S100A10, human, recombinant, full length
- Known as:
- S100A10, H. sapiens, Rec., length
- Catalog number:
- 201SA10
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- ProtEra
- Gene target:
- S100A10 human recombinant full length
Related genes to: S100A10, human, recombinant, full length
- Gene:
- S100A10 NIH gene
- Name:
- S100 calcium binding protein A10
- Previous symbol:
- ANX2LG, CAL1L
- Synonyms:
- P11, 42C, CLP11
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-09-10
- Date modifiied:
- 2018-05-02
Related products to: S100A10, human, recombinant, full length
Related articles to: S100A10, human, recombinant, full length
- To investigate the effects of electroacupuncture (EA) on cognitive function and neuroinflammation in a rat model of vascular dementia (VD) and the underlying mechanism. - Source: PubMed
Gao JianhongShi CeLi WeiranShang XiangWang FeiYang QiqiLi Fei - Non-small cell lung cancer (NSCLC) is the most common lung cancer subtype and a leading cause of cancer-related mortality due to asymptomatic early stages and poor 5-year survival, and tumor-infiltrating lymphocytes (TILs) play a pivotal but poorly defined role in NSCLC progression and prognosis within the tumor microenvironment (TME). - Source: PubMed
Publication date: 2026/07/23
Su WenyaWu YudiHe QianZhou LinZhou Jun - Cigarette smoke (CS) exposure is a significant environmental trigger for childhood asthma. Although S100 calcium-binding protein A10 (S100A10) is upregulated in asthma patients, its regulatory mechanism in CS-associated asthma remains unclear. This study aimed to elucidate how insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) influences S100A10 expression via the N-methyladenosine (mA) modification pathway and to investigate the role of the IGF2BP3/S100A10 axis in CS-exposed childhood asthma. A total of 120 asthmatic children were enrolled, with 120 healthy children selected as controls. Serum levels of S100A10 and IGF2BP3 were measured. A murine model of asthma was established using ovalbumin (OVA) induction combined with CS exposure. Lentivirus-mediated overexpression or knockdown of IGF2BP3 or S100A10 was performed to evaluate lung function, inflammatory infiltration, immune cell proportions, and immunoglobulin E (IgE) levels. Airway epithelial cells (AECs) were isolated and treated with cigarette smoke extract (CSE) and OVA to assess apoptosis and inflammatory cytokine levels. RNA immunoprecipitation, m6A methylated RNA immunoprecipitation, and crosslinking immunoprecipitation (CLIP) were conducted to validate the regulatory mechanism between IGF2BP3 and S100A10. The expression of S100A10 and IGF2BP3 was elevated in asthmatic children and OVA-induced asthmatic mice. In OVA-induced asthmatic mice, CS exacerbated OVA-induced asthma phenotypes, including increased lung resistance, enhanced inflammatory infiltration, elevated T helper 2 (Th2) and T helper 17 (Th17) cell proportions, and raised IgE levels. Knockdown of S100A10 or IGF2BP3 ameliorated these pathological changes, while overexpression of S100A10 reversed the protective effects of IGF2BP3 knockdown. Mechanistically, IGF2BP3 bound to m6A modification sites on S100A10 mRNA and enhanced its stability. CSE and OVA promoted IGF2BP3 expression, thereby increasing S100A10 mRNA stability, leading to enhanced epithelial apoptosis and release of inflammatory factors (interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha). CS exposure aggravates childhood asthma by promoting IGF2BP3 expression and enhancing m6A-dependent stabilization of S100A10 mRNA. Targeting the IGF2BP3/S100A10 axis may provide a novel therapeutic strategy for CS-associated asthma. - Source: PubMed
Publication date: 2026/08/05
Guo LuYangWang LiFeng MingZhaoKong LingFengChai YaHuiLiu BaoZhang He - Epilepsy, characterized by recurrent seizures, is associated with dysregu-lated Fatty Acid (FA) metabolism and metabotropic glutamate receptor 5 (mGluR5) signaling. However, the contribution of FA metabolism-related molecules (FAMs) to these pathological pro-cesses remains poorly characterized. - Source: PubMed
Publication date: 2026/07/26
Li SijunZhou MuhuaWei XingCao YingyingLuo XibaoLi DongmeiKang BaorenWang XiaojuanHe KunmeiHe JunruiLv Yuan - Pancreatic adenocarcinoma (PAAD) is an extremely invasive malignancy with limited effective treatment options. S100 calcium-binding protein A10 (S100A10), a protein-coding gene, plays a critical role in tumor progression. However, its correlation with immune cell infiltration and PAAD prognosis has not been previously reported. This study aimed to systematically explore the expression pattern, biological function and clinical value of S100A10 in PAAD. - Source: PubMed
Publication date: 2026/05/21
Song PengzhaoChen TianqiGuo QingqunSun YahuiGu PengfeiHan Yong