mProX™ Human CHRM1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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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-KX630 | Magic™ Rat CHRM1 in Vitro Calcium Flux Assay | Rat | CHO-K1 | Calcium Flux Assay |
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Published Data
Fig.1 A375 cell proliferation was inhibited by CRISPR-Cas9-mediated CHRM1 knockdown.
To further corroborate the findings observed using siRNA, a complementary gene-editing technique involving CRISPR-Cas9 was employed, using guide RNAs designed to target CHRM1 in A375 melanoma cells. While achieving complete CHRM1 knockout proved elusive, possibly due to the hypotriploid karyotype characteristic of this model, CRISPR-Cas9-mediated CHRM1 reduction nonetheless substantially impeded the antiproliferative effects induced by DOPA/carbidopa. The proliferation of A375 cells, subjected to CRISPR-Cas9-mediated CHRM1 depletion, both with and without CHRM1 transgene rescue, was assessed following treatment with a vehicle control or 25 µM L-DOPA and 6.25 µM carbidopa. This experiment was conducted with a sample size of n=5.
Ref: Doepner, Miriam, et al. "CHRM1 is a Druggable Melanoma Target Whose Endogenous Activity is Determined by Inherited Genetic Variation in DOPA Production." bioRxiv (2021): 2021-03.
Pubmed: NA
DOI: 10.1101/2021.03.03.433757
Research Highlights
Zhang H, et al. "Bioinformatic Analysis on the Prognostic Value of Neurotransmitter ." Alternative therapies in health and medicine, 2023.
Kidney renal clear-cell carcinoma (KIRC) is a malignant tumor that often presents with nonspecific symptoms, which can delay treatment. To address this issue, researchers from Wannan Medical College in China conducted a case-control study to investigate the potential of neurotransmitter receptor-related genes (NRRGs) as predictive biomarkers for KIRC. They obtained transcriptome data from the Cancer Genome Atlas (TCGA) and ArrayExpress databases, and used machine learning and functional enrichment analyses to identify 52 NRRGs that were differentially expressed in KIRC samples. Subsequently, they identified eight prognostic biomarkers and developed a predictive model using multivariate Cox analyses. The model was used to create a nomogram to predict patient outcomes. They also found significant differences in immune cell infiltration between high-risk and low-risk individuals, and identified potential therapeutic targets for KIRC treatment. The study's findings provide a new perspective for understanding and treating KIRC, and further research is needed to determine the exact mechanisms by which NRRGs affect KIRC progression.
Pubmed:
37632962
DOI:
No
Sabbir MG, et al. "Hippocampal versus cortical deletion of cholinergic receptor muscarinic 1 in mice ." Frontiers in cell and developmental biology, 2023.
In a previous retrospective study, it was demonstrated that the loss of Cholinergic Receptor Muscarinic 1 (CHRM1) in the temporal cortex of a subset of Alzheimer's patients is associated with poor survival, while a similar loss in the hippocampus shows no such association. To investigate the underlying mechanistic basis of these findings, cortical mitochondrial phenotypes were evaluated in Chrm1 knockout (Chrm1(-/-)) mice. The results showed that Chrm1 loss resulted in reduced respiration, decreased supramolecular assembly of respiratory protein complexes, and abnormal mitochondrial structure. This study aims to further understand the impact of Chrm1 loss on mouse hippocampal mitochondrial characteristics. Methods included measuring respiration, protein assembly, post-translational modifications, and ultrastructure in wild-type and Chrm1(-/-) mice. The results revealed an increase in respiration and assembly of OXPHOS-associated proteins in the hippocampus, with no changes in mitochondrial structure. These findings suggest that loss of Chrm1 in the cortex leads to detrimental effects on mitochondrial function, while its loss in the hippocampus may actually enhance function. This region-specific effect of Chrm1 loss on mitochondria supports our previous human tissue-based observations and mouse behavioral phenotypes. Furthermore, the study suggests that Chrm1-mediated post-translational modifications of Atp5a may play a role in regulating mitochondrial structure and function.
Pubmed:
37293125
DOI:
10.3389/fcell.2023.1179252