CHI3L2 protein
- Known as:
- CHI3L2 protein
- Catalog number:
- 80R-4391
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- CHI3L2 protein
Related genes to: CHI3L2 protein
- Gene:
- CHI3L2 NIH gene
- Name:
- chitinase 3 like 2
- Previous symbol:
- -
- Synonyms:
- YKL-39, YKL39
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-20
- Date modifiied:
- 2016-10-05
Related products to: CHI3L2 protein
Related articles to: CHI3L2 protein
- Bronchopulmonary Dysplasia (BPD) is a major complication in preterm infants, lacking effective diagnostic biomarkers to facilitate early detection and intervention. - Source: PubMed
Publication date: 2026/07/14
Sun YanchunYou JingyeTao JinhaoDai JialeChen AijuLuo FeiChen Yun - Glioblastoma (GBM), the most common and aggressive subtype of glioma, currently lacks effective therapeutic targets. This study aimed to elucidate the role of chitinase-3-like protein 2 (CHI3L2) and its underlying mechanism in GBM cell proliferation and migration. - Source: PubMed
Publication date: 2026/02/26
Liu ZhihongChen DihuiLiao SijiaFan XiuyueWang JiameiYue HongshuangShen HuilinWang JijinZhao ChengningHu RongDu GuangshiHan Feng - This study determines the phenotypic and functional characteristics that define distinct fibroblast-like synoviocyte (FLS) populations in rheumatoid arthritis (RA) vs psoriatic arthritis (PsA). - Source: PubMed
Publication date: 2026/04/11
Tynan ÓrlaBrugman Aenea A ISmith Conor MCanavan MaryO'Rourke Aoife MFloudas AchilleasAnton DumitruWade SiobhánSundanum SoniaFletcher Jean MOrr CarlVeale Douglas JFearon Ursula - Polymorphisms of mouse chitinase-like protein 3 (Chil3), a member of the mammalian chitinase-like protein (CLP) family, have been demonstrated to be associated with inflammatory diseases by regulating lipid metabolism. However, the specific immunomodulatory impacts of CLPs, mainly mouse CHIL3 and its human functional homologue chitinase-3-like 2 (CHI3L2), on macrophage cholesterol metabolism and atherosclerosis have remained unclear. Here, we find CLPs (CHIL3 and CHI3L2) accelerate atherogenesis in a macrophage-dependent manner. Mechanistically, we identify an autocrine mechanism through which CLPs regulate cholesterol metabolism in macrophages. Macrophage-secreted CLPs exacerbate lipid uptake by binding to CD36. CLPs exhibit glycosidase activity, targeting and hydrolyzing N-glycosylated glycans on CD36, predominantly at sites N220 and N321, thereby enhancing lipid uptake. Increased lipid influx activates mTOR in macrophages, driving their transition to a pro-inflammatory phenotype while simultaneously suppressing peroxisome proliferator-activated receptor gamma (PPARγ) expression and thus impairing ABCG1-mediated cholesterol efflux. Single-cell sequencing reveals that CLPs increase atherosclerotic foamy macrophages, favoring vascular smooth muscle cells (VSMC) transformation into foam and osteoblast-like cells. Additionally, neutralizing antibodies targeting CHI3L2 prevent and treat atherosclerosis. These findings highlight the potential of CLPs as targets for disease diagnosis and therapy. - Source: PubMed
Publication date: 2026/04/08
Wang YuZhang JingFan MeiyangHou XianbinLi XiaomengZhang WentaoLiu WenbinLi YueLu YaqiLi FeiGuan YanglongWang YudanYuan BingyuLi XiaoweiGong HuilinNing FengZhuo XiaozhenLu SheminMeng LiesuHolmdahl RikardZhu Wenhua - Glioblastoma multiforme (GBM), the most aggressive primary brain tumor, is characterized by high recurrence, metabolic plasticity, and complex tumor microenvironmental interactions. The human chitinase and chitinase-like protein family includes five members (CHI3L1, CHI3L2, CHIA, CHID1, and CHIT1) that share conserved chitinase-related domains but exhibit diverse biological functions in immune regulation and tissue remodeling. While chitinase-like proteins are recognized as mesenchymal-associated markers, however, the role of CHID1 in GBM remains largely unexplored. An integrative multi-omics strategy combining TCGA-GBM and CGGA transcriptomic datasets, single-cell RNA sequencing, and enrichment analyses (GSEA, GO, KEGG, and MetaCore) were used to investigate CHID1 expression patterns and associated transcriptional programs. Pharmacogenomic correlations and molecular docking were used to explore potential drug-response associations. CHID1 showed higher expression in GBM compared to the normal brain and was associated with poor overall survival. A single-cell analysis showed tumor-associated expression patterns of CHID1 across malignant samples. Pathway enrichment analyses identified transcriptional programs related to oxidative phosphorylation, redox-related processes, DNA repair, and cell cycle pathways. Collectively, this study provides a comprehensive multi-cohort and multi-modal characterization of CHID1 expression in GBM, integrating bulk transcriptomics, single-cell RNA sequencing, and tissue-level validation. The findings establish CHID1 as a GBM-associated transcriptional marker linked to metabolic and redox-related programs and provide a systematic resource for future investigations into chitinase family-related biology in GBM. - Source: PubMed
Publication date: 2026/03/17
Kumar SachinWu Chung-CheSolomon Dahlak DanielNgadio Juan LorellXuan Do Thi MinhKo Ching-ChungPalekkode NeethuFathima AymanLin Hung-YunLin Hui-RuWang Chih-YangLee Yung-KuoNguyen Ngoc Uyen Nhi