mProX™ Human ADGRF1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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 ADGRF1 Stable Cell Line (S01YF-0923-PY161). Click the button above to contact us or submit your feedback about this product.
Karen (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Amanda (Verified Customer)
Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 GPR110 (ADGRF1) knockdown resulted in a significant decrease in number of colonies in parental as well as LTR derivatives of BT474 and SKBR3 cell line models.
In HER2+ breast cancer cell lines, the inhibition of anchorage-independent cell growth through GPR110 knockdown exhibited greater efficacy in LTR derivatives than in the parental cells, as determined by the soft agar assay. Two distinct siRNAs targeting GPR110 resulted in a significant reduction in colony numbers in both BT474 and SKBR3 models, encompassing both parental and LTR derivatives. However, the reduction was notably more prominent in the LTR cells when compared to their parental counterparts. This observed effect was statistically significant (* indicating P<0.05), as determined by Repeated Measures ANOVA followed by Dunnett's post hoc test.
Ref: Bhat, Raksha R., et al. "GPCRs profiling and identification of GPR110 as a potential new target in HER2+ breast cancer." Breast cancer research and treatment 170 (2018): 279-292.
Pubmed: 29574636
DOI: 10.1007/s10549-018-4751-9
Research Highlights
Wu M, et al. "Amelioration of non-alcoholic fatty liver disease by targeting adhesion G ." eLife, 2023.
Recent research has shown that the adhesion G protein-coupled receptor F1 (Adgrf1) is an oncogene. This evidence is based on the high expression of Adgrf1 in various cancer types and its ability to promote cell migration, invasion, and proliferation. Adgrf1 is predominantly expressed in the liver of healthy individuals, but its function in this organ is still unknown. Interestingly, the expression of Adgrf1 is significantly decreased in obese individuals. To investigate its potential role in liver metabolism, the researchers utilized a recombinant adeno-associated virus-mediated gene delivery system and antisense oligonucleotide to manipulate Adgrf1 expression in obese mice. Their study found that Adgrf1 expression was directly correlated to fat content in the liver and that it regulated fat metabolism through controlling the expression of a key enzyme, stearoyl-coA desaturase 1. These results were confirmed in human liver tissue samples from non-alcoholic fatty liver disease patients. The research was supported by various grants and proposes a new therapeutic approach for treating NAFLD by targeting Adgrf1.
Pubmed:
37580962
DOI:
10.7554/eLife.85131
Banerjee S, et al. "Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation ." Journal of neuroinflammation, 2023.
In this study, the authors examined the effects of acute ethanol exposure and GPR110 activation on neuroinflammation, a key factor in various neurodegenerative diseases. The aim was to determine the impact of single-dose ethanol exposure on the mechanisms of neuro-inflammation and how GPR110 activation could mitigate its effects. In vivo and in vitro experiments were conducted using mice to assess gene and protein expressions, as well as microglial activation. Results showed that ethanol exposure prior to lipopolysaccharide (LPS) injection amplified pro-inflammatory cytokine expression, while GPR110 ligand synaptamide reduced these effects in wild type (WT) mice but not in knockout (KO) mice. This demonstrates the potential therapeutic role of GPR110 activation in mitigating ethanol-induced inflammation.
Pubmed:
37580715
DOI:
10.1186/s12974-023-02868-w