CRISP3 antibody
- Known as:
- CRISP3 (anti-)
- Catalog number:
- orb100349
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CRISP3 antibody
Related genes to: CRISP3 antibody
- Gene:
- CRISP3 NIH gene
- Name:
- cysteine rich secretory protein 3
- Previous symbol:
- -
- Synonyms:
- SGP28, CRISP-3, CRS3, dJ442L6.3, Aeg2
- Chromosome:
- 6p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-04-25
Related products to: CRISP3 antibody
Related articles to: CRISP3 antibody
- Extracellular matrix (ECM) remodeling contributes to retinal vascular basement membrane thickening, an early structural hallmark of diabetic retinopathy (DR). This study aimed to identify key ECM-related genes (ECMGs) associated with DR. Transcriptomic data of DR and ECMGs from MatrixDB were integrated to identify differentially expressed ECMGs. Six machine learning (ML) models, including Extra Trees (ET), Logistic Regression, Adaptive Boosting, Random Forest, Extreme Gradient Boosting, and naive Bayes classifier, were employed to construct DR classification models, with SHapley Additive exPlanation (SHAP) used to interpret feature contributions. Functional enrichment analysis using GSEA and immune infiltration analysis using CIBERSORT were conducted to explore the potential mechanisms by which key ECMGs regulate DR. Regulatory networks were constructed using predicted miRNAs, lncRNAs, and transcription factors (TFs) via the ENCORI, miRWalk, and miRNet databases. Drug-key ECMGs-DM-related diseases interactions were further explored using the DGIdb and CTD databases. Nine candidate ECMGs were identified by overlapping 356 DM-associated DEGs, 1,626 DR-associated DEGs, and 1,023 ECMGs, including CILP2, FN1, DEFA3, COL17A1, CRISP3, TPSAB1, SFRP1, GPHA2, and ECM2. Among the six ML algorithms, the ET classifier exhibited the best overall performance, and five ECMGs (SFRP1, CILP2, FN1, TPSAB1, and ECM2) with non-zero SHAP values were retained as key genes. These genes showed distinct expression patterns across the healthy, DM, and DR groups, and were enriched in neural-related pathways, such as axon guidance, glycosphingolipid biosynthesis ganglio series, and neuroactive ligand receptor interaction. Immune profiling and correlation analysis revealed that FN1, TPSAB1, and CILP2 were correlated with memory/naive B cells, CD8 + T cells, activated memory CD4 + T cells, Tregs, monocytes, and neutrophils. Additionally, the ceRNA network contained five miRNAs, 7 lncRNAs, and two ECMGs, and further regulatory and pharmacologic analysis further linked key ECMGs to specific TFs, drugs, and diabetes-related diseases. This study identified SFRP1, CILP2, FN1, TPSAB1, and ECM2 as key ECMGs in DR, revealing their coordinated involvement in ECM remodeling, neural signaling, and immune modulation. These findings provide novel insights into DR pathogenesis and potential therapeutic targets. - Source: PubMed
Publication date: 2026/06/10
Xin WangYing WangQiang FengYan ChenWei Zhang - Parthanatos, a Poly polymerase 1 mediated programmed cell death pathway, remains poorly characterized in asthma pathogenesis. This study integrated transcriptomic data from public asthma datasets and parthanatos-related genes (PRGs) to identify the key molecular players. - Source: PubMed
Publication date: 2026/01/22
Zhao JiaweiLi DanniYang ChunliLiu ChunyanMa Xiaolin - A newly discovered mode of cell death is called cuprotosis. Current evidence confirms that cuprotosis is involved in the occurrence and development of malignant tumors. However, the prognostic significance and function of cuprotosis-related genes (CRGs) in breast cancer (BC) remain unclear. The aim of this study is to establish a model for predicting the prognosis of BC patients with cuprotosis-related pattern-related gene (CRPRG) score, and explore the functional role of CRGs in the tumor microenvironment (TME). - Source: PubMed
Publication date: 2026/02/12
