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
- 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 - In mammals, the postnatal increase in cardiac workload coincides with the loss of cardiomyocyte proliferative capacity, rendering adult cardiomyocytes permanently post-mitotic. Whether reducing load can restore regenerative potential in the adult heart remains unknown. Here we use a heterotopic heart transplantation model, in which the donor heart is vascularized but nonpumping, to show that mechanical unloading induces adult cardiomyocyte proliferation, revealed by Ki67-based and MADM (mosaic analysis with double markers) lineage tracing. Applying heterotopic transplantation to infarcted hearts to achieve mechanical unloading similarly promoted regeneration within peri-infarct regions. Single-nucleus RNA sequencing of unloaded hearts identified enhanced epicardial-cardiomyocyte communication via the NRG1-ERBB4-STAT3 axis. Epicardial Nrg1 deletion blocked STAT3 activation and cardiomyocyte proliferation. CUT&Tag revealed STAT3 directly upregulates H6pd in cardiomyocytes, boosting pentose phosphate pathway activity to supply nucleotides and reducing equivalents for proliferation. These findings delineate a mechanotransductive pathway linking epicardial signals to cardiomyocyte cell-cycle re-entry, providing a framework for leveraging unloading to promote cardiac regeneration. - Source: PubMed
Publication date: 2026/08/05
Jiang ChenyuLiu TianyuDai ZihaoXiang LiZhu YifanZhou XingliangHuang XuShen YiLiu JianJi YuxiCheng LinYu FangYan YiFeng BeiPan TuoChen JinhaiNie YuZhang HaoLiu Yiwei - Age-related cataracts (ARC), a disease associated with aging, is the leading cause of blindness worldwide. To better understand the heterogeneous pathogenesis of ARC and identify potential therapeutic targets, we generate a comprehensive atlas of age-related cataracts at a single-cell resolution, encompassing three disease states-mild cataract group (Mild), severe cortical cataract group (Severe_C), and severe nuclear cataract group (Severe_N)-with a total of 230 838 lens epithelial cells (LECs) derived from the lens capsules of 554 patients. We find that ARC involves seven distinct lens capsule cell types, with notable differences in cellular composition and functional states across disease severities. Unexpectedly, we discover that neuronal axon-like structures ingrowth into the lens is associated with cataractogenesis and its progression. All three disease groups show significant enrichment of the neurotrophic SLIT-ROBO signaling pathway. Cluster 0 exhibits high expression of the neurotrophic factor NRG1, which forms a stable ligand-receptor axis with the ERBB3 receptor on sympathetic neurons. These findings not only reveal the heterogeneity of ARC at the levels of cellular composition and signaling pathways but also suggest that neuro-lens interactions may play a critical role in cataract development. This provides a new perspective for understanding the pathogenesis of age-related cataracts. - Source: PubMed
Publication date: 2026/08/05
Tang QiaomeiTong ZiyangFan ChunmeiChen SilongGuo JiaruiHu JianghuaYao KeYin ZiChen XiaoYu Yibo