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
- 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 - To investigate the molecular interaction patterns between CD46/TREM1 and LC3B/ATG5 in the development of oral squamous cell carcinoma (OSCC), providing novel targets for elucidating the mechanism of inflammatory-to-cancer progression and for the early diagnosis and treatment of OSCC. - Source: PubMed
Publication date: 2025/12/03
Xie HuixianXu YingjieCong BeibeiGao MeihuaWang Wanchun - Hypertrophic cardiomyopathy (HCM) is a prevalent cardiovascular disorder affecting populations worldwide, characterized by abnormal thickening of the heart muscle.(Supporting S1) The development of HCM is influenced by multiple factors, including genetic mutations, geographical conditions, lifestyle, and environmental exposures. The availability of extensive genomic datasets in public repositories provides an opportunity to identify potential genetic contributors and functional biomarkers associated with HCM. Previous studies have highlighted the pivotal role of the MYBPC3 gene in the pathogenesis of HCM. In this study, computational analyses were performed to predict gene mutations and functional biomarkers using RNA-sequencing and whole exome sequencing datasets. A total of 12 RNA-sequencing samples, comprising four healthy controls and eight HCM cases, along with 12 exome sequencing datasets, were retrieved from the Gene Expression Omnibus (GEO) database. RNA-sequencing analysis identified the top 20 differentially expressed genes associated with HCM, including MIB2, ZBTB48, MYBPC3, PRPF40B, CD27-AS1, MYH7, WDR90, KDM8, BCAM, ZSWIM9, KANK3, CCDC85A, ZNF512B, POLR3H, NUP210, PSMG4, GPLD1, GNL1, SH2D3C, and COL4A6. Among these, MYH7 exhibited the highest expression level, showing strong similarity to MYBPC3 in its association with HCM. Whole exome sequencing analysis further identified a panel of variant genes including MYBPC3, MYH6, MYH7, TNT, Titin, Desmin, ACE1, TGF-beta, Ang-2, SGCG, SGCA, DMD, and LaminA/C, all previously implicated in HCM pathophysiology. This integrative study underscores the correlation between differential gene expression patterns and clinical variants in HCM, providing valuable insights into the molecular mechanisms underlying the disease. - Source: PubMed
Publication date: 2025/11/21
Cn PrashanthaR RamachandraNm GuruprasadReddy Vaddi Damodara