Ask about this productRelated genes to: AZGP1 antibody
- Gene:
- AZGP1 NIH gene
- Name:
- alpha-2-glycoprotein 1, zinc-binding
- Previous symbol:
- -
- Synonyms:
- ZA2G, ZAG
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-12
- Date modifiied:
- 2014-11-19
Related products to: AZGP1 antibody
Related articles to: AZGP1 antibody
- Blood-Heat syndrome is a core syndrome of Traditional Chinese Medicine (TCM) in Henoch-Schönlein purpura nephritis (HSPN), yet its biological basis remains unclear. This study aimed to systematically elucidate the scientific basis of Blood-Heat syndrome within the context of HSPN and to identify its objective biomarkers using a multidimensional biological approach. - Source: PubMed
Publication date: 2026/04/10
Xu ShuangXu YanBi YuefengDing YingZhang XiaXi LeyingRen Xianqing - Macrophage homeostasis is disrupted in periodontitis, a condition often exacerbated by diabetes. AZGP1 is an inflammation-associated factor capable of modulating macrophage polarization. Hyperglycemia alters O-GlcNAcylation dynamics in pathological contexts. This study investigated the regulatory role of AZGP1 in macrophage polarization during diabetic periodontitis and explored whether O-GlcNAcylation mediated this effect. Raw264.7 cells were exposed to lipopolysaccharide (LPS) and high glucose (HG) to simulate the periodontitis and hyperglycemia microenvironment, respectively. Macrophage polarization was analyzed by quantifying M1 and M2 markers via qRT-PCR and immunofluorescence. O-GlcNAcylation of AZGP1 regulated by OGT was examined using immunoprecipitation, immunoblotting, and cycloheximide-chase assays. A hyperglycemic periodontitis mouse model was established, and bone-related parameters and macrophage polarization were assessed. Porphyromonas gingivalis LPS induced M1 polarization and suppressed M2 polarization in Raw264.7 cells, while HG further amplified LPS-driven polarization. Following LPS/HG treatment, AZGP1 expression increased; its knockdown inhibited M1 polarization and enhanced M2 polarization. OGT depletion reduced AZGP1 protein stability by blocking O-GlcNAcylation at the tryptophan (T205) residue. AZGP1 overexpression counteracted the M1/M2 polarization inhibition caused by OGT knockdown. In vivo, AZGP1 knockdown mitigated alveolar bone destruction in periodontitis mice with hyperglycemia by promoting M1 to M2 polarization. O-GlcNAcylation of AZGP1, mediated by OGT, enhances its stability, promoting M1 polarization and suppressing M2 polarization under hyperglycemic conditions, thereby exacerbating periodontitis progression under hyperglycemic conditions. These findings offer novel insights into the pathogenesis and therapeutic strategies for diabetic periodontitis. - Source: PubMed
Publication date: 2026/04/11
Zeng XiaofangXia HongMa Yulong - Prognostic biomarker panels identified through bulk sequencing approaches have shown utility in localized prostate cancer but are limited by underlying molecular heterogeneity. Spatial transcriptomics offers a complementary approach to investigate spatial gene expression patterns and the tissue- and cell-type-associated localization of their constituent biomarker genes. - Source: PubMed
Publication date: 2026/03/30
Taylor Kristofer GJohannessen BjarneMills Ian GRye Morten BAxcrona KarolSkotheim Rolf I - Transcriptional activity perturbation holds promise for selectively modulating harmful transcriptional networks, but its therapeutic potential remains largely unexplored. We employed a network-based analysis of single-cell heart transcriptomes to identify transcription factor activities linked to pathological cardiomyocytes in vivo. This analysis revealed that transcriptional activity of Krüppel-like factor 15 (KLF15) exhibited the most significant change in pathological cardiomyocytes, characterized by less effective repression of disease-associated genes in stressed hearts, which correlated with reduced KLF15 expression. To restore KLF15 activity, we utilized CRISPR/nuclease-dead (d)Cas9-based transcriptional enhancement (CRISPRa) in cardiomyocytes, which effectively abolished fetal reprogramming by simultaneously suppressing pathological gene expression and restoring metabolic homeostasis under sustained stress conditions. Furthermore, we identified a novel cell-nonautonomous anti-fibrotic effect mediated by cardiomyocyte-fibroblast crosstalk, and revealed the contribution of KLF15-dependent Alpha-2-glycoprotein 1, zinc-binding (AZGP1) regulation in this process. We also elucidated the upstream mechanisms of KLF15 regulation, highlighting its role as a cell-specific downstream target of the broad TGF-β canonical signaling pathway, along with its downstream-dependent mechanisms in human cardiomyocytes. Finally, to enhance the therapeutic potential of this approach, we engineered and validated an adeno-associated viral (AAV) vector with a small CRISPRa system for endogenous regulation in human cardiomyocytes suitable for clinical applications. Overall, we elucidated a regulatory circuit involving TGF-β, KLF15, and AZGP1, which coordinates critical pathological responses through cellular crosstalk between cardiomyocytes and fibroblasts. Importantly, we demonstrated the efficacy of CRISPRa as an epigenetic intervention restoring a critical transcriptional function disrupted in non-genetic heart failure. This approach provides a promising blueprint for future adaptation targeting additional non-hereditary pathologies. - Source: PubMed
Publication date: 2026/03/03
Schoger EricKim RosaBleckwedel FedericoPeralta Tomás MPriesmeier LauraFischer Janek AStengel LauraRocha CheilaSantos Gabriela LLutz SusanneBoileau EtienneBaumgarten NinaSchulz Marcel HDieterich ChristophMüller Oliver JCyganek LukasCabrera-Orefice AlfredoEberl HannaMaack ChristophStreckfuss-Bömeke KatrinPavez-Giani Mario GDoroudgar ShirinSossalla SamuelZelarayán Laura C - Maternal-fetal communication involves complex molecular exchanges that can be perturbed by chromosomal abnormalities. Despite the growing use of omics approaches in prenatal research, maternal urine remains underexplored as a non-invasive source of molecular information reflecting both systemic and pregnancy-specific processes. This study performed an exploratory, label-free mass spectrometry-based proteomic analysis of maternal urine from pregnancies with normal karyotype ( = 15) and those affected by fetal aneuploidy ( = 9; trisomy 21, 18, 13, or monosomy X). A total of 861 proteins were identified across all samples, of which 42 significantly differed between groups ( ≤ 0.05, |fold change| ≥ 1.2). Ten proteins, including TFF1, TFF3, KRT76, CD300, PVR, VWA1, FBLN1, FGA, AZGP1, and MAT1, were more abundant in aneuploid pregnancies, suggesting roles in immune modulation, epithelial restitution, metabolic control, and extracellular matrix remodeling. Conversely, 32 proteins with lower abundance were primarily involved in immune regulation, structural organization, and energy metabolism, consistent with impaired placental and vascular adaptation. These findings reveal distinct urinary proteomic signatures associated with fetal aneuploidy, highlighting biologically relevant pathways that may advance understanding of maternal-fetal metabolic communication. - Source: PubMed
Publication date: 2025/11/24
Jurca Răzvan LucianSoporan Maria-AndreeaPralea Ioana-EcaterinaGheorghiu IoanaRus IuliaStamatian FlorinIuga Cristina-Adela