BAM01 Amyloid, Beta-
- Known as:
- BAM01 Amyloid, Beta-
- Catalog number:
- mc-733
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- BAM01 Amyloid Beta-
Related genes to: BAM01 Amyloid, Beta-
- Gene:
- BHLHE22 NIH gene
- Name:
- basic helix-loop-helix family member e22
- Previous symbol:
- TNRC20, BHLHB5
- Synonyms:
- CAGL85, Beta3, bHLHe22
- Chromosome:
- 8q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-27
- Date modifiied:
- 2016-10-05
- Gene:
- BHLHE23 NIH gene
- Name:
- basic helix-loop-helix family member e23
- Previous symbol:
- BHLHB4
- Synonyms:
- bA305P22.3, Beta4, bHLHe23
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2016-04-25
- Gene:
- KCNAB1 NIH gene
- Name:
- potassium voltage-gated channel subfamily A member regulatory beta subunit 1
- Previous symbol:
- -
- Synonyms:
- AKR6A3, KCNA1B, hKvBeta3, Kvb1.3, hKvb3
- Chromosome:
- 3q25.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-13
- Date modifiied:
- 2016-10-05
- Gene:
- MAPK11 NIH gene
- Name:
- mitogen-activated protein kinase 11
- Previous symbol:
- PRKM11
- Synonyms:
- p38-2, p38Beta, SAPK2
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2015-08-25
- Gene:
- PPBP NIH gene
- Name:
- pro-platelet basic protein
- Previous symbol:
- THBGB1
- Synonyms:
- SCYB7, TGB, NAP-2-L1, LA-PF4, MDGF, LDGF, Beta-TG, CTAP3, CXCL7, PBP, b-TG1, TGB1, CTAPIII, NAP-2
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-21
- Date modifiied:
- 2016-10-05
Related products to: BAM01 Amyloid, Beta-
Related articles to: BAM01 Amyloid, Beta-
- Calcification often occurs as a characteristic pathological manifestation in the progression of atherosclerosis (AS) plaques, but its mechanism is not fully understood yet. The purpose of this research was to supplement the exploration of key candidate genes and key cells involved in the calcification process of AS, building on existing insights into its underlying mechanisms. Through the examination of our internally generated single‑cell RNA sequencing (scRNA-seq) dataset derived from human carotid plaque samples, pivotal cellular populations associated with AS calcification were successfully identified. Following this identification, a comprehensive analytical approach was employed, incorporating differential gene expression profiling alongside the establishment of protein-protein interaction (PPI) networks, thereby enabling the extraction of critical genetic markers within these cellular subsets. Furthermore, a molecular regulatory framework was assembled, aiming to elucidate the mechanistic pathways through which these genetic determinants contribute to the calcification phenomena in AS pathology. Moreover, analysis of cell communication was applied to explore the interactions among cells. Pseudo-time analysis was employed to explore the expression of key candidate genes during the differentiation of key cells. Finally, monocytes were identified as key cells. WARS1, IFITM1, ANXA1, ADGRE2, and S100P were identified as key candidate genes. Moreover, 115 transcription factors such as THRB and 118 miRNAs such as hsa-miR-196a-5p were predicted to be associated with the key candidate genes. Across both calcified and non-calcified control specimens, the cellular communication between endothelial cells and natural killer (NK) T cell populations was consistently orchestrated via the PPBP-CXCR2 signaling axis. During monocytic differentiation trajectories, ADGRE2 expression exhibited a biphasic pattern characterized by initial gradual elevation followed by subsequent decline. Conversely, both ANXA1 and S100P demonstrated progressive upregulation throughout the differentiation process. The expression of IFITM1 and WARS1 first decreased, then increased, and finally decreased again. The present investigation successfully pinpointed five critical genes alongside one key cellular population, collectively providing potential molecular insights and candidate targets for further investigation into AS calcification. - Source: PubMed
Publication date: 2026/08/11
Yuan Huai WuWang WeiyeCheng WeiWang HongzheSong BoyanChen Tian XiangPeng Guo Ping - Platelets have been increasingly recognized as versatile regulators of ageing, immunity, and cancer, yet their functional heterogeneity has remained poorly defined. We performed the first large-scale single-cell RNA sequencing of 28,192 platelets from healthy, aged, metastatic, and treated mice using the BD Rhapsody platform. Our analysis revealed four conserved and functionally distinct platelet transcriptional states: haemostatic platelet (HP), neural gene-enriched platelet (NEP), platelet-leukocyte aggregate (PLA) and platelet-erythrocyte aggregate (PEA). Among these states, Tpm2-high HP is linked to ageing-associated lung metastasis and is characterized by cytoskeletal remodelling gene signatures. The PLA state was predicted to be a signalling hub for immunothrombosis, with a PLA-Bridge subpopulation coordinating immune-adherent platelets via the Ppbp-Cxcl2 and Thbs1-Cd47 checkpoint axes. Strikingly, AAV-mPf4 gene therapy was associated with a neural gene-enriched platelet-associated transcriptional program, which mitigates age-related functional decline. This study provides a single-cell transcriptomic atlas of murine platelets under ageing and metastasis conditions and reveals transcriptional state-specific heterogeneity. This study also proposes PF4-based interventions and cytoskeletal candidates for diagnosis and therapy. - Source: PubMed
