Ask about this productRelated genes to: CHI3L1 antibody
- Gene:
- CHI3L1 NIH gene
- Name:
- chitinase 3 like 1
- Previous symbol:
- -
- Synonyms:
- GP39, YKL40, YK-40
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-20
- Date modifiied:
- 2018-08-01
Related products to: CHI3L1 antibody
Related articles to: CHI3L1 antibody
- The CHI3L1 protein supports various types of cancer progression and metastasis, where the background players were the upregulation of angiogenesis and microenvironment modulation. In glioblastoma (GB), high vascularisation is a key feature of these tumours, making anti-angiogenic therapy a pivotal treatment option. Autophagy, a dual-faced mechanism, may be useful as a target in GB treatment. This work presents the role of the CHI3L1 protein in autophagy in GB. U-87 MG glioblastoma cells and a GB spheroid model consisting of U-87 MG cells, macrophages and endothelial cells were used in the studies. A new tissue-like phantom was designed for the radiotherapy of spheroids. The role of CHI3L1 in autophagy regulation was analysed after cell starvation and treatment with G721-0282, a small molecule inhibitor of CHI3L1, as well as X-ray doses. The biological responses were evaluated using the Western blot method, immunohistochemical reactions, DHT (digital holographic tomography) and O-PTIR (optical phototermal infrared spectroscopy) to analyse biological responses in GB spheroids. Induction of autophagy in glioblastoma cells after CHI3L1 inhibition was observed, as well changes in CHI3L1 expression levels occurred after cell starvation and different X-ray radiation doses. Secondary structure changes in glycoproteins and decreases in nucleic acids were observed in O-PTIR. The expression of CHI3L1 in glioblastoma cells may be precisely regulated by an adverse environment, such as nutrient depletion or anti-tumour treatment. Inhibiting the CHI3L1 protein leads to upregulation of autophagy, meaning that CHI3L1 inhibitors could be used as a new therapy to upregulate autophagy in GB. - Source: PubMed
Publication date: 2026/03/22
Rusak AgnieszkaJaniszewska MarzenaRaczkowski MaciejCael SupatchareeGuźniczak MateuszBuzalewicz IgorKrawczyńska KlaudiaEl-Mashtoly Samir FKulus MichałGórnicki TomaszDzięgiel PiotrPodhorska-Okołów MarzennaPopp JürgenKrafft Christoph - CHI3L1, a chitinase-like protein, is implicated in pulmonary fibrosis, yet its mechanisms incompletely understood. In this study, we demonstrated that CHI3L1 coordinates profibrotic macrophage activation and invasive myofibroblast differentiation, and their crosstalk. In vitro, CHI3L1 drove M2-like macrophage polarization as evidenced by increased CD163, CD206, and PD-L1, and amplified TGF-β1-induced fibroblast responses, including myofibroblast transformation, migration, and invasion. Mechanistically, CHI3L1 enhanced TGF-β1 signaling through SMAD, AKT, and ERK pathways, and PD-L1 was required for CHI3L1/TGF-β1-driven myofibroblast transformation. Co-culture studies further demonstrated the ability of CHI3L1 to induce profibrotic macrophage activation that enhanced myofibroblast transformation mediated via a CD44-PD-L1 axis. In vivo, following bleomycin challenge, CHI3L1 transgenic mice exhibited increased PD-L1+ M2 macrophages, PD-L1+/PDGFRα+ fibroblasts, and PD-1+ immune cells compared with wild-type controls. Therapeutically, combined anti-CHI3L1 and anti-PD-1 antibodies, as well as a bispecific anti-CHI3L1-anti-PD-1 antibody, produced greater anti-fibrotic efficacy than monotherapy. These findings demonstrate crosstalk between CHI3L1 and the PD-1/PD-L1 pathway that promotes profibrotic macrophage activation and invasive fibroblast differentiation and support dual targeting of CHI3L1 and PD-1/PD-L1 as a promising therapeutic strategy for pulmonary fibrosis. - Source: PubMed
Publication date: 2026/04/28
Jeong Han-SeokSadanaga TakayukiLee Joyce HKamle SuchitraMa BingZhou YangShin Sung JaeElias Jack ALee Chun Geun - Autoimmune glial fibrillary acidic protein astrocytopathy (A-GFAP-A) is a recently defined immune-mediated disorder of the central nervous system (CNS). At present, diagnosis relies primarily on the detection of GFAP-IgG in cerebrospinal fluid (CSF); however, the limited specificity of this biomarker restricts its clinical utility. This study aimed to investigate the expression profiles and clinical relevance of additional protein biomarkers in A-GFAP-A. - Source: PubMed
Publication date: 2026/04/08
Liu LuMa BoyaPeng JiahuiLi NingZhang YinghuiLiu QiangYang JuanZhao LiLi YiWang YanbaiYang Xiao - Metabolic dysfunction-associated steatotic liver disease (MASLD) affects about one-quarter of adults worldwide, and liver fibrosis is its strongest predictor of liver-related morbidity and mortality. Using combined in-silico screening and experimental evaluation, we aimed to identify circulating biomarkers associated with fibrosis progression. Fibulin-3 was identified, and its diagnostic performance was evaluated in biopsy-proven MASLD cohorts. - Source: PubMed
Publication date: 2026/04/20
Laraño Allen AnthonyPalmisano SilviaBonazza DeborahMarina DiscipioMeroni MaricaFracanzani Anna LudovicaCrocè Lory STiribelli ClaudioDongiovanni PaolaRosso NataliaGiraudi Pablo - Glioblastoma recurrence is driven by diffuse microscopic infiltration beyond the contrast-enhancing tumour margin. GlioMap is an open-access AI model predicting voxelwise infiltration and recurrence risk from multiparametric MRI. This prospective study aimed to validate GlioMap's biological accuracy and prognostic relevance through histopathological assessment, transcriptomic profiling, and survival analysis within the SupraGlio trial (NCT05735171). - Source: PubMed
Publication date: 2026/04/20
Cepeda SantiagoHernando-Pérez ElenaPérez-Riesgo EnriqueRodríguez-Valle IsabelEsteban-Sinovas OlgaArrese IgnacioLucero-Salaverry María MiguelZamora TomásTorres-Nieto María ÁngelesLuppino Luigi TommasoKuttner SamuelWodzinski MarekEscudero TrinidadGarzón JesúsRomero-Oraá RobertoHornero RobertoNúñez LucíaVillalobos CarlosSarabia Rosario