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-
- [This corrects the article DOI: 10.3389/fcell.2026.1914540.]. - Source: PubMed
Publication date: 2026/09/17
Li FengXu XingHu Yi-QiuZhang Cheng-PengShen Yi-WeiGeng ChiChu Jia-PengBai Hui-YuGu Xiao-SongLi Hui - Chronic stress activates the hypothalamic-pituitary-adrenal (HPA) axis and induces systemic physiological changes. This study aimed to identify stress-associated serum biomarker candidates in chronically stressed beagle dogs and to evaluate the anti-stress effects of var. (Maxim.) Kitam. extract (CZE). Beagle dogs were subjected to movement restriction-induced chronic stress for 42 days, with or without repeated oral administration of CZE. Serum cortisol and corticosterone concentrations were measured using ELISA, and hematological and serum biochemical parameters were analyzed. Serum samples collected at day 0 and day 42 of the 84-day chronic stress model were subjected to LC-MS/MS-based proteomic analysis. Chronic stress increased serum cortisol and corticosterone concentrations and induced alterations in hematological and serum biochemical parameters, whereas CZE administration tended to attenuate or stabilize these stress-associated changes. Proteomic analysis identified 380 serum proteins, of which 348 quantified proteins were subjected to differential expression analysis. The differentially expressed proteins were primarily associated with immune response, inflammatory response, extracellular matrix organization, angiogenesis, neurogenesis, and secretion. TIMP1, TREM2, RAB8A, KRT9, PPBP, THBS1, and HSPB1 were identified as candidate stress-associated serum biomarkers. These findings indicate that chronic stress induces endocrine, hematological, biochemical, and serum proteomic alterations in beagle dogs. Changes in proteins related to immune-inflammatory regulation and extracellular matrix organization suggest that prolonged stress may affect systemic immune responses and tissue remodeling. CZE may contribute to the maintenance of physiological homeostasis under chronic stress conditions and may have potential as a functional anti-stress material, while the identified serum proteins may provide a basis for the development of biomarkers for chronic stress. - Source: PubMed
Publication date: 2026/08/26
Yang Ye JinKim Min JungKim Hee HoHeo Ji WoongChun Ju LanShin Eui-CheolKim Kyeong SooKim Hyun-WookJeong Eun JuLee DongbinPark Kwang Il - Obstructive sleep apnea (OSA) is an independently modifiable risk factor for atrial fibrillation (AF). However, the molecular mechanism of OSA-related AF is elusive. This study aims to identify the key genes and pathophysiological changes underlying OSA-related AF. - Source: PubMed
Publication date: 2026/08/20
Li FengXu XingHu Yi-QiuZhang Cheng-PengShen Yi-WeiGeng ChiChu Jia-PengBai Hui-YuGu Xiao-SongLi Hui - Tendon regeneration remains limited by the unmet challenge of precisely controlling the intensity and duration of local inflammation, often resulting in scarred healing. Here, we present a novel, micro-thin, nano-layered patch that employs Layer-by-Layer (LbL) self-assembly for the precisely controlled release of small molecules, Oxo-M and 4-PPBP, to address this technical challenge. This novel combination of small molecules exhibits distinct functions in modulating the polarization of macrophages and the tenogenic differentiation of tendon stem/progenitor cells (TSCs). The customized, temporal release of these small molecules effectively modulated the critical crosstalk between TSCs and macrophages, thereby promoting regenerative tendon healing. The nano-LbL tendon patch successfully mitigated early inflammation, promoted matrix synthesis, and regulated later tissue remodeling in vivo. Robust scRNA-seq and CellChat analysis delineated the temporal-orchestrated communication between cell types across healing phases, confirming the critical interplays between TSCs, tenocytes, and macrophages. We then validated the key signaling pathways regulating cell-cell communication modulating inflammation. Our nano-layered LbL nanopatch represents a highly translational approach for achieving scarless tendon regeneration. In addition, this study elucidated the essential signaling pathways regulating TSC-macrophage crosstalk, advancing our understanding of tendon biology and pathology. - Source: PubMed
Publication date: 2026/08/24
Sarker M DZong ChenHoang Lan Anh PJeong Hun JinKumar VivekZhu ElenPark RachelComito Samuel JLee Chang H - Diagnostic evaluation of suspected neuromyelitis optica spectrum disorder (NMOSD) integrates AQP4-IgG testing, clinical assessment, neuroimaging, and exclusion of alternative inflammatory demyelinating disorders; nevertheless, some patients remain diagnostically unresolved or may be misclassified as multiple sclerosis (MS) or other disorders. This single-center retrospective exploratory study analyzed quantitative serum proteomics from 20 patients with MS and 20 with NMOSD. Proteins meeting nominal < 0.05 together with prespecified fold-change criteria were considered exploratory candidates. VWF, PPBP, and SERPINA3 were subsequently assessed by ELISA in a separate, non-overlapping cohort from the same center, together with routine hematological variables. Among 261 protein entries, 34 met the exploratory nominal threshold and fold-change criteria, but none remained significant after Benjamini-Hochberg correction (lowest q = 0.0734). VWF and PPBP showed no significant differences across the four validation groups. SERPINA3 differed across groups (Kruskal-Wallis H = 44.982, = 9.34 × 10) and was higher in NMOSD than in MS, TBI, and HCs after Holm adjustment (adjusted = 0.036, 1.49 × 10, and 1.13 × 10, respectively). In the full ELISA cohort, the AUC was 0.928 for NMOSD versus HC and 0.800 for NMOSD versus MS. In a post hoc sensitivity analysis excluding participants with preceding infection, the NMOSD-MS separation was attenuated. In smaller complete-case analyses, adding an additional laboratory variable to SERPINA3 did not significantly improve apparent discrimination. SERPINA3 is therefore an exploratory adjunctive serum biomarker candidate rather than a stand-alone diagnostic test; prospective external validation in clinically representative cohorts is required. - Source: PubMed
Publication date: 2026/08/20
Xu TingHan BingqingZheng GuanghuiJiang WencanZhang HanyuZhang Guojun