Publication date: 2026/08/11
Li RunzeChen YuyiSong YuanyuanZhang AoLiang TuliangLian LirongMi JianingZhou NanjieWang JingrongBai YingnanPan HudanLiu QuanZhao YichengLiu Liang - Ovarian endometrioma (OEM) is a common manifestation of endometriosis and is associated with both local lesions and systemic alterations. While immune dysregulation and metabolic disturbances have been individually reported in endometriosis, whether these changes are coordinated at the circulating molecular level in OEM remains unclear. - Source: PubMed
Publication date: 2026/07/22
Chen NaHu YubingXiao TianxiaMa YunZhu LitongGao JiahongZhang Jian VJin Ping - Cyanidin-3-O-galactoside(C3G) has a variety of biological activities. Pulmonary fibrosis (PF) is a fatal interstitial lung disease. To define its pathogenic networks, we performed transcriptomic sequencing of lung tissues from five mouse groups: WT_Control, WT_Model, WT_Model_C3G, Control_Ccl3-/-, Model_Ccl3-/-. Comprehensive assessment of immune infiltration, weighted gene co-expression network, and functional enrichment verified that PF is tightly linked to immune microenvironment dysregulation. Seven machine learning algorithms identified five core immune-related targets: Ccl3, Xcl1, Pyy, Il31ra, Ppbp. Subsequent analysis prioritized Ccl3 and Ppbp as the key core pathogenic genes. Molecular docking clarified their binding modes and key interaction sites with C3G. Histopathological and biochemical assessments showed that the WT_Model group exhibited elevated expressions of Ccl3 and Ppbp, accompanied by marked inflammatory infiltration and collagen deposition. C3G intervention significantly ameliorated these PF phenotypes. Ccl3 knockout improved survival and ameliorated fibrotic pathology. Interaction modeling and correlation analyses identified Slc2a3 as a key Ccl3 downstream target. WB and IHC validation revealed reduced expression of Ccl3, Slc2a3, and α-SMA proteins in Model_Ccl3-/- compared to WT_Model, which suggested Ccl3 may positively regulate the expression of Slc2a3. Through transcriptome and external metabolome verification, it was found that Slc2a3 can regulate PF through metabolic pathways. In conclusion, this study confirmed the potential role of C3G in regulating Ccl3-related inflammation and metabolic pathways in bleomycin-induced PF, which is expected to become a new strategy for targeted therapy of PF and provide a theoretical basis for the development of clinical treatment. - Source: PubMed
Publication date: 2026/07/31
Tang XianZhao MengLi FeiBao XiaochaoWang DongxuHe YujingGao JunZhang GuokunWei Jie - This study aimed to identify candidate shared transcriptomic signals between major depressive disorder and dermatomyositis through an integrative bioinformatic reanalysis of public GEO datasets with single-cell contextualization. The analytical workflow included Weighted Gene Co-expression Network Analysis (WGCNA) for key module identification, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses for functional characterization, GeneMANIA- and a network visualization platform-based network analysis for candidate-gene prioritization, and evaluation of 113 machine-learning models combined with SHapley Additive exPlanations (SHAP) for diagnostic feature selection. Gene Set Enrichment Analysis (GSEA), immune infiltration analysis, and single-cell RNA-seq-based contextualization were subsequently performed to further characterize the immune-related cellular context of the identified signals. Integration of dermatomyositis-related GEO datasets identified 570 differentially expressed genes, from which 33 candidate shared genes were obtained via WGCNA. Functional enrichment and network analyses highlighted immune defense, cytotoxicity, and pathways including PPAR, IL-17, and antigen processing, with ELANE, PPBP, and CTSG emerging as highly connected nodes. Machine-learning-based feature prioritization retained 8 candidate model-selected genes, namely KIF4A, OLR1, KIR2DL4, KRT23, KIR3DS1, AZU1, SCG5, and LRRC37E. Immune infiltration analysis associated these shared genes with regulatory T cells (Tregs), resting mast cells, resting dendritic cells, and both classically activated (M1) and alternatively activated (M2) macrophages. Single-cell RNA-seq contextualization further suggested that CD8⁺ T-cell subsets with different candidate-gene score states showed distinct intercellular communication patterns. Among these, the MIF-(CD74+CD44) axis and signals from naive/central memory T cells were notable features requiring further validation. Overall, this study identified candidate shared transcriptomic signals between major depressive disorder and dermatomyositis and highlighted immune-related cellular contexts that warrant further validation in true comorbid cohorts. - Source: PubMed
Publication date: 2026/06/26
Teng FeiZheng SisiZhang XiatianLu ZhongwenWang PengruiWang PengYin Dongqing