Anti_Human, mab ErbB4 Source Mouse
- Known as:
- Anti_Human, mab ErbB4 Source Mouse
- Catalog number:
- 101-M396
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab ErbB4 Source Mouse
Related genes to: Anti_Human, mab ErbB4 Source Mouse
- 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: Anti_Human, mab ErbB4 Source Mouse
Related articles to: Anti_Human, mab ErbB4 Source Mouse
- 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 - Obsessive compulsive disorder (OCD) is significantly heritable, but only a fraction of the contributory genetic variation has been identified, and the molecular etiology involved remains obscure. Identifying rare contributory variants of large effect would be an important milestone in helping to elucidate the mechanisms involved. Analysis of densely affected pedigrees is a potentially useful strategy to bypass the sample size challenges of standard case-control approaches. Here we performed whole genome sequencing (WGS) of 25 individuals across two multiplex OCD pedigrees. We prioritised rare variants using a Bayesian inference approach which incorporates variant pathogenicity and co-segregation with OCD. In the first pedigree, we identified a highly deleterious missense variant in , carried by the majority of affected individuals. This gene is brain-expressed and has previously been implicated in panic disorder and internet addiction GWAS studies. In the second pedigree, we identified a large deletion of and a missense variant in , that perfectly co-segregated in a specific branch of the family: both genes have previously been implicated in OCD and autism. Both genes contribute to a protein interaction network including and which we had previously identified in a large Tourette Syndrome pedigree. Our analysis suggests that both energy homeostasis and downstream signalling from the post-synaptic density may both be important avenues for future research. - Source: PubMed
Publication date: 2026/04/22
Ormond CathalCap MathieuChang Yi-ChiehRyan NiamhChavira DeniseWilliams KyleGrant Jon EMathews CarolHeron Elizabeth ACorvin Aiden - A novel series of palladium(ii) coordination complexes of the formula [Pd(CHC(NAr)CHC(O)CH)] (4a-j) were synthesized by the reaction of enaminone ligands (3a-j) with [PdCl(NCCH)] in a molar ratio of 2 : 1 in the presence of BuOK. The square planar coordination geometry around Pd(ii) of the 4c complex, with electrostatic potential calculations rationalizing the formation of C-H⋯π contacts, leading to chain structures, was confirmed by single-crystal X-ray diffraction. UV-vis spectra, supported by TD-DFT (B3LYP) calculations, indicated that the long-wavelength absorptions arose from intra-ligand charge transfer transitions (π → π*) involving HOMO-LUMO+1 excitations, with Pd(ii) orbitals contributing to the HOMO. Thermogravimetric analysis demonstrated high thermal stability of the series. Biological evaluation revealed notable cytotoxicities of the compounds 4b, 4d, 4h, 4i, and 4j. The compound 4i shows the strongest activity (IC = 5.42 µM, MCF-7; 17.20 µM, and HCT-116) and high selectivity toward cancer cells. Molecular docking against oncogenic targets (PIK3CA-E545K, ERBB4-Y1242C, KRAS-G13D, PIK3CA-H1047R, and ATM-A112V) identified - and -substituted analogues (4b, 4c, and 4h) as the most favorable binders, while bulky substituents reduced the affinity due to steric effects. Docking against PIK3CA-E545K produced binding energies that qualitatively paralleled several of the measured MCF-7 selectivity indices, with planar aromatic interactions and hydrophobic contacts defining the structure-activity relationships. - Source: PubMed
Publication date: 2026/04/29
Taher DeebKhalil BelalAlNaimat SaraMustafa MoradIshtaiwi ZakariyyaHelal WissamKorb MarcusThiab Tuqa AbuImraish AmerAlhindi TareqMakahleh AhmadAmer Mohammad WAbdelrahman Duha H