HLA-DQA2 Blocking Peptide
- Known as:
- Human leukocyte antigen-DQA2 Blocking Peptide
- Catalog number:
- 33r-5275
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HLA-DQA2 Blocking Peptide
Related products to: HLA-DQA2 Blocking Peptide
Related articles to: HLA-DQA2 Blocking Peptide
- Neoadjuvant chemoradiotherapy (nCRT) is the main treatment for Locally Advanced Rectal Cancer (LARC). The response to nCRT varies from a complete response to no response. The impact of the B cells in this process is poorly understood. This study aimed to characterize the B cells types associated with response or resistance to nCRT. We applied the "Scissor" algorithm to integrate single-cell RNA-seq data with bulk transcriptome data from colorectal cancer samples, thereby identifying B cell subpopulations associated with nCRT response and exploring the clinical significance of B cell-related characteristic genes in nCRT for rectal cancer. At the single-cell level, we identified a B cell subpopulation characterized by the expression of HLA-DRB5, HLA-DQA2, HLA-DQB1, CD74, and ACTG1, which was associated with nCRT response in rectal cancer. Using subpopulation-specific trait genes, rectal cancer patients were classified into three distinct subtypes with unique features. Subtype A shows higher PD-L1 expression suggesting that patients in this subgroup are more likely to achieve favorable responses to immunotherapy. Subtype C shows lower hypoxia scores and a higher proportion of patients deriving clinical benefit from nCRT, suggesting that this subgroup may be more sensitive to neoadjuvant treatment. We developed a machine learning-based predictive model for pathological complete response (pCR) to nCRT in rectal cancer, achieving an area under the curve (AUC) of 0.911 in the training set and 0.819 in the 64-sample validation cohort. This study reveals that a B cell subpopulation characterized by the co-expression of HLA-DRB5, HLA-DQA2, HLA-DQB1, CD74, and ACTG1 is significantly associated with nCRT response in rectal cancer. These findings offer actionable insights for optimizing clinical treatment strategies, including patient stratification and personalized therapy selection. - Source: PubMed
Publication date: 2026/01/02
Xia HuangLin YuLi ZeyuanZeng LijingYao QiweiXu BenhuaZheng Rong - Immune dysfunction and systemic inflammation are hallmarks of decompensated liver cirrhosis (DLC), associated with an increased risk of developing sepsis. Rapid immune degradation is poorly understood in DLC patients; therefore we performed single-cell RNA (scRNA) transcriptomics in DLC patients. Twenty-one DLC patients (all males, 42 ± 7 year) with sepsis ( = 10) and without sepsis (w/o, = 11) and ten healthy controls PBMCs, were analysed for scRNA transcriptomics using the BD Rhapsody. Cell clustering and cell types were determined using gene expression data and validation of specific genes was done by qRT-PCR. Retrospectively analyzed proteomics data from same patients was used for RNA-Protein interactions. Ten clusters and 7 cell types were detected, with high heterogeneity in the monocyte cluster in DLC patients. All DLC patients irrespective of sepsis showed down regulation of O6-methylguanine-DNA methyltransferase (MGMT) mediated DNA damage reversal, mitochondrial transcription termination, and melanin biosynthesis, with upregulated lactose synthesis, hydroxycarboxylic acid, FGFR1b and FGFR1c receptors. DLC-sepsis showed down regulation of NF-kβ, TNF-α, and IL-17 signaling in classical monocytes compared to w/o sepsis. Serotonin and DNA repair genes were significantly increased in DLC sepsis ( < 0.05). In addition to HLA-DR, HLA-A, HLA-B, and HLA-DQA1 were also decreased but HLA-DRB1, HLA-C, HLAE, HLA-DRA, and HLA-DQA2 were raised in sepsis. RNA-protein interaction revealed the down regulation of PROS1, CDC42, CD62L, FCGR3B, CX3CR1, Rpl31 genes in sepsis. Chances of sepsis increased in DLC patients due to monocytic defects in genes and signaling pathways. These markers further can be explored for diagnostic purposes and early detection of sepsis. - Source: PubMed
Publication date: 2025/12/30
Sehgal RashiGautam PramodIslam MojahidulKumar Sevak JayeshJaved MaryamKaur NavkiranRamakrishna GayatriMaiwall RakhiSarin Shiv KumarTrehanpati Nirupama - Moyamoya disease (MMD) is a rare, progressive cerebrovascular disorder characterized by internal carotid artery stenosis and compensatory vascular network formation. While its pathogenesis remains unclear, multi-omics approaches provide crucial molecular insights. Genomic studies identify significant associations with the RNF213 p.R4810K variant and other susceptibility loci like HLA-DQA2 and GUCY1A3. Transcriptomics reveals dysregulation in extracellular matrix organization and mitochondrial oxidative phosphorylation, with specific markers such as AQP4 and non-coding RNAs (e.g., miR-107). Proteomic analyses highlight alterations in proteins including VEGF, apolipoproteins (APOC1, APOD), and ferroptosis-related pathways. Metabolomics identifies diagnostic amino acid markers (L-lysine, L-glutamate) and altered lysophosphatidylcholine (LPC 16:1) levels. Epigenomics implicates DNA methylation changes in genes like SOX6 and KCNMA1. Integrated multi-omics facilitates the development of multifaceted treatments, including revascularization surgery, targeted molecular therapies, and personalized interventions based on individual omics profiles, advancing precision medicine for MMD. This article outlines the omics techniques' application progress in MMD, discussing their pros and cons in disease analysis, prevention, and treatment, aiming to guide future research and inform clinical decisions. - Source: PubMed
Publication date: 2025/12/07
Guo QingbaoLi Na - Recently, the role of peripheral blood mononuclear cells (PBMCs) in neurodegenerative activities has garnered significant attention, yet the role in Alzheimer's disease (AD) remains unclear. Based on our previous single-cell RNA sequencing data sets of PBMCs from healthy controls and AD patients, we identified differentially expressed genes (DEGs) between healthy individuals and AD patients. These DEGs are involved in pathways related to apoptosis regulation, cognition, synaptic organization, and other AD pathology-associated biological processes using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. JUN, CHCHD10, HSPA8, RETN, S100A8, ITGA2B, HBG2, PPBP, and HLA-DQA2 have high correlation with these pathways. To further investigate the role of PBMCs in AD, PBMCs from 9- or 6-month-old wild-type mice were, respectively, injected into 9- or 6-month-old AD mice; we found that PBMCs could reduce Aβ plaques and phosphor-tau deposition and improve cognitive function in AD mice without side effects. Additionally, intersection analysis with AD pathogenic genes, quantitative real-time polymerase chain reaction validation, and receiver operating characteristic curves demonstrated increased JUN expression in PBMCs of AD patients with higher specificity in the diagnosis of AD, with no significant sex- and age-dependent differences observed in its expression. This study provides a critical theoretical foundation for the clinical application of PBMCs and identifies JUN as a key regulatory gene within PBMCs. - Source: PubMed
Xue Lu-LuYang Ya-QiDu Ruo-LanGan Zong-JinZhao Yang-YangWang Wen-JingBi NingWang Qiu-LinWang Ting-HuaXiong Liu-Lin - BK polyomavirus-associated nephropathy (BKVAN) is a major cause of graft dysfunction in kidney transplant recipients, and is often triggered by BK virus reactivation due to immunosuppression. This study used GeoMx digital spatial profiling (DSP) to investigate molecular changes during BK virus infection. - Source: PubMed
Publication date: 2025/07/28
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