Rat COL9a1 ELISA
- Known as:
- Rat COL9a1 Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-32227
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Rat COL9a1 ELISA
Related genes to: Rat COL9a1 ELISA
- Gene:
- COL9A1 NIH gene
- Name:
- collagen type IX alpha 1 chain
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6q13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-08
- Date modifiied:
- 2016-07-20
Related products to: Rat COL9a1 ELISA
Related articles to: Rat COL9a1 ELISA
- Chronic Chagas cardiomyopathy (CCC) remains a major cause of heart failure (HF)-related mortality in Latin America and is increasingly recognized as a global health concern. Prognostic models developed in non-Chagas populations often perform poorly in CCC, highlighting the need for etiology-specific risk stratification. - Source: PubMed
Publication date: 2026/06/08
Patané José S LGiugni Fernando RRosa Rogério SMarcondes-Braga Fabiana GMansur Alfredo JPereira Alexandre CKrieger Jose E - Mechanical loading is essential for the assembly and maintenance of the articular cartilage extracellular matrix (ECM), whereas alterations in ECM composition profoundly affect cartilage mechanics and function. Type IX collagen is a heterotrimeric fibril-associated collagen with interrupted triple helices (FACIT) that is covalently linked to type II collagen. It restricts lateral fibril growth and mediates interactions with other ECM components. Although type IX collagen expression is mechanosensitive and implicated in cartilage mechanotransduction, its precise functional role is not yet fully understood. This study investigated the combined effects of type IX collagen deficiency and moderate mechanical loading on articular and growth plate cartilage. Twelve-week-old female wild-type (WT) and mice were randomly assigned to control (CON) or forced running exercise (EXE) groups ( = 10-12 per group). EXE animals underwent treadmill training for 6 wk (20% incline, 18 m/min, 40 min/day, 5 days/wk). Type IX collagen deficiency resulted in an abnormal growth plate architecture and a reduction of all matrilins and cartilage oligomeric matrix protein (COMP) in articular cartilage. Moderate forced running exercise induced a significant increase ( < 0.05) in cartilage thickness at the lateral femoral condyle and altered ECM composition in mice, without evidence of cartilage degeneration. WT mice showed no comparable structural changes. In conclusion, moderate mechanical loading elicits localized, nondegenerative, structural and molecular adaptations in articular cartilage and only modestly modulates the cartilage phenotype associated with type IX collagen deficiency. These findings suggest a limited, yet context-dependent role of type IX collagen in cartilage mechanoadaptation. Moderate forced running exercise only slightly enhances the cartilage phenotype in aging female type IX collagen knockout mice and induces local, nondegenerative, structural and molecular adaptations in the articular cartilage ECM. Alterations in the cartilage phenotype do not depend on the age of the mice. - Source: PubMed
Publication date: 2026/05/19
Weyers MiriamLi ThomasDreiner MarenMählich DanielaLorenz Charlottede Roy LuisaZigrino PaolaHan LinBrachvogel BentZaucke FrankNiehoff Anja - Metastasis and recurrence of triple-negative breast cancer (TNBC), are mainly attributed to the presence of dormant cancer cells (DCCs), yet the molecular mechanisms governing the maintenance and reactivation of DCC dormancy remain poorly elucidated. This study identified collagen IX alpha 1 chain (Col9a1) as a gene specifically expressed in TNBC dormant cells and confirmed that it is a key molecule sustaining DCC dormancy. Mechanistic studies revealed that COL9A1 sustains TNBC cell dormancy by suppressing the FAK-AKT-p27 signaling axis, thereby inducing G0/G1 cell cycle arrest. Col9a1 knockdown reactivates DCCs, and the reactivated cells recruit natural killer (NK) cells by upregulating retinoic acid early inducible 1γ (RAE-1γ) and secreting proinflammatory cytokines (IL-15/IL-18), thus abrogating the immune evasion capacity of DCCs and enhancing the chemosensitivity of reactivated TNBC cells to docetaxel. This study uncovers a novel mechanism by which COL9A1 regulates TNBC cell dormancy, indicating that COL9A1 can serve as a potential biomarker for assessing the dormant phenotype of TNBC and predicting tumor recurrence, as well as a novel therapeutic target for TNBC. This study also provides preclinical evidence for developing COL9A1-targeted combination therapies for TNBC. - Source: PubMed
Publication date: 2026/05/18
Liu WeiSong Zhe - Presently, we investigated hypothesized roles and mechanisms of cell type-specific, selective activation of different vascular NOX (NADPH oxidase) isoforms in obesity and metabolic syndrome. - Source: PubMed
Publication date: 2026/04/23
Huang KaiHuang YuanliZhang YuhanZhang YixuanHatch Nicholas WFreed Julie KCai Hua - Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy, and cervical lymph node metastasis significantly impacts patient prognosis. This study aimed to develop interpretable artificial intelligence models based on transcriptomics to predict PTC occurrence and cervical lymph node metastasis, while exploring the heterogeneity of risk factors across different regions. We obtained 419 samples from the GEO database, originating from Asia, Europe, and America, comprising 158 normal samples, 203 PTC samples, and 58 metastatic samples. After comparing multiple machine learning algorithms, deep neural networks (DNN) demonstrated superior performance and were used to construct the PTC diagnostic and metastasis predictive models. The optimized PTC diagnostic model achieved an AUC of 0.987 with an accuracy of 0.945, while the PTC metastasis predictive model reached an AUC of 0.998 with an accuracy of 0.987. Model interpretation using SHapley Additive exPlanations (SHAP) and Kolmogorov-Arnold Networks (KAN) methods identified SYT1, REN, CNTN5, and ADAM12 as critical features for PTC diagnosis, whereas COL9A1, CYP4F3, and GAD1 were key predictors for PTC metastasis. Stratification analysis revealed regional differences in risk factors for PTC occurrence, while factors promoting PTC metastasis exhibited commonalities across different regions. Pathway enrichment analysis indicated that regulation of hormone levels and cell population proliferation were common pathways involved in both PTC occurrence and metastasis. Finally, we developed online predictive platforms based on the Streamlit framework to facilitate transparent model exploration and risk estimation. These tools are publicly accessible research-use prototypes intended for model demonstration and interpretability visualization. Because they require standardized gene-expression inputs and have not undergone prospective clinical validation, they should not be used as standalone tools for clinical diagnosis, risk stratification, or treatment decision-making. Overall, our findings identify candidate transcriptomic markers associated with PTC occurrence and lymph node metastasis and provide a basis for future translational evaluation. - Source: PubMed
Publication date: 2026/04/18
Zhang ZhigangLiu HongyuZhao ZhengTan GuoyuZhao YangLiu Xun