OSM & COL4A6 Protein Protein Interaction Antibody Pair
- Known as:
- OSM & COL4A6 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0105
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- OSM & COL4A6 Protein Interaction Antibody Pair
Related genes to: OSM & COL4A6 Protein Protein Interaction Antibody Pair
- Gene:
- COL4A6 NIH gene
- Name:
- collagen type IV alpha 6 chain
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-01
- Date modifiied:
- 2019-04-23
Related products to: OSM & COL4A6 Protein Protein Interaction Antibody Pair
Related articles to: OSM & COL4A6 Protein Protein Interaction Antibody Pair
- Pulmonary hypertension (PH) is a progressive disease that severely compromises right ventricular function, characterized by two major pathological features: pulmonary arterial constriction and pulmonary arterial remodeling. Bellidifolin (BEL), a natural ketone compound, exhibits potent anti-inflammatory and antioxidant effects; however, its role in PH remains unexplored. This study evaluated the impact of BEL on the two pathological processes: pulmonary arterial constriction and pulmonary arterial remodeling. First, the effects of BEL on pulmonary arterial constriction were evaluated using wire myography. The study revealed that BEL (6-96 μmol/L) inhibited the contraction response of intact endothelial and denuded pulmonary arterial rings precontracted with norepinephrine (1 μmol/L) in a concentration-dependent manner. BEL (90 μmol/L) suppressed pulmonary constriction induced by intracellular calcium release and extracellular calcium influx. In cellular experiments, BEL inhibited the proliferation, migration, and phenotypic transformation of pulmonary arterial smooth muscle cells (PASMCs) induced by 10 μmol/L CoCl (72 h), as evidenced by upregulation of the contractile phenotype markers α-SMA and SM22α and downregulation of the synthetic phenotype markers OPN, vimentin, and PCNA. Multi-omics analysis identified Aldh1A1, Mgp, Col4a6, and Igfbp5 as significantly enriched candidates. Among these candidates, Cellular Thermal Shift Assay demonstrated that BEL enhanced the thermal stability of Igfbp5 in PASMCs, suggesting that Igfbp5 may be a potential direct target of BEL. Moreover, KEGG pathway analysis revealed significant enrichment of the PI3K-AKT-mTOR pathway, which is known to be involved in cell proliferation and is regulated by Igfbp5. BEL may inhibit the PI3K-AKT-mTOR pathway by suppressing Igfbp5. The results indicate that BEL may regulate Igfbp5 to inhibit the PI3K-AKT-mTOR pathway, thereby exerting anti-proliferative and inhibitory effects on migration and phenotypic transformation. - Source: PubMed
Publication date: 2026/07/19
Hu QiuqinWang HongmaiQiao YujieXia QingqingHu JiachengGai XiangyunLi YulinChen TaoLi Zhanqiang - Idiopathic Pulmonary Fibrosis (IPF) is a progressive interstitial lung disease characterized by aberrant extracellular matrix remodeling. While type I and III collagens are known contributors, the broader transcriptional landscape of diverse collagen genes in IPF fibroblasts and their potential associations with clinical outcomes remain incompletely understood. This study aimed to comprehensively characterize gene expression of collagen genes in IPF fibroblasts and to explore its relationship with patient survival. - Source: PubMed
Publication date: 2026/06/22
Seo Eun-JeongPark Seung-LeeKim Min-KyungChoi Jae-SungHwang Hun-GyuKim Jung-HyunChang Hun-SooPark Choon-SikLee Jong-Uk - Post-traumatic joint contracture (PTJC), characterized by progressive fibrosis, is a frequent complication following joint injury. Nevertheless, the molecular mechanisms driving its progression remain elusive. To address this, our study aims to delineate the dynamic transcriptomic alterations during arthrofibrosis development and to identify potential biomarkers associated with PTJC. - Source: PubMed
Publication date: 2026/02/23
Wang YijiaZeng HongLi ZilinCheng LiZhu XintongLiang MengtingFang ZhongyiLai ShujingCai Bin - The progression of gastric cancer (GC) is profoundly influenced by extracellular matrix (ECM) remodeling within the tumor microenvironment (TME); however, the compartment-specific roles of key ECM proteins (e.g., epithelium vs. stroma) remain incompletely understood. By integrating multi-omics bulk transcriptomic data with single-cell sequencing data, we observed a bulk-compartment discrepancy for COL4A6: COL4A6 carries an inverse association (OR < 1) in bulk transcriptome-based risk models, whereas its protein is markedly upregulated and predominantly localized to the CAF compartment in clinical specimens. We constructed a Matrisome Risk Score (MRS) model and identified ECM subtypes with distinct prognoses, confirming that the high-matrix subtype (MC1) is closely associated with immunosuppression and chemotherapy resistance. Functional experiments demonstrated that COL4A6 from CAF-enriched fibroblast cultures promotes tumor progression and stromal remodeling by inducing CAF activation (upregulation of α-SMA and FAP, remodeling of stress fibers) and promoting EMT in gastric cancer cells. Collectively, our findings support a compartment-dependent model in which epithelial silencing/loss may bias bulk mRNA associations, whereas CAF-compartment COL4A6 accumulation is a functional driver of GC progression. This highlights CAF-compartment COL4A6 as a potential target for therapies aimed at ECM remodeling within the TME. - Source: PubMed
Publication date: 2026/02/24
Sun QiangWei ShuxunYao JunWang FuqinWu HanHu ZunqiZhang XinYang DejunWang WeijunXu Kai - Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disorder characterized by the development of fluid-filled cysts in the kidneys. Tolvaptan is the only FDA-approved drug to treat ADPKD, which has significant side effects, prompting the need for safer novel treatments. Given the pathophysiological similarities between ADPKD and malignant tumors, repurposing anti-cancer compounds signifies a promising strategy. In this study, we explored the therapeutic potential of a novel spirocyclic compound 4l with anti-cancer effects in ADPKD. Our preliminary results demonstrated that 4l reduced cell viability in a dose-dependent manner and inhibited cyst growth in 3D culture. Transcriptomic analysis indicated hypoxia-related pathways, mitophagy, and necroptosis (Ripk1 and Mlkl activation) as key mechanisms, alongside cell cycle arrest via Cdkn1a-Rb1 pathway and inhibition of fibrotic markers (Tgfb2 and Col4a6). To strengthen the translational relevance, we established an ADPKD iPSC-derived renal epithelial model, confirming successful differentiation into proximal tubule/collecting duct-like cells (LTL/DBA staining and upregulation of renal markers AQP1, LRP2, and GATA3). Differentiated ADPKD cells exhibited hyperproliferation, reflecting the cystic epithelium observed in vivo. 4l treatment significantly reduced cell viability without immediate cytotoxicity, suggesting a cytostatic effect. Our findings emphasize 4l as a multi-target agent, proficient in reducing cystogenesis through mitophagy induction, modulation of necroptosis, cell cycle inhibition, and suppression of fibrosis. 4l's efficiency across 2D, 3D, and iPSC-derived models highlights its therapeutic potential. This study also recognizes mitophagy and necroptosis as novel targets in ADPKD and corroborates iPSC-derived renal cells as a powerful platform for drug screening. - Source: PubMed
Devapatla PallaviTeng Yu-HanSettipalli Poorna ChandrasekharYeruva Pavan Kumar ReddyHsieh-Li Hsiu MeiShaik Anwar