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-
- Infected wounds represent a formidable clinical challenge, as persistent bacterial colonization and disrupted bio-signaling collectively hinder effective tissue repair. Conventional passive dressings lack the capacity to actively modulate this complex microenvironment. Here, we report a wireless, dual-responsive hydrogel (PVA/P(VDF-TrFE)/BiOClBr@PDA, PPBP) based on porous poly(vinyl alcohol) (PVA), piezoelectric poly(vinylidene fluoride-trifluoroethylene) (P(VDF-TrFE)), and polydopamine-modified bismuth oxybromide chloride (BiOClBr@PDA). The constructed hydrogel orchestrates piezoelectric stimulation and piezo-photocatalysis to simultaneously eradicate infection and accelerate tissue regeneration. Under concurrent ultrasonic and optical stimulation, this platform efficiently transduces mechanical and light energy into therapeutic electrical cues and reactive oxygen species (ROS). This dual-mode activation enables enhanced antibacterial efficacy against diverse bacterial strains, significantly outperforming single-mode treatments while maintaining favorable biocompatibility. In an infected wound model, the constructed composite hydrogel PPBP effectively inhibits bacteria and attenuates inflammatory responses via controlled ROS generation, while piezoelectric stimulation supports re-epithelialization and collagen deposition. Together, these effects promote accelerated and structurally improved wound healing. This work establishes a paradigm for utilizing multi-source energy-responsive hydrogels as an active strategy for regulating infected wound environments and supporting functional skin regeneration. - Source: PubMed
Publication date: 2026/08/17
Dai BaoyingQie WenxuanLi XiaoyeZheng JingbenHe AoDong HengYan JiangjiangZhang HaoPan ZihengYin HangZhou ChuyiKong RuiWang HaoDai BinghanXie YannanLin Zhiqun - 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-Cxcr2 and Thbs1-Cd47 checkpoint axes. Strikingly, AAV-mPf4 gene therapy was associated with a NEP-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