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  • mProX™ Human CHRM1 Stable Cell Line

    [CAT#: S01YF-0923-PY127]
    Product Category:
    Membrane Protein Stable Cell Lines
    Subcategory:
    GPCR Cell Lines

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    Host Cell Type:
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    Based 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

    Product Information

    Target Protein
    CHRM1
    Target Family
    Muscarinic Acetylcholine Family
    Target Protein Species
    Human
    Host Cell Type
    A375;CHO-K1;HEK293
    Target Classification
    GPCR Cell Lines
    Target Research Area
    CNS Research
    Related Diseases
    Anxiety;Trichothiodystrophy 7, Nonphotosensitive
    Gene ID
    Human: 1128
    UniProt ID
    Human: P11229

    Product Properties

    Biosafety Level
    Level 1
    Activity
    Yes
    Quantity
    10⁶ cells per vial
    Applications
    The CHRM1 gene encodes the muscarinic acetylcholine receptor M1, which plays a crucial role in mediating various physiological responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides, and modulation of potassium channels through the action of G proteins. In the realm of scientific research, CHRM1 has been implicated in various neurological and physiological processes. For instance, the receptor has been associated with cognitive functions, particularly in the context of Alzheimer's disease, where its dysregulation may contribute to cognitive decline. Additionally, CHRM1's role in modulating neurotransmission has made it a target of interest in the study of various neuropsychiatric disorders.

    Protocols

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    FAQ

    chat Kevin (Verified Customer)

    How is CHRM1 associated with Alzheimer's Disease and other neurological disorders? Oct 30 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    A severe reduction of CHRM1 has been observed in a subset of patients with Alzheimer's Disease (AD) and Parkinson's Disease (PD), potentially explaining the low efficacy of AChE inhibitors as a treatment for these patients. Oct 30 2020

    chat Paul (Verified Customer)

    What is the role of CHRM1 in melanoma suppression? Apr 15 2020

    chat Patrick Liam (Creative Biolabs Scientific Support)

    CHRM1 is inhibited by endogenous DOPA, which regulates melanocyte proliferative capacity and susceptibility to malignant transformation, indicating a potential role in melanoma suppression. Apr 15 2020

    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

    Please note: All products are "FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR CLINICAL PROCEDURES" For licensing inquiries, please contact
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