mProX™ Human TLR5 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Immune Checkpoint Cell Lines
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Published Data
Fig.1 TLR5 downregulation promoted EMT in 4T1 cells.
A western blot analysis was conducted in triplicate to detect the protein expression levels of TLR5, E-cadherin, N-cadherin, vimentin, fibronectin, TRAF6, SOX2 and Twist1 in TLR5 positive and TLR5 negative 4T1 cells. The results demonstrated statistically significant differences (p < 0.05) in the expression of all proteins examined between the two cell types, with TLR5 positive 4T1 cells exhibiting higher levels of mesenchymal markers and lower levels of epithelial markers. Further investigation into the phenotypic and functional variances induced by TLR5 signaling in this murine breast cancer model is warranted.
Ref: Shi, Dai, et al. "TLR5: A prognostic and monitoring indicator for triple-negative breast cancer." Cell Death & Disease 10.12 (2019): 954.
Pubmed: 31852883
DOI: 10.1038/s41419-019-2187-8
Research Highlights
Bhardwaj, Ananya. et al. "Role of toll-like receptor in the pathogenesis of oral cancer." Cell biochemistry and biophysics, 2023.
The significance of toll-like receptors as vital components of innate immunity is well recognized. These receptors are classified as pattern recognition receptors as they have the ability to identify specific molecules, known as pathogen-associated molecular patterns, on pathogens. Upon recognition, they release chemical signals that promote an inflammatory response. Toll-like receptors play a crucial role in eliminating infected cells and preventing the spread of infection, making them potential targets for cancer research. Oral cancer is a prevalent issue in many countries, and it has been found that toll-like receptors are involved in its development. Certain variations in toll-like receptor genes have been linked to an increased susceptibility to oral cancer. By identifying toll-like receptors and their associated genotypes, they can potentially serve as biomarkers for this disease. Recent studies have also shown that specific toll-like receptors, such as TLR7 and TLR5, inhibit the progression of oral cancer, while others, such as TLR4 and TLR2, are linked to its advancement. Therefore, toll-like receptors have the potential to be targeted for the development of effective therapeutic strategies for oral cancer.
Bhardwaj, Ananya. et al. "Role of toll-like receptor in the pathogenesis of oral cancer." Cell biochemistry and biophysics, 2023.
Pubmed:
37853249
DOI:
10.1007/s12013-023-01191-8
Gautam, Priyanka. et al. "Genome-wide expression profiling reveals novel biomarkers in epithelial ovarian cancer." Pathology, research and practice, 2023.
Epithelial ovarian cancer (EOC) is a highly aggressive and common form of cancer affecting women globally. Understanding the pathophysiology of EOC is crucial in order to identify new biomarkers for early detection, management, and prognostication. In this study, the researchers aimed to analyze RNA-seq data to investigate the transcriptomic landscape and biomarkers. This was followed by further analysis using Protein Protein network, which identified the top 10 Differentially Expressed Genes (DEGs). The team also conducted KEGG pathway enrichment analysis, revealing the significant enrichment of DEGs in basal cell carcinoma, cell cycle, and FoxO signalling pathway. To validate their findings, the researchers used QRT-PCR and TCGA database. Correlation studies between gene expression and clinical characteristics were also performed, as well as survival analysis. This study identified 8 DEGs (CDKN1A, BCL6, CDC45, WNT2, TLR5, AQP5) and 2 novel DEGs (CSN1S1 and NKILA) that showed significant correlations with EOC characteristics. These DEGs could potentially be used as biomarkers and treatment targets, and further research on their functional outcomes is warranted.
Gautam, Priyanka. et al. "Genome-wide expression profiling reveals novel biomarkers in epithelial ovarian cancer." Pathology, research and practice, 2023.
Pubmed:
37844484
DOI:
10.1016/j.prp.2023.154840