S100A12, human, recombinant, full length
- Known as:
- S100A12, H. sapiens, Rec., length
- Catalog number:
- G02S1A12
- Product Quantity:
- 5 mg
- Category:
- -
- Supplier:
- Giotto Biotech
- Gene target:
- S100A12 human recombinant full length
Related genes to: S100A12, human, recombinant, full length
- 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
Related articles to: S100A12, human, recombinant, full length
- Bacterial lipopolysaccharide (LPS) play a crucial role in triggering dysregulated immune responses in pediatric septic shock, profoundly influencing disease onset and progression. This study systematically investigated the differential expression of LPS-related genes, constructed diagnostic models, explored regulatory networks, analyzed immune cell infiltration, and identified potential therapeutic targets of traditional Chinese medicine for pediatric septic shock. - Source: PubMed
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Qiao JunyingZou LanlanZhao JianchuangCui ChenhangHuang XianjieFan Yazhen - Gouty arthritis (GA) has long been considered a disease primarily driven by innate immune activation, whereas the contribution of adaptive immune remodeling remains incompletely understood. - Source: PubMed
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Zhang PengZhu FangjieXiao YuntingShen ZhengdongFan ChunxiaoKe PeifengXu YaoZhan ChenguangLi XinWu XiaodongMei LiyanGao KaixinDu HaifangChen XiuminJiao YangHuang RunyueWang Maojie - To integrate multi-cohort transcriptomic, single-cell, and experimental data to identify diagnostic signature genes for septic shock, establish a peripheral blood molecular diagnostic model, and elucidate the m6A regulatory mechanisms of key genes. - Source: PubMed
Publication date: 2026/05/25
Li LingLi KexunQian WeiweiJiang HuiPeng HongqiongZhang YangChen ZhengjunZeng Xia - This study describes the distribution of non-reactive brain-resident microglia densely populated along the borders of the lateral ventricles and choroid plexus in premature rabbit pups during early forebrain development. Following intraventricular hemorrhage (IVH) injury, activated microglia expand by proliferation, and migrate deeper into parenchymal regions. During this process, activated microglia exhibit a disproportionate elevation of the proinflammatory microglia phenotype (M1 nomenclature) from the total IBA-1 microglia cell population along with tissue iron accumulation; this shift was reduced by sulforaphane (SFN; Nrf2-antioxidant response element [ARE] activator of anti-inflammatory pathways) plus deferoxamine (DFN; iron chelator) treatment. A separate DFN monotherapy transcriptome analysis identified over expression of pro-inflammatory calcium-binding proteins S100A8 and S100A12 (intracellular damage signals), as well as chemokines CXCL8 and CXCL10 by microglia and other cells, along with upregulated ferroptosis interactive network genes in IVH including: HMOX1, CTSB, FTL, PRM2, LPCAT1, and CDK1. Importantly, the expression of multiple key genes involved in iron metabolism and transport function included: ACSL4, TFRC, SLC7A11 and ABCA4 which were all downregulated in IVH and this trend was reversed after DFN treatment. Taken together, in the developing postnatal brain, the combination treatment of SFN-DFN mitigated M1 infiltration, reduced iron deposition in the tissue and in the CSF, suppressed the magnitude of inflammation and reduced cell death after IVH. Moreover, DFN monotreatment reversed most dysregulated genes in inflammation and iron homeostasis networks, revealing potential molecular targets for additional pharmacologic interventions after IVH. We speculate that reducing the toxic microcellular environment will attenuate injurious inflammatory responses and improve recovery of the trajectory toward normal brain development. - Source: PubMed
Publication date: 2026/05/25
Castro Diaz VanessaSunshine MichelleHu FurongShah SohanHuang WeihuaThompson Carl IWolin Michael SSubbian SelvakumarLaGamma Edmund FVinukonda Govindaiah - Parkinson's disease (PD) is a progressive neurodegenerative disorder lacking established clinical biomarkers. We performed an exploratory multi‑omics analysis of transcriptome and proteome data from small PD and control cohorts at Huaihe Hospital of Henan University. Using two local datasets, we identified 124 differentially expressed genes (DEGs) and 28 proteins, then performed protein‑protein interaction (PPI) and gene set variation analysis (GSVA). After intersecting with 2,964 DEGs from Gene Expression Omnibus (GEO) Dataset 3, we obtained a 28‑gene panel. Potential markers were prioritized via random forest (RF), support vector machine (SVM) and principal component analysis (PCA), and evaluated in external GEO data, clinical serum samples and a 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine (MPTP)‑induced PD mouse model. PPI highlighted C‑X‑C motif chemokine ligand 1 (CXCL1), C‑X‑C chemokine receptor type 4 (CXCR4), S100 calcium‑binding protein A12 (S100A12) and C‑X‑C motif chemokine ligand 11 (CXCL11) as hub genes. GSVA indicated upregulated cardiac muscle contraction and oxidative phosphorylation (OXPHOS). C‑C motif chemokine ligand 4 (CCL4), CKLF like MARVEL transmembrane domain containing 2 (CMTM2), tudor domain containing 6 (TDRD6), potassium voltage‑gated channel subfamily S member 1 (KCNS1) and member RAS oncogene family (RAB15) were identified as candidate markers. They showed consistent expression changes in clinical samples and mice. Immune infiltration differed in B cells, CD8 + T cells and natural killer (NK) cells. LY‑303511 and HC‑toxin were predicted as candidate compounds. These five genes represent preliminary candidate biomarkers for PD; however, further validation in larger independent cohorts is warranted for clinical translation. - Source: PubMed
Publication date: 2026/06/01
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