mProX™ Human ANO1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryProduct Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
There are currently no Customer reviews or questions for mProX™ Human ANO1 Stable Cell Line (S01YF-1023-PY257). Click the button above to contact us or submit your feedback about this product.
Casey Davis (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Morgan Miller (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 The phosphorylation of FADD is promoted by the silencing of endogenous ANO1.
In the left panel, immunoblots were observed in lysates derived from PC-3 cells that had been transfected with ANO1-siRNAs or NCsi for a duration of 72 hours. On the right panel, lysates from normal RWPE-1 cells were utilized for the stable expression of ANO1, while the IRES2-GFP vector was employed as the control. A bar graph was constructed to display the quantitative analysis of phospho-FADD and total FADD protein expression in PC-3 cells with ANO1 knockdown.
Ref: Song, Yan, et al. "Inhibition of ANO1/TMEM16A induces apoptosis in human prostate carcinoma cells by activating TNF-α signaling." Cell Death & Disease 9.6 (2018): 703.
Pubmed: 29899325
DOI: 10.1038/s41419-018-0735-2
Research Highlights
Wang, Ying. et al. "Researches of calcium-activated chloride channel ANO1 intervening amyotrophic lateral sclerosis progression by activating EGFR and CaMKII signaling." Brain research bulletin, 2023.
According to recent studies, ANO1 has been found to have a strong correlation with the activation of EGFR and CaMKII. However, in amyotrophic lateral sclerosis (ALS) models, both EGFR and CaMKII exhibit low levels of activation. Based on this observation, the researchers conducted experiments to investigate the potential protective function of ANO1 on motor neurons in ALS, through its ability to activate EGFR and CaMKII. These findings suggest a potential therapeutic target for ALS treatment.
Wang, Ying. et al. "Researches of calcium-activated chloride channel ANO1 intervening amyotrophic lateral sclerosis progression by activating EGFR and CaMKII signaling." Brain research bulletin, 2023.
Pubmed:
37858681
DOI:
10.1016/j.brainresbull.2023.110792
J Hancock, Edward. et al. "A dual-clock-driven model of lymphatic muscle cell pacemaking to emulate knock-out of Ano1 or IP3R." The Journal of general physiology, 2023.
The lymphatic system is known to be involved in a variety of diseases, including obesity, cardiovascular disease, and neurological disorders like Alzheimer's disease. The returning of fluid through the lymphatic vascular system is primarily facilitated by muscle contractions in the walls of the vessels, which are driven by electrochemical oscillations that cause rhythmic action potentials and surges in calcium ion concentration. However, there is still limited understanding of the underlying mechanisms involved in these events, making it difficult to develop effective pharmacological treatments. In a previous study, the researchers proposed a model where autonomous oscillations in the membrane potential (M-clock) drove passive oscillations in calcium concentration (C-clock). In this paper, the authors extend their model to include active coupled M-clock and C-clock oscillators, which are both responsible for driving the action potentials. This extension was made by modifying the model's description of the IP3 receptor, a crucial mechanism in the C-clock. Through phase-plane analysis, the researchers were able to explain the coupling mechanisms of the dual clocks. The model has the potential to aid in understanding the mechanisms and identifying targets for pharmacological treatment of lymphoedema.
J Hancock, Edward. et al. "A dual-clock-driven model of lymphatic muscle cell pacemaking to emulate knock-out of Ano1 or IP3R." The Journal of general physiology, 2023.
Pubmed:
37851028
DOI:
10.1085/jgp.202313355