PLA2G3 polyclonal antibody
- Known as:
- PLA2G3 pab (anti-)
- Catalog number:
- PAB16527
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PLA2G3 polyclonal antibody
Related genes to: PLA2G3 polyclonal antibody
- Gene:
- PLA2G3 NIH gene
- Name:
- phospholipase A2 group III
- Previous symbol:
- -
- Synonyms:
- GIII-SPLA2
- Chromosome:
- 22q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-04-29
- Date modifiied:
- 2015-11-18
Related products to: PLA2G3 polyclonal antibody
Related articles to: PLA2G3 polyclonal antibody
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Publication date: 2026/04/13
Xing HaihuaZhao XunwuWang QianghuiMa YukaiGuo XingjianZhang YujieJiang QiLi Heping - Microplastics and nanoplastics are commonly found in our everyday environments. So far, microplastics and nanoplastics have been detected in various tissues and bodily fluids, including hair, sputum, digestive tissue, lungs, blood, placental and endometrial tissue. Although some studies indicate that microplastics and nanoplastics can promote tumor development, their impact on endometrial cancer (EC) remains unclear. In this study, we examined the effect of polystyrene nanoplastics (PS-NPs) on EC development and explored the underlying pathogenic mechanisms. We observed the uptake and accumulation of PS-NPs in HEC-1B cells and EC organoids. Through cell and organoid experiments as well as mouse models, we demonstrated that PS-NP exposure can accelerate EC progression in vitro and in vivo. Next, through transcriptomic sequencing and targeted metabolomic sequencing, We found that adenosine 5'-monophosphate-activated protein kinase (AMPK) can activate ACSS2 and promote its nuclear translocation. The nuclear entry of ACSS2 is associated with increased levels of H3K9 acetylation, which may be a potential mechanism through which it regulates PLA2G3 expression. PLA2G3 mRNA levels are upregulated, increasing the production of arachidonic acid (AA), and ultimately leads to the epithelial-mesenchymal transition (EMT) in EC cells. The relevant molecular markers in this study can provide new strategies for early warning and targeted intervention, reducing the potential impact of PS-NPs on EC. - Source: PubMed
Publication date: 2026/03/26
Huang XiangchunXu LiWang JielinCheng JiachenYuan JingLiu XinLarionova IrinaKzhyshkowska JuliaChen ShuoZhao Yang - Cervical cancer, in which cervical squamous cell carcinoma (CSCC) accounts for 60-70% of cases, has a poor prognosis and poses a significant health threat to global patients. Lipid metabolism reprogramming is a key driver of tumor progression and tumor microenvironment (TME) regulation, making it a promising target for improving the efficacy of immunotherapy. This study aimed to construct a lipid metabolism prognostic signature (LMPS) in CSCC and identify key genes involved in tumor progression. - Source: PubMed
Publication date: 2025/10/14
Bai GaigaiChen FanghuaQiu JunjunHua Keqin - The study examined the induction and mechanism of bone regeneration facilitated by the P24-loaded Gelatin-Hydroxyapatite-Tricalcium Phosphate (Gelatin-HA-TCP (P24)) scaffold. The prepared Gelatin-HA-TCP (P24) scaffold was employed to treat human bone marrow mesenchymal stem cells (hBMSCs) and human umbilical vein endothelial cells (HUVECs). Various assays were conducted to assess the impact of the Gelatin-HA-TCP (P24) scaffold on the osteogenic differentiation of hBMSCs and angiogenesis in HUVECs. For mechanistic investigations, hBMSCs were exposed to both the Gelatin-HA-TCP (P24) scaffold and the ERK inhibitor SCH772984. A rat cranial bone defect model was treated through the implantation of the Gelatin-HA-TCP (P24) scaffold. Micro-computed tomography, histological staining, and immunofluorescence techniques were utilized to evaluate the effect of the Gelatin-HA-TCP (P24) scaffold on cranial bone regeneration. Osteogenic differentiation of hBMSCs was facilitated by the Gelatin-HA-TCP (P24) scaffold, as evidenced by increased ALP activity, enhanced Alizarin Red S staining, and upregulated RUNX2, OSX, OCN, and BMP2. Angiogenesis in HUVECs was induced, as demonstrated by improved migration, tube formation, and upregulated CD31. However, the ability of the Gelatin-HA-TCP (P24) scaffold to promote osteogenic differentiation in hBMSCs was counteracted by SCH772984. In the rat cranial bone defect model, implantation of the Gelatin-HA-TCP (P24) scaffold reduced the bone defect area, increased the bone volume/tissue volume ratio, enhanced bone regeneration, decreased bone fibrosis, and upregulated CD31, RUNX2, and BMP2 in bone tissues. Therefore, the Gelatin-HA-TCP (P24) scaffold enhances the osteogenic differentiation of hBMSCs and promotes bone regeneration in cranial bone defects by activating the ERK/ELK1/PLA2G3 pathway. It has potential for bone regeneration therapies. - Source: PubMed
Fu LaihuaLiu YuanxinXu SongfengZhou YangHuang Jing-YangQiu JinHuang Peng-ZhouZhang ChaoYang Ji-LongSong JianZhao Zhi-Gang - Psoriasis is a chronic inflammatory skin disorder with complex molecular mechanisms. While previous studies have demonstrated altered levels of arachidonic acid and its metabolites in psoriatic lesions, the specific roles of arachidonic acid metabolism (AAM) genes in the molecular pathogenesis and immune dysregulation of psoriasis remain poorly understood. This study aimed to investigate the role of AAM genes in the pathogenesis and immune dysregulation of psoriasis using an integrative bioinformatics approach. - Source: PubMed
Publication date: 2025/03/17
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