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
- Psoriasis is a chronic inflammatory skin disorder driven by immune dysregulation and keratinocyte hyperproliferation. Calcitriol, the active form of vitamin D, shows therapeutic potential, but its molecular mechanisms remain incompletely understood. CHI3L2 (chitinase-3-like protein 2) is a member of the chitinase-like protein family implicated in inflammatory and tissue-remodelling processes, yet its role in psoriasis has not been explored. Here, we investigated whether CHI3L2 mediates the anti-psoriatic effects of calcitriol. Topical application of calcitriol alleviated imiquimod (IMQ)-induced psoriasiform lesions in both unilateral and bilateral mouse ear models, as evidenced by reduced clinical scores, epidermal thickening and pro-inflammatory cytokine expression (IL-1α, IL-6, IL-17A, IL-23A). In M5-stimulated HaCaT cells, calcitriol reversed aberrant proliferation, migration and inflammatory responses, and restored keratin expression (KRT1/KRT6). RNA-seq identified CHI3L2 as the most significantly downregulated gene following calcitriol treatment. CHI3L2 knockdown phenocopied the protective effects of calcitriol, suppressing cell proliferation, migration and inflammation. Mechanistically, calcitriol downregulated CHI3L2 via inhibition of STAT3 phosphorylation at Tyr705. Collectively, these findings demonstrate that calcitriol ameliorates psoriatic inflammation and keratinocyte hyperproliferation through CHI3L2 downregulation mediated by the STAT3 pathway, highlighting CHI3L2 as a potential therapeutic target for psoriasis. - Source: PubMed
He QingqingLiu Junlin - 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