Abcam, ab261818, Human ACHE (Acetylcholinesterase) knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
ACHE KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 2. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 11 bp deletion in exon 2,
Antibiotic resistance:Puromycin 1µg/mL,
Disease:Adenocarcinoma

Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-ACHE, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Acetylcholinesterase also known as AChE is an enzyme with a molecular mass of approximately 67 kDa. It plays a critical role in neurotransmission by catalyzing the hydrolysis of the neurotransmitter acetylcholine into acetate and choline. This reaction occurs at neuromuscular junctions and cholinergic synapses therefore terminating synaptic transmission. AChE is highly expressed in muscle and brain tissue particularly in the synaptic cleft where it regulates the nerve signal terminations.
Biological function summary
Acetylcholinesterase is essential for maintaining neurotransmission dynamics by ensuring timely acetylcholine breakdown. It does not function as part of a larger enzyme complex but its activity is necessary for efficient synaptic signaling in the nervous system. This enzymatic action prevents continuous stimulation of muscles and nerves by rapidly degrading acetylcholine thereby ensuring proper muscle contraction and cognitive processes.
Pathways
Acetylcholinesterase participates significantly in the cholinergic system. It influences cholinergic signaling pathways by inactivating acetylcholine after its release into the synaptic cleft. This function aligns acetylcholinesterase closely with receptors like nicotinic and muscarinic acetylcholine receptors. It indirectly affects signal transduction pathways that involve these receptors with potential downstream effects on ion channels and intracellular messengers.
Acetylcholinesterase plays a significant role in Alzheimer's disease and myasthenia gravis. In Alzheimer's disease decreased acetylcholinesterase function can lead to accumulations of acetylcholine and disrupted signaling contributing to cognitive dysfunction. Acetylcholinesterase inhibitors are therapeutic in such contexts. For myasthenia gravis a disorder affecting neuromuscular transmission the enzyme’s interaction with antibodies targets synaptic acetylcholine receptors. This interaction results in weakened muscle contractions correlating with condition severity.