Sun Tian-WeiLi Min-YuanMa JieWu Jin-Wei - BACKGROUND: Women with prior gestational diabetes mellitus (GDM) have an elevated risk of developing cardiometabolic diseases, including type 2-diabetes and cardiovascular disease. While physical fitness is protective, circulating molecular biomarkers linking fitness to long-term metabolic health in this population remain poorly understood. This study aimed to identify serum proteins associated with aerobic capacity and muscle strength 10 years after GDM, and explore their biological functions related to cardiometabolic risk. METHODS: We assessed aerobic fitness (VO2peak), peak fat oxidation, and maximal isometric muscle strength of five muscle groups in 38 women from the post-GDM PONCH-cohort. Serum proteins were analysed using mass spectrometry-based proteomics. Associations between proteins, fitness variables, and clinical markers were tested using Spearman correlations with FDR correction, and age- and medication-adjusted sensitivity analysis. Group differences across four fitness-level groups (defined by aerobic fitness and muscle strength) and glycaemic status groups were analysed using linear regression models and Kruskal-Wallis tests, with age- and medication-adjusted sensitivity analyses. Exercise responsiveness of selected proteins was assessed in an independent cohort of untrained men undergoing six weeks of supervised aerobic training (n = 28), with pre-post changes assessed using Wilcoxon signed-rank tests. RESULTS: Thirty-five proteins were associated with at least one fitness variable, of which 21 remained significant after age- and medication-adjusted sensitivity analysis. Nine proteins correlated with both VO2peak and muscle strength. Identified proteins mapped to key cardiometabolic pathways, including metabolic regulation, immune response, complement activation, oxidative stress, and extracellular matrix remodelling. Five proteins (PON3, IGF1, CRISP3, COL6A3, C3) emerged as particularly interesting, showing the largest and most consistent effect sizes across fitness variables and associations with central adiposity, blood lipids, blood pressure, and insulin resistance. Stratified analysis across the four fitness-level groups identified IGF1, PON3, and PRG4 as markers of higher overall-fitness. In the independent training cohort, nine of the fitness-associated proteins changed following aerobic training without significant weight-loss. CONCLUSIONS: This study identified circulating proteins linked to physical fitness and cardiometabolic health in women after GDM. These findings suggest fitness-associated serum proteins may serve as biomarkers of early metabolic dysfunction and potential targets for exercise-based prevention of T2D and cardiovascular disease. - Source: PubMed
Publication date: 2026/02/27
Kristiansson EmiliaHolmäng AgnetaWallenius KristinaChung H SophiaHess SonjaPettersson StefanMadsen KlavsAndersson-Hall Ulrika - : Ovarian cancer (OC) remains the most common cause of gynecological cancer-related death, and about 70% of these deaths are from advanced high-grade serous ovarian cancer (HGSOC). Cysteine-rich secretory protein 3 (CRISP3) is related to various human diseases; however, the roles and mechanisms of CRISP3 in HGSOC remain unclear. : The clinical significance of CRISP3 in patients with OC was analyzed using the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. CRISP3 expression in OC tissues was validated by RNA-sequencing (RNA-seq), quantitative PCR, and immunohistochemistry. Furthermore, we explored the effect of CRISP3 expression modulation on the biological behavior of HGSOC through CCK-8, EdU, and Transwell assays in vitro, and the differences in CRISP3 during the progression of HGSOC in vivo. We utilized RNA-seq, GSEA and Western blotting to detect CRISP3's regulatory mechanisms. Finally, we employed data from the IMvigor210 cohort and TCGA to assess the correlation of CRISP3 with clinical response to immunotherapy, and the landscape of immune cell infiltration. : CRISP3 expression was markedly reduced in HGSOC. In vitro studies demonstrated that CRISP3 knockdown significantly enhanced proliferation, migration, and invasion of HGSOC cells, whereas its overexpression suppressed these malignant phenotypes. Moreover, CRISP3 expression was found to be downregulated during OC progression in vivo. Mechanistically, CRISP3 acted as a tumor suppressor through the PI3K/AKT signaling pathway to inhibit the progression and metastasis of HGSOC. Additionally, we observed an association between CRISP3 expression and CD8 T cell, macrophage, neutrophil and Th1 cell infiltration. : We demonstrate that CRISP3 suppresses tumorigenesis in HGSOC by regulating the PI3K/AKT pathway, and that alterations in its expression correlate with disease progression, supporting its utility as a biomarker. - Source: PubMed
Publication date: 2026/02/20
Ma MingjunTian XiuCao WeiweiWang ChaoZhang YueYang JianiCheng ShanshanGu SijiaLi JianxiaoZhao YaqianShao YaodiHuang ChaoShi ShuoXue RenhaoChu ChenSheng JindanWang Yu