Ask about this productRelated genes to: ERBB4 antibody
- Gene:
- ERBB4 NIH gene
- Name:
- erb-b2 receptor tyrosine kinase 4
- Previous symbol:
- -
- Synonyms:
- ALS19, HER4
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-07
- Date modifiied:
- 2016-10-05
Related products to: ERBB4 antibody
Related articles to: ERBB4 antibody
- Epilepsy is a complex central nervous system disease with a high incidence and a significant social health burden. Although there are many antiepileptic drugs, about 30% of patients are insensitive to existing drug treatments, and it is urgently required to identify reliable molecular markers and therapeutic targets. Traditional research has focused on a single omics level, and it is difficult to establish a complete connection from genetic variation to changes in cell function. In this study, a multi-level analysis framework integrating transcriptome, proteome, Mendelian randomization, and single-cell omics was constructed, and the E3 ubiquitin ligase RNF149 was systematically screened and multi-dimensionally verified as a key candidate molecular marker for epilepsy. In external datasets (GSE88992, GSE127871, GSE255223) and animal models, RNF149 showed a stable trend of differential expression and was associated with hippocampal sclerosis and the severity of epileptic seizures. Single-cell communication investigation revealed that RNF149 may influence the pathological process of epilepsy by modulating the interaction between excitatory neurons and oligodendrocytes, particularly the NRG3-ERBB4 signaling axis. In conclusion, multi-omics integrated analysis highlighted RNF149's potential relevance as a molecular biomarker and treatment target for epilepsy, generating new ideas for precision diagnosis and mechanism research in temporal lobe epilepsy. - Source: PubMed
Publication date: 2026/05/09
Wei BiQian XuehongMao RunningYu KaiWang YusenChen HongbingXiong HongliLi Jianbo - Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. - Source: PubMed
Publication date: 2026/05/11
Keating TreasaStranahan LaurenWiener DominiqueKeating M KellyLeon RenatoBanovic Frane - Gliosarcoma of the central nervous system (CNS) is a rare and aggressive neoplasm exhibiting biphasic differentiation into glial and mesenchymal components. We report a primary gliosarcoma with mesenchymal differentiation resembling follicular dendritic cell sarcoma (FDCS). A 72-year-old man presented with a rim-enhancing lesion in the left frontotemporal parenchyma. Histologically, the tumor was biphasic, comprising a glioblastoma (GBM) component of diffusely infiltrative GFAP- and Olig2-positive oligodendroglial-like cells with microvascular proliferation, and an FDCS component composed of cohesive sheets, nests, and fascicles of CD21-, CD23-, and CD35-positive plump spindle cells. NGS analysis performed on the microdissected components revealed shared PTEN p.N48S mutations with high variant allele frequencies and MGMT promoter methylation, suggesting a monoclonal origin. Furthermore, the two components exhibited divergent genetic profiles: the glial component was characterized by an FGFR1 mutation, PDGFRA fusion, KIT/KDR amplification, and a whole-arm 1p/19q codeletion, whereas the sarcomatous component harbored an ERBB4 p.S853F mutation. These alterations predominantly converged on the RAS-MAPK and PI3K-AKT-mTOR signaling pathways. No IDH1/2 mutations, EGFR gene amplification, or TERT promoter mutations were detected in either component. This case represents the first documented instance of primary gliosarcoma with FDCS differentiation, thereby expanding its known differentiation spectrum. Furthermore, it demonstrates the necessity of separately analyzing each histological component in the diagnosis of challenging cases. - Source: PubMed
Zhou JingZhao ShaLi HaiYang ShudongPan Minhong - The neuregulin-1 (NRG1)/ERBB signaling system is essential for cardiac embryonic development and function. Its activation during heart failure (HF) exerts compensatory effects by acting on cardiomyocytes and mitigating ventricular fibrosis. - Source: PubMed
Publication date: 2026/05/05
van Fraeyenhove JensTubeeckx Michiel R LGoovaerts BoFu YileZhang JuanDekker Sven OBezerra ArthurDe Coster TimCools JulieWülfers Eike MVan den Bogaert SielBruyns TineThienpont BernardMurphy Samuel Lde Vries Antoine A FFransen ErikVandersickel NelePijnappels Daniël ADe Meyer Guido R YHeidbuchel HeinRoderick H LlewelynSegers Vincent F MDe Keulenaer Gilles W - The mammalian pineal gland maintains normal circadian rhythms and homeostasis by secreting melatonin. However, the lack of a single-cell-resolved regulatory map limits our understanding of how these neuroendocrine functions are orchestrated. Here, we constructed a multiomics atlas of the pineal gland from by integrating snRNA-seq, snATAC-seq, and spatial transcriptomics. We identified pinealocytes as the predominant cell type, alongside six glial and vascular lineages. Chromatin accessibility analysis delineated cell-type-specific regions enriched for melatonin synthesis and phototransduction genes. Notably, we resolved a dual-layer regulatory architecture: While melatonin synthesis programs are robustly organized, circadian clock regulators exhibit a distinct, sparse spatial pattern. Coexpression networks further identified core modules and regulatory hubs-including CRX/OTX2, LHX4, and RORA-that integrate these circadian and light-responsive signals. Cell-cell communication analysis identified signaling axes, such as -/, -, and -, that potentially coordinate this spatial functional organization. Integrating genetic traits showed that sleep and neuropsychiatric risk variants preferentially map to these pineal regulatory modules. Specifically, sleep-associated loci converged on -linked elements, while bipolar disorder-associated loci highlighted candidate genes of and . Overall, this study reveals the cellular diversity and spatial regulatory logic of the primate pineal gland, providing a physiological foundation for investigating circadian and neuroendocrine regulation in healthy and disease models. - Source: PubMed
Publication date: 2026/05/05
Zheng JihongXiao YuchenLyu JianjunXu HongtaoZhang YaqunLi YanchuanLi YihaoWang TianjunLiu LiuJin LingjingZhou XuhuiZhang Chao