Panoply™ Human CHRM1 Knockdown Stable Cell Line

Name: Panoply™ Human CHRM1 Knockdown Stable Cell Line
SKU: CSC-DC003124
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-DC003124

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

Inquire for Price

Cell Line Information

Safety and Packaging

Gene Information

Cat. No.	CSC-DC003124
Description	Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene	CHRM1
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

Mycoplasma	Negative
Format	One frozen vial containing millions of cells
Storage	Liquid nitrogen
Safety Considerations	The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship	Dry ice

Gene Name	CHRM1 cholinergic receptor, muscarinic 1 [ Homo sapiens ]
Gene Symbol	CHRM1
Synonyms	M1; HM1; M1R
Gene Description	cholinergic receptor, muscarinic 1
GeneID	1128
Uni ProtID	P11229
mRNA Refseq	NM_000738.2
Protein Refseq	NP_000729.2
Chromosome Location	11q13
Function	G-protein coupled acetylcholine receptor activity; drug binding; phosphatidylinositol phospholipase C activity;
Pathway	Amine ligand-binding receptors, organism-specific biosystem; Calcium Regulation in the Cardiac Cell, organism-specific biosystem; Calcium signaling pathway, organism-specific biosystem; Calcium signaling pathway, conserved biosystem; Cholinergic synapse, organism-specific biosystem; Class A/1 (Rhodopsin-like receptors), organism-specific biosystem; G alpha (q) signalling events, organism-specific biosystem;
MIM	118510

Quick Inquiry

Case Study

Q & A

Customer Reviews

Alzheimer's disease (AD) is a common neurodegenerative disorder characterized by neuronal degeneration and tau hyperphosphorylation. Magnolol, an active component isolated from Magnolia officinalis, has potential neuroprotective activity. However, the role and mechanism of magnolol in AD progression remain unclear. This study used bioinformatics analysis to predict biomarkers associated with AD and magnolol. The results showed that CHRM1 is a key biomarker for magnolol's anti-AD effects. Magnolol attenuates Aβ-induced SH-SY5Y cell viability inhibition, tau hyperphosphorylation, and apoptosis by upregulating CHRM1 levels. Furthermore, cAMP signaling may be a potential pathway for CHRM1 in AD. Magnolol activates the cAMP/PKA/CREB pathway by increasing CHRM1 levels. Inhibition of the cAMP/PKA/CREB pathway reverses the inhibitory effects of magnolol on Aβ-induced tau hyperphosphorylation and apoptosis in SH-SY5Y cells. In summary, magnolol alleviated Aβ-induced Tau hyperphosphorylation and neuronal apoptosis by upregulating CHRM1 and activating the cAMP/PKA/CREB pathway.

To analyze the role of magnolol in Aβ-induced neuronal injury, SH-SY5Y cells were transfected with si-con or si-CHRM1 and then treated with 10 μM magnolol and Aβ. The results showed that Aβ treatment significantly reduced CHRM1 expression and significantly increased p-Tau/Tau levels in SH-SY5Y cells (Figure 1A-C). Magnolol had little effect on CHRM1 and p-Tau/Tau levels, but it reversed the Aβ effects on these levels, while CHRM1 knockdown abolished the Aβ effects on these levels (Figure 1A-C). Furthermore, magnolol attenuated the Aβ-induced increase in cleaved-caspase-3 levels and caspase-3 activity, while CHRM1 knockdown attenuated the effects of magnolol on Aβ-stimulated SH-SY5Y cells (Figure 1D-F). Furthermore, although magnolol did not affect apoptosis under normal conditions, it attenuated Aβ-induced apoptosis, and CHRM1 knockdown reversed the inhibitory effect of magnolol on Aβ-induced apoptosis (Figure 1G, H). These results suggest that magnolol may alleviate Tau hyperphosphorylation and apoptosis by increasing CHRM1 levels in Aβ-stimulated SH-SY5Y cells.

Figure 1. Effect of magnolol on hyperphosphorylation of Tau and apoptosis in Aβ-treated SH-SY5Y cells. (Zhu G, et al., 2022)

Ask a Question

If your question is not addressed through these resources, you can fill out the online form below and we will answer your question as soon as possible.

Question *

Name

Country *

Email *

Write a Review

Write a review of your use of Biogene products and services in your research. Your review can help your fellow researchers make informed purchasing decisions.

Product Name *

Catalog Name *

Rating

Needs improvement

Satisfaction

General satisfaction

Very satisfaction

Product Review Title *

Summary *