S100A9, human, unlabelled
- Known as:
- S100A9, H. sapiens, unlabelled
- Catalog number:
- 201SA09_H
- Category:
- -
- Supplier:
- ProtEra
- Gene target:
- S100A9 human unlabelled
Related genes to: S100A9, human, unlabelled
- Gene:
- S100A9 NIH gene
- Name:
- S100 calcium binding protein A9
- Previous symbol:
- CAGB, CFAG
- Synonyms:
- P14, MIF, NIF, LIAG, MRP14, MAC387, 60B8AG, CGLB
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-19
- Date modifiied:
- 2018-05-02
Related products to: S100A9, human, unlabelled
Related articles to: S100A9, human, unlabelled
- Antimicrobial peptides (AMPs) are essential components of the innate immune system, exhibiting diverse mechanisms of action. - Source: PubMed
Pinheiro da Silva FabianoSoriano Francisco GarciaHajjar Ludhmila Abrahão - Psoriasis, a chronic inflammatory skin disease affecting 2-3% of the global population, is driven by dysregulated immune responses. Despite advancements in biologic therapies, treatment challenges persist due to high recurrence rates. This study aimed to identify immune-related hub genes and elucidate their clinical implications in psoriasis pathogenesis and therapy. - Source: PubMed
Publication date: 2026/04/20
Sun YuzhenZhou ZiguangMao YuLiu NiuLi YanfengFang Weiyuan - Type 1 diabetes mellitus (T1DM) compromises the mechanical adaptive capacity of bones, posing challenges in orthodontic treatment and increases periodontal complication risks. Mechanical loading is the main inducer of craniofacial bone adaptation; however, the early proteomic responses of the maxillary bone to stress under diabetic conditions remain unexplored. Therefore, we aimed to characterize the early proteomic signatures of the maxillary bone in T1DM rats subjected to controlled mechanical stress and identify potentially relevant molecular pathways for orthodontic treatment in patients with diabetes. - Source: PubMed
Publication date: 2026/04/06
Tobias-López Luis FernandoTrejo-Iriarte Cynthia GeorginaGarcía-Muñoz AlejandroGómez-Clavel José Francisco - Radiation-induced heart disease (RIHD) is a serious complication of thoracic radiotherapy, and its pathogenesis involves systemic immune alterations. To elucidate these mechanisms, we profiled peripheral blood mononuclear cells (PBMCs) from patients before and after thoracic radiotherapy using single-cell RNA sequencing (scRNA-seq), with key findings validated via multiparameter flow cytometry and ELISA assays. Our analysis revealed that radiotherapy markedly reshaped the immune composition, expanding innate myeloid cells (monocytes and neutrophils) and reducing lymphocytes (T and NK cells); these compositional shifts were independently confirmed by flow cytometric analysis. Cell-cell communication networks showed that postradiotherapy monocytes evolved into central signaling hubs, exhibiting heightened proinflammatory ligand-receptor interactions. Consistent with this, monocytes showed broad transcriptional reprogramming with upregulation of canonical inflammatory pathways (IL-6/STAT3, TNF/NF-κB) and metabolic regulators (mTORC1, glycolysis). ELISA assays corroborated these transcriptomic signatures, demonstrating significantly elevated plasma levels of IL-6 and TNF-α post-treatment. Notably, scRNA-seq identified a selective expansion of the highly plastic intermediate (CD14++CD16+) monocyte subset, a specific population shift further verified by flow cytometry. These intermediate monocytes exhibited an immature, progenitor-like profile and were enriched at the origin of a Monocle3 pseudotime trajectory. Trajectory analysis indicated they differentiate into mature classical monocytes that upregulate proinflammatory effector genes such as S100A8, S100A9, and S100A12. Furthermore, pseudotime gene clustering revealed a functional bifurcation in monocyte behavior: one module drove inflammatory activation, while a second module simultaneously engaged oxidative stress responses and antioxidant defenses (e.g., glutathione metabolism). In summary, by integrating single-cell transcriptomics with experimental validation, we demonstrate that radiotherapy drives a systemic immune shift characterized by intermediate monocyte expansion and bifurcated programs of inflammation and stress adaptation. Intermediate monocytes emerge as key drivers of postradiotherapy inflammation, offering a potential cellular biomarker of RIHD risk and a target for immunomodulatory interventions to mitigate cardiovascular injury in cancer survivors. - Source: PubMed
Publication date: 2026/04/17
He JinchenKong DejunZhang ChengweiChen QiuhongYang HongWang YuyuanWu TianqiWu Qi - Oxidative stress (OS) plays a role in hypertension development, but the underlying genetic mechanisms are not completely understood. This study aimed to investigate the association between OS-related genes and hypertension by performing an integrative multi-omics analysis using summary-data-based Mendelian randomization (SMR) and colocalization approaches. - Source: PubMed
Publication date: 2026/03/25
Zhang YueMeng JinyangYan YuchengTang HongZhong DonglingLi YuxiXue PeiwenZhang AnrenJin RongjiangLi Juan