S100A12, human, recombinant, full length, unlabelled
- Known as:
- S100A12, H. sapiens, Rec., length, unlabelled
- Catalog number:
- 201SA12_H
- Category:
- -
- Supplier:
- ProtEra
- Gene target:
- S100A12 human recombinant full length unlabelled
Related genes to: S100A12, human, recombinant, full length, unlabelled
- Gene:
- S100A12 NIH gene
- Name:
- S100 calcium binding protein A12
- Previous symbol:
- -
- Synonyms:
- p6, MRP6, CGRP, CAAF1, CAGC, ENRAGE
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-30
- Date modifiied:
- 2018-05-02
Related products to: S100A12, human, recombinant, full length, unlabelled
Related articles to: S100A12, human, recombinant, full length, unlabelled
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Publication date: 2026/08/12
Su YueLuo XiaohuiXu Haitao - In order to investigate the therapeutic mechanism of Jianpiyiqi Granule in juvenile myasthenia gravis (JMG) and find the immune-associated cytokines or signaling pathways targeted by this intervention. - Source: PubMed
Geng YuanyuanLiu PengJin MinQi GuoyanLin XiaotingZhang Yousheng - Intravenous immunoglobulin (IVIG) resistance occurs in 10-20% of children with Kawasaki disease (KD) and is associated with a 3- to 5-fold higher risk of coronary artery lesions (CALs). Yet the mechanistic basis for why some patients progress from reversible inflammation to irreversible vascular damage after IVIG remains poorly understood. Most existing reviews have focused on risk prediction rather than the mechanistic chain linking resistance to CALs. Here, we synthesize current evidence across three interconnected pathways. First, autophagy dysfunction-particularly impaired mitophagy-sustains inflammation through cGAS-STING activation. Second, neutrophil extracellular traps (NETs) play a controversial role in KD vasculitis, with PAD2 and PAD4 possibly acting redundantly via the NLRP3 inflammasome. Third, endothelial-to-mesenchymal transition (EndMT), driven by the IL-1β/TNF axis and the USP7-TGFβ2/SMAD pathway, emerges as a core event in vascular remodeling. Building on these findings, we propose the "autophagy-inflammasome axis" as a candidate molecular switch that dictates whether inflammation resolves or persists. This hypothesis is actionable: it generates three explicit, testable predictions linking autophagic integrity to inflammatory outcomes and therapeutic response. Direct experimental validation in IVIG-resistant KD models and patient samples is now urgently needed. This review provides a systematic framework for understanding how IVIG resistance transitions to irreversible CALs. It also identifies candidate biomarkers (e.g., S100A12, mtDNA, and MCM8) and therapeutic targets (autophagy inducers, NLRP3 inhibitors, USP7 inhibitors, and anakinra) that could enable earlier intervention. - Source: PubMed
Publication date: 2026/07/18
Zhang RongZhang JiaqiYang YanzhiWang YaCao Haijun - Acute empyema refers to suppurative inflammation of the pleural cavity secondary to pulmonary infection. Prompt diagnosis and intervention are required upon identification to prevent progression to chronic empyema; hence, clinically effective biomarkers are needed to predict the development of acute empyema. - Source: PubMed
Publication date: 2026/07/09
Zhou Xiao-LianLi Dong-QiongLi Duo - Juvenile idiopathic arthritis (JIA) and acute lymphoblastic leukemia (ALL) share overlapping musculoskeletal presentations in pediatric patients, and the misclassification of ALL as JIA carries life-threatening consequences due to inappropriate initiation of corticosteroid or immunosuppressive therapy. A rigorous synthesis of contemporary evidence identifying the most reliable clinical and laboratory discriminators between these two conditions is long overdue. This systematic review and meta-analysis aimed to evaluate clinical, laboratory, and biomarker-based features that differentiate ALL from JIA in pediatric patients. The primary focus was on studies published between January 2021 and April 2026, while selectively incorporating seminal pre-2021 studies with major diagnostic relevance and extractable comparative data to strengthen quantitative synthesis. - Source: PubMed
Publication date: 2026/06/30
Reyad Heba MEltrafi NarmenAli Walaa HAbdelrazek MohamedAbd Elwahab Marwa KhairyIbrahim EimanRamdan Seham NabilAkef AhmedEid Jumana AhmedAbdou Mohamed Hashem YoussefEltokhy Soad AMosaid SedeekHashem Mona EKassem Iman AhmedAbdelghany Ramy Saleh