mProX™ Human ADORA2A Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Knockdown of ADORA2A-AS1 inhibits cell proliferation.
The CCK8 assessment revealed diminished OD values in cells silenced for ADORA2A-AS1 through specific si-transfection compared to their negative control counterparts.
Ref: Liu, Yabo, et al. "Knockdown of ADORA2A antisense RNA 1 inhibits cell proliferation and enhances imatinib sensitivity in chronic myeloid leukemia." Bioengineered 13.2 (2022): 2296-2307.
Pubmed: 35034552
DOI: 10.1080/21655979.2021.2024389
Research Highlights
Allard B, et al. "Adenosine A2A receptor is a tumor suppressor of NASH-associated hepatocellular ." Cell reports. Medicine, 2023.
The inhibition of adenosine A2A receptor (A2AR) has shown potential for cancer immunotherapy and is currently being evaluated in clinical trials. A study was conducted to investigate the role of A2AR in hindering the development of hepatocellular carcinoma (HCC). It was found that A2AR is responsible for anti-obesogenic and anti-inflammatory functions, which restrict HCC development. Mice with Adora2a deletion displayed obesity, non-alcoholic steatohepatitis (NASH), and systemic inflammation, leading to spontaneous HCC and promoting DMBA or DEN-induced HCC. The conditional deletion of Adora2a revealed the critical involvement of myeloid and hepatocyte-derived A2AR signaling in restraining HCC by limiting hepatic inflammation and steatosis. Interestingly, the impact of A2AR pharmacological blockade on HCC development was found to be dependent on pre-existing NASH. This finding was also observed in humans, where low ADORA2A gene expression in human HCC was associated with cirrhosis, hepatic inflammation, and poor survival. The study discovered a previously unknown tumor-suppressive role for A2AR in the liver and suggests caution in using A2AR antagonists in patients with NASH and NASH-associated HCC.
Pubmed:
37729873
DOI:
10.1016/j.xcrm.2023.101188
Cuaycal AE, et al. "Lactobacillus johnsonii N6.2 phospholipids induce immature-like dendritic cells ." Gut microbes, 2023.
Dysbiosis, a disturbance in the gut microbiota composition, has been linked to both acute and chronic illnesses. However, the biological mechanisms connecting gut dysbiosis to systemic inflammatory diseases remain unclear. Phospholipids (PLs) serve as precursors for inflammatory and resolving molecules and their disruption is associated with ailments such as cancer. Specifically, unique gut microbial-derived lipids have the ability to modulate the host's immune system. The Gram-positive symbiont Lactobacillus johnsonii N6.2 exhibits probiotic properties and has been shown to reduce the incidence of autoimmunity and promote anti-inflammatory responses in animal and human studies. Through bioassay-guided fractionation methods with bone marrow-derived dendritic cells (BMDCs), researchers found that purified lipids from L. johnsonii N6.2 induced a transcriptional profile similar to that of migratory dendritic cells. RNA sequencing analysis showed upregulation of genes related to both maturation and migration in BMDCs stimulated with L. johnsonii N6.2 total lipids, as well as various immunoregulatory genes. Further research revealed that PLs were the bioactive lipids responsible for triggering the BMDCs' response. Additionally, blocking a key surface receptor known as Toll-like receptor 2 resulted in enhanced pro-inflammatory effects, while inhibiting a specific pathway restricted expression of certain inflammatory genes. Morphologically, PL-stimulated BMDCs exhibited an immature-like phenotype and had elevated levels of surface ICAM-1. These findings provide insight into the immunoregulatory capabilities of Gram-positive, gut microbial-derived phospholipids on the innate immune response.
Pubmed:
37675983
DOI:
10.1080/19490976.2023.2252447