. Collectively, our findings define a novel biochemical paradigm wherein C. albicans utilizes a stress-responsive membrane protein to fine-tune ergosterol remodeling and membrane permeability, structurally coupling stress adaptation to signal transduction. - Source: PubMed
Publication date: 2026/08/07
Gao WenxiaZhou YiJiang SunaTang XingyiFeng Jinrong - Growth differentiation factor 15 (GDF-15), a stressful cytokine of the transforming growth factor-β (TGF-β) superfamily, plays pivotal roles in diverse physiological and pathological processes. Most recently, its pleiotropic effects regarding energy metabolism and nutritional modulation are of intense scrutiny. Its physiological functions involve signaling pathways such as GDF-15/glial cell-derived neurotrophic factor family receptor α-like protein (GFRAL)/rearranged during transfection (RET), phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (Akt)/mammalian target of rapamycin (mTOR), nuclear factor kappa B (NF-κB), and reactive oxygen species (ROS). The mechanism of action involves regulation of energy metabolism, inflammation, oxidative stress, and muscle-fat-bone metabolism, and it holds important prognostic value and potential therapeutic significance. Mounting evidence has suggested that GDF-15 levels are significantly increased in the context of cancer cachexia, metabolic syndrome (MetS), and amongst older patients, paralleling multiple indicators of nutrition. Notably, this association appears to be gender- and age-specific, therefore serving as a good biomarker alongside a therapeutic target to mitigate or even reverse disease-related nutritional deficiency and aggravation. However, the precise contribution of GDF-15 to evaluate nutritional status and its mechanistic basis across varying disorders is not fully elucidated. In light of these knowledge gaps, we sought to delve into basic research, clinical information and translational evidence, aiming to analyze the molecular regulatory network of GDF-15 and clarify its clinical implications as a novel diagnostic tool and assessment metric, and in turn provide a theoretical basis for early intervention and personalized treatment. Future research should focus on elucidating GDF-15's neuroanatomical basis and signaling pathways, validating gender-disparity mechanisms, establishing clinical diagnostic thresholds, optimizing targeted therapeutic strategies, and developing dynamic monitoring approaches, so as to bridge the gap from biomarker discovery to precision intervention. - Source: PubMed
Publication date: 2026/07/22
Peng BinbinZhao WeiKong MingChen YuSun Chao