mProX™ Mouse ADGRA1 Stable Cell Line
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- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 Overexpression of ADGRA1 in Neuro2A cells.
In the experimentation, Neuro2A cells were subjected to transfection with pcDNA3.1b (−) and pcDNA3.1-Adgra1 vectors. Subsequent examination of cell lysates from these transfected cells via western blot analysis revealed a noteworthy dosage-dependent inhibition of both the PI3K/AKT/GSK3β and MEK/ERK signaling pathways associated with the expression of ADGRA1. Interestingly, the integrity of the remaining pathways remained unaltered throughout the investigation.
Ref: Zhang, Xiao-Hong, et al. "ADGRA1 negatively regulates energy expenditure and thermogenesis through both sympathetic nervous system and hypothalamus-pituitary-thyroid axis in male mice." Cell Death & Disease 12.4 (2021): 362.
Pubmed: 33824276
DOI: 10.1038/s41419-021-03634-7
Research Highlights
Xiao-Hong Zhang et al. "Increased Anxiety-like Behaviors in Adgra1-/- Male But Not Female Mice are Attributable to Elevated Neuron Dendrite Density, Upregulated PSD95 Expression, and Abnormal Activation of the PI3K/AKT/GSK-3β and MEK/ERK Pathways." Neuroscience, 01 Nov. 2022
In their study, the researchers investigated the role of Adhesion G protein-coupled receptor A1 (ADGRA1) in neurobehaviors of mice. This highly expressed brain receptor belongs to the G protein-coupled receptor (GPCR) family, and its function is not fully understood. Through a comprehensive analysis of ADGRA1-deficient male and female mice, the researchers found that ADGRA1 shows an important role in regulating anxiety, depression, learning, and memory in male mice. They discovered that ADGRA1 deficiency leads to increased anxiety levels and altered synaptic function in male mice, potentially through abnormal activation of the PI3K/AKT/GSK-3beta and MEK/ERK pathways in the amygdala. This suggests that targeting ADGRA1 may have therapeutic potential in the development of anti-anxiety drugs.
Xiao-Hong Zhang et al. "Increased Anxiety-like Behaviors in Adgra1-/- Male But Not Female Mice are Attributable to Elevated Neuron Dendrite Density, Upregulated PSD95 Expression, and Abnormal Activation of the PI3K/AKT/GSK-3β and MEK/ERK Pathways." Neuroscience, 01 Nov. 2022
Pubmed:
36115515
DOI:
10.1016/j.neuroscience.2022.09.003
Tingting Liu et al. "A Genome-Wide Association Study of Prediabetes Status Change." Frontiers in endocrinology, 2022
The first genome-wide association study of prediabetes status change was conducted by a team of researchers. The study included 900 White participants from the Atherosclerosis Risk in Communities (ARIC) study. Using logistic regression models, the researchers performed a single nucleotide polymorphism (SNP)-based analysis while controlling for age, gender, body mass index, and genetic principal components. They also conducted a gene-based analysis by combining SNP-based p values using an effective Chi-square test method. Promising SNPs (p < 1x10^-5) and genes (p < 1x10^-4) were further evaluated for replication in 514 White participants from the Framingham Heart Study (FHS). In order to account for familial correlations, the researchers used generalized estimation equation models for SNP-based analyses in the FHS. They then combined the analysis results from both the ARIC and FHS studies using an inverse-variance-weighted meta-analysis method for SNPs and Fisher's method for genes. The researchers were able to identify 5 novel genes associated with prediabetes status change, including SGCZ, HPSE2, ADGRA1, GLB1L3, and PCSK6. These genes were found to be highly expressed in tissues related to diabetes development. However, no novel loci were identified in the single SNP-based analysis. The researchers recommend that future large-scale genomic studies are needed to further understand prediabetes status change.
Tingting Liu et al. "A Genome-Wide Association Study of Prediabetes Status Change." Frontiers in endocrinology, 2022
Pubmed:
35769078
DOI:
10.3389/fendo.2022.881633