IGHG3 Antibody (OASA09213)
- Known as:
- IGHG3 Antibody (OASA09213)
- Catalog number:
- oasa09213
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- IGHG3 Antibody (OASA09213)
Related genes to: IGHG3 Antibody (OASA09213)
- Gene:
- IGHG3 NIH gene
- Name:
- immunoglobulin heavy constant gamma 3 (G3m marker)
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q32.33
- Locus Type:
- immunoglobulin gene
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: IGHG3 Antibody (OASA09213)
Related articles to: IGHG3 Antibody (OASA09213)
- Class-switch recombination (CSR) allows B cells to produce antibodies with distinct effector functions, but its dynamics during a primary human response remain poorly understood. We sampled COVID-19-naive healthy volunteers every other day during the first 3 weeks after SARS-CoV-2 vaccination, combining bulk and single-cell B cell receptor repertoires, single-cell transcriptomics, immunophenotyping, and IGHC sterile transcript analysis. Vaccine-specific B cells show sterile transcription across all IGHC genes up to IGHG2, contradicting the prevailing idea of single-gene sterile transcription. Clonal tracking confirms that sequential CSR exists: e.g., IGHG3 to IGHG1 and IGHG1 to IGHA1 and IGHG2, with sparse switching beyond IGHG2. VDJ gene usage associates with specific isotype subclasses and differential CSR timing. CSR and somatic hypermutation are temporally decoupled, with antigen-specific clones remaining hypomutated up to 10 weeks post-immunization. These findings complement textbook models of CSR and inform strategies for vaccines requiring switching to key isotypes such as IgG1 or IgA2. - Source: PubMed
Publication date: 2026/06/04
Montamat-Garcia GuillemNg Joseph C FStewart Alexander TSinclair EmmaMensah Benedicta BGiam Yan HuiBlair PaulKateregga DianaGander AmirKipling DavidGuo DongjunServius LuteciaPiper Christopher J MBaig ZaraFraternali FrancaMauri ClaudiaDunn-Walters Deborah K - Breast cancer transcriptional programs span malignant epithelial cells, and the tumor microenvironment (TME), yet tumor-normal contrasts are often confounded by lineage identity and cell-type composition, limiting clinically actionable signatures. - Source: PubMed
Publication date: 2026/06/02
Le BaoNguyen Doan Phuong QuyBinh Doan Huu NhatVo Bao LongAnh Le DucKhoa Ta Hoang Dang - Activation of oncogenes by hijacking immunoglobulin gene loci (IG) enhancers via chromosomal translocation is a common pathogenetic mechanism in B-cell malignancies, affecting 5-10% of chronic lymphocytic leukemia (CLL). The oncogenic partners in many of these cases remain unidentified. Therefore, we conducted a comprehensive analysis of 144 CLL samples with IGH-translocation excluding IGH::BCL2, IGH::CCND1, IGH::BCL3 and IGH::MYC. By combining fluorescence in situ hybridization (FISH) with whole-genome, targeted sequencing, and RNA expression profiling, we identified 25 IG-translocation partners; 12 were previously unreported. Of 142 cases, 107 (75%) displayed an unmutated IGHV. Genetic profiling showed a heterogenous distribution of chromosomal aberrations and recurrently mutated genes across the groups. Of 41 informative cases, 32 (78%) exhibited breakpoints driven by aberrant class-switch recombination (CSR), with prominent involvement of IGHM (9/41) and IGHG3 (9/41). Three cases with unmutated IGHV carried a juxtaposition of the IGH locus 5' to the intact NKX2.6 gene in chromosome 8p21.2 due to illegitimate VDJ recombination, associated with significant ectopic upregulation of NKX2.6 transcriptional expression (FDR < 0.001, logFC: 15). Similarly, METRNL, located at the telomere of chromosome 17q25, was identified as a translocation partner gene in four cases. Our findings expand the spectrum of the oncogenic translocation partners targeting IGH in CLL. - Source: PubMed
Publication date: 2026/04/23
Drewes CosimaLópez CristinaOkeke NnamdiJebaraj BillyWiegreffe ChristophKraus IsabelleHillebrecht SinaAwada AmaniBens SusanneChteinberg EmilEichhorst BarbaraDatismann SarahDyer Martin J SFischer AnjaFischer KirstenGlaser SelinaHallek MichaelKretzmer HeleneMottok AnjaPfaff DominickSchnitzler KarolineMeier-Kolthoff Jan PSchlesner MatthiasSchneider ChristofBritsch StefanAmmerpohl OleStilgenbauer StephanTausch EugenSiebert Reiner - Circulating proteomics acts as an intermediate phenotype linking genetic susceptibility to MASLD. However, current evidence rarely establishes a direct concordance between serum protein levels and hepatic gene expression. We aimed to perform a multi-cohort joint analysis of serum proteomics and transcriptomics to characterize essential molecular features for MASLD. - Source: PubMed
Publication date: 2026/04/17
Xu JinjianGou WanglongWang XinyueRu DongmeiHu WeiChen JietengLi Bang-YanXi YueZheng Ju-ShengChen Yu-Ming - This study analyzed B-cell heterogeneity in lacrimal gland tissues from 4 patients with IgG4-related ophthalmic disease (IgG4-ROD) and 2 patients with IgG4-positive MALT lymphoma using single-cell transcriptome sequencing (scRNA-seq). The results revealed that while the B-cell differentiation trajectories have similarities between the two diseases, critical differences were evident. IgG4-ROD was predominantly composed of naïve B cells, with memory B cells mainly being the central memory type. These cells were enriched in hormone/innate immunity pathways, and the plasma cells exhibited features of functional exhaustion. Conversely, MALT lymphoma was dominated by memory B cells, particularly enriched in terminally differentiated subtypes, with aberrant activation of oncogenic pathways (BCR/NF-κB). In MALT lymphoma, naïve B cells showed upregulated expression of immunoglobulin genes (IGHG3/IGHG4) and abnormal activation of EBV/BCR/T-cell differentiation pathways, despite having suppressed basal metabolism. Germinal center-like B cells in MALT lymphoma revealed upregulated gene expression enriched in T-cell activation and PD-1/PD-L1 pathways. Plasma cells in MALT lymphoma displayed monoclonal expansion (high expression of IGHG2/IGHG3/IGHG4) and enhanced antibody secretion. Therefore, MALT lymphoma is characterized by abnormal activation and malignant transformation of B cells, whereas IgG4-ROD manifests as functional exhaustion and metabolic suppression. The differentiation state of memory B cells may represent a critical juncture for malignant transformation. - Source: PubMed
Publication date: 2026/03/19
Liu RuiRen TingtingXu LiangyuanWang NanZhang YufeiYan HaihanWang TaiyaoYang RunziMa JianminLi Jing