PTX3 Monoclonal Antibody [MNB4]
- Known as:
- PTX3 Monoclonal Antibody [MNB4]
- Catalog number:
- a-0568-100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- PTX3 Monoclonal Antibody [MNB4]
Ask about this productRelated genes to: PTX3 Monoclonal Antibody [MNB4]
- Gene:
- PTX3 NIH gene
- Name:
- pentraxin 3
- Previous symbol:
- TNFAIP5
- Synonyms:
- TSG-14
- Chromosome:
- 3q25.32
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2016-10-05
Related products to: PTX3 Monoclonal Antibody [MNB4]
Related articles to: PTX3 Monoclonal Antibody [MNB4]
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Saptarini IkaMasyeni SriHarahap Alida RoswitaGiantini AstutiNugroho PringgodigdoHandito AgusHendarwan HarimatSusilo AdityoHaryanto SotianingsihFitriani DesiSasmono R TedjoNelwan Erni Juwita - Silica nanoparticles (SiNPs) are considered as one of the excellent alternative negative electrode materials for optimizing the storage performance of lithium-ion batteries. Therefore, with the global transition to new energy, their production may rapidly increase, but there is still a lack of relevant research on occupational exposure risks, especially respiratory toxicity mechanisms and biomarkers, associated with lithium-ion battery-related SiNPs. This study investigated the mechanism of toxic effects and possible biomarkers of SiNPs on human bronchial epithelial cells (BEAS-2B) using integrative transcriptomic, proteomic, and metabolomic approaches. SiNPs used in this study were selected as the most relevant type of negative electrode material for lithium-ion batteries, and their physical and chemical properties were characterized in detail. It was found that SiNPs induced significant concentration- and time-dependent cytotoxicity on BEAS-2B cells. SiNPs could alter the multiomics phenotype of cells after treatment with 50 μg/mL for 24 h. Multiomic joint analysis found that SiNPs may have induced cytotoxicity through toxic pathways, including oxidative stress, inflammation, and fibrosis, screening possible biomarkers such as PTX3, SESN2, STC2, IL-6, CLDN1, and COL14A1. This study revealed the possible mechanisms and biomarkers of respiratory toxicity of lithium-ion battery-related SiNPs and also suggested that integrative omic analyses could be a useful approach for evaluating the toxicity of novel nanoparticles. - Source: PubMed
Publication date: 2026/06/03
Zhou XinyanShi JiaqiMa YingZhang YiLi XiaojinPeng BinshuaiJia GuangChen Zhangjian - Diabetic kidney disease (DKD) is characterized by tubular EMT and fibrosis. So far, the pathogenesis of DKD is still not fully understood. Pentraxin 3 (PTX3), an inflammatory regulator, is overexpressed in DKD due to hyperglycemia. PTX3 amplifies inflammation by promoting inflammatory cytokine release (TNF-α, IL-6) and activating the nuclear factor kappa-B (NF-κB) pathway. Subsequently, it triggers the c-Jun N-terminal kinase (JNK) signaling pathway, enhancing AP-1-mediated transcription of inflammatory genes (MCP-1, ICAM-1). JNK also upregulates EMT markers (α-SMA, N-cadherin) through increased transforming growth factor TGF-β1, accelerating renal fibrosis. Targeting the PTX3-JNK axis with neutralizing antibodies or inhibitors mitigates inflammation and EMT, suggesting PTX3 as a potential anti-fibrotic target in DKD. - Source: PubMed
Publication date: 2026/05/20
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Publication date: 2026/05/29
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