mProX™ Human CHRM2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Made to Order Inquiry
InquiryBased on this stable cell line, we also provide cell-based in vitro assays to evaluate the effects of your compounds or antibodies.
Sub Cat | Product Name | Target Protein Species | Host Cell Type | Assay Types | Inquiry | Datasheet |
---|---|---|---|---|---|---|
S01YF-1122-KX635 | Magic™ Rat CHRM2 in Vitro Calcium Flux Assay | Rat | CHO-K1-Gα16 | Calcium Flux Assay |
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Published Data
Fig.1 Quantitative PCR revealed that CHRM2 and miR-490-3p were downregulated in the GBM cell lines U87MG and A172.
In two GBM cell lines, namely U87MG and A172, CHRM2 and miR-490-3p expression levels were assessed through qRT-PCR analysis. It was evident that both CHRM2 and miR-490-3p exhibited significant downregulation. For normalization of miRNA and mRNA data, RNU6B (U6) and GAPDH were utilized as controls. The data were processed using the 2−ΔΔCt method, and the graphical representation reflects the mean ± SD derived from a minimum of three independent experiments (*p < 0.05, **p < 0.01).
Ref: Vinchure, Omkar S., et al. "Polycomb complex mediated epigenetic reprogramming alters TGF-β signaling via a novel EZH2/miR-490/TGIF2 axis thereby inducing migration and EMT potential in glioblastomas." International journal of cancer 145.5 (2019): 1254-1269.
Pubmed: 31008529
DOI: 10.1002/ijc.32360
Research Highlights
Tegegne BS, et al. "Phenotypic but not genetically predicted heart rate variability associated with ." Communications biology, 2023.
The link between low heart rate variability (HRV) and mortality has been well documented. However, the specific molecular mechanisms behind this association remain unclear. To address this gap, a study was conducted to identify new genetic variations associated with HRV and investigate their relationship with mortality. Using data from the UK Biobank, 46,075 individuals of European ancestry were included in a genome-wide association study. The study identified 17 genetic variants in 16 loci that were significantly associated with HRV traits. Interestingly, eight of these loci (RNF220, GNB4, LINCR-002, KLHL3/HNRNPA0, CHRM2, KCNJ5, MED13L, and C160rf72) have not been previously reported. A follow-up analysis examining the relationship between HRV and mortality over a median follow-up of seven years found that individuals with lower HRV were at a higher risk of death from any cause. However, genetically predicted HRV, as determined by genetic risk scores, was not found to be associated with mortality. These results provide important insights into the underlying biological mechanisms of HRV and highlight the significance of the cardiac autonomic nervous system in predicting mortality.
Pubmed:
37803156
DOI:
10.1038/s42003-023-05376-y
Zeng H, et al. "Unbiased multitissue transcriptomic analysis reveals complex neuroendocrine ." Journal of neuroinflammation, 2023.
Spinal cord injury (SCI) is a devastating central nervous system disease that results in loss of sensory and motor function below the level of injury. A common secondary effect of SCI is SCI-induced immunodeficiency syndrome (SCI-IDS), which increases the risk of infection and worsens neurological dysfunction. Previous studies have shown that SCI-IDS is an independent risk factor for poor neurological outcomes, particularly in cases of injury above the T5 levels. While the mechanism behind SCI-IDS is unclear, research utilizing experimental rats has revealed changes in neuroendocrine-immune regulation following SCI. Atrophy of secondary immune organs and elevated cortisol levels suggest impaired immune function and autonomic disturbance. A differential gene regulation analysis showed disrupted inflammatory and circadian rhythm pathways, potentially contributing to a systemic suppression of peripheral adaptive immunity. Ultimately, SCI-induced neuroinflammation impedes nerve repair and increases susceptibility to infection, leading to poor neurological prognosis.
Pubmed:
37775760
DOI:
10.1186/s12974-023-02906-7