ACSL3 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 4 and Insertion of the selection cassette in exon 4.
ACS3, ACSL3_HUMAN, Acyl CoA synthetase long chain family member 3, FACL3, Fatty acid Coenzyme A ligase long chain 3, LACS 3, Lignoceroyl CoA synthase, Long-chain acyl-CoA synthetase 3, Long-chain-fatty-acid--CoA ligase 3, PRO2194
ACSL3 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 4 and Insertion of the selection cassette in exon 4.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our limited use license and patent pages.
The ACSL3 protein also known as Acyl-CoA synthetase long-chain family member 3 plays a central role in lipid metabolism. It is an enzyme with a mass of approximately 79 kDa that activates long-chain fatty acids by converting them into acyl-CoA thioesters. This process is critical for their subsequent use in metabolic pathways. ACSL3 expression occurs mainly in the liver adipose tissue and brain tissues involved in energy balance and storage. By catalyzing the initial step in the fatty acid metabolic pathway ACSL3 influences lipid biosynthesis and degradation.
ACSL3 contributes to cellular processes involving lipid synthesis and energy production. It functions as part of a larger lipid metabolic framework where it facilitates the incorporation of fatty acids into complex lipids like phospholipids and triglycerides. Though not a member of a molecular complex in terms of protein structure its activity complements other enzymes involved in lipid metabolism indicating an indirect association with lipid-binding proteins and transport mechanisms. The metabolic activity of ACSL3 therefore plays a significant role in maintaining cell membrane integrity and energy balance.
ACSL3 integrates into the peroxisome proliferator-activated receptor (PPAR) signaling and fatty acid metabolism pathways. These pathways coordinate the regulation and utilization of lipids for energy storage and consumption. The ACSL3 protein interacts with proteins such as PPARα and PPARγ which are transcription factors that regulate gene expression associated with lipid metabolism. Through these interactions ACSL3 affects lipid metabolism at a genomic level promoting the adaptive responses necessary for cellular energy requirements.
ACSL3 association with metabolic conditions like obesity and non-alcoholic fatty liver disease (NAFLD) is evident. In obesity ACSL3 expression may alter lipid metabolism contributing to excess fat accumulation and energy imbalance. Additionally elevated ACSL3 levels in the liver could be linked to NAFLD enhancing lipid storage and steatosis. The protein interacts indirectly with other players in metabolic diseases such as SREBP-1c and AMPK which are critical regulators of lipid homeostasis and energy balance in cells. These connections suggest that ACSL3 is a potential target for therapeutic interventions in metabolic disorders.
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Terms & Conditions.
Allele-2: 1 bp insertion in exon 4.
Allele-1: Insertion of the selection cassette in exon 4.
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