mProX™ Human BDKRB1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Effect of overexpression of Bdkrb1 gene in RAW264.7 cells on NF-κB activation.
Plasmids with full cDNAs of specified genes, or a negative control, positioned after a certain promoter, were co-introduced with two other plasmids. Post-transference, cells received a specific stimulation for a set duration, after which their immune reactivity was gauged via luciferase output. Averages from three separate tests, showcasing variability, are illustrated; a delineated threshold highlights a twofold augmentation in a particular immune response due to gene amplification. Statistical significance is denoted for certain comparisons.
Ref: Alper, Scott, et al. "Novel innate immune genes regulating the macrophage response to Gram positive bacteria." Genetics 204.1 (2016): 327-336.
Pubmed: 27356610
DOI: 10.1534/genetics.115.185314
Research Highlights
Torres-Mendez JK, et al. "Nicotinamide Prevents Diabetic Brain Inflammation via NAD+-Dependent ." Nutrients, 2023.
In this study, the effects of dietary nicotinamide (NAM) supplementation in treating brain inflammation in type 1 diabetic (T1D) mice were investigated. The T1D mice were divided into three groups: non-treated, low-dose NAM (NAM LD), and high-dose NAM (NAM HD). The results showed that the markers of inflammation and microglial activation were significantly reduced in the NAM-treated mice compared to the non-treated T1D mice. Moreover, the nuclear NFκB (p65) signaling was also alleviated in the NAM-treated diabetic mice. These findings indicate that dietary NAM supplementation can prevent brain inflammation through NAD+-dependent deacetylation mechanisms, possibly through increased sirtuin signaling.
Pubmed:
37513501
DOI:
10.3390/nu15143083
Punapart M, et al. "Chronic Stress Alters Hippocampal Renin-Angiotensin-Aldosterone System Component ." Genes, 2023.
Biallelic mutations in the gene WFS1 have been identified as the cause of Wolfram syndrome (WS), a rare neurodegenerative disorder with no current cure. Previous studies have shown that WFS1 deficiency can disrupt the renin-angiotensin-aldosterone system (RAAS). In a rat model of WS, our team observed downregulation of key receptors in various organs, including angiotensin II receptor type 2 (Agtr2) and bradykinin receptor B1 (Bdkrb1). Our latest research reveals dysregulation of RAAS components in neural tissue from older WS rats, unaffected by treatments such as liraglutide (LIR), 7,8-dihydroxyflavone (7,8-DHF), or a combination of both. Furthermore, we observed decreased expression of angiotensin II receptor type 1a (Agtr1a), angiotensin II receptor type 1b (Agtr1b), Agtr2, and Bdkrb1 in the hippocampus of WS rats experiencing long-term experimental stress. These results suggest that under chronic stress, Wfs1 deficiency impairs RAAS functioning and contributes to neurodegeneration in WS.
Pubmed:
37107585
DOI:
10.3390/genes14040827