GPD2 KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided. Knockout achieved by CRISPR/Cas9; X = 32 bp deletion, 31 bp deletion, 4 bp deletion; Frameshift: 100%.
GDH2, GPDH-M, GPDM_HUMAN, Glycerol 3 phosphate dehydrogenase 2, Glycerol 3 phosphate dehydrogenase 2 (mitochondrial), Glycerol 3 phosphate dehydrogenase mitochondrial, Glycerol-3-phosphate dehydrogenase, Mitochondrial glycerophosphate dehydrogenase, OTTHUMP00000162788, OTTHUMP00000204452, OTTHUMP00000204453, OTTHUMP00000204458, mGPDH, mitochondrial, mtGPD
GPD2 KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided. Knockout achieved by CRISPR/Cas9; X = 32 bp deletion, 31 bp deletion, 4 bp deletion; Frameshift: 100%.
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 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 and patent pages.
Glycerol-3-phosphate dehydrogenase 2 (GPD2) also known as GPDM-m and mGPDH is an enzyme that belongs to the glycerol-3-phosphate dehydrogenase family. GPD2 weighs approximately 74 kDa and is expressed in several tissues including the liver kidney and muscle. It primarily localizes in the mitochondrial inner membrane. Mechanically GPD2 catalyzes the oxidation of glycerol-3-phosphate to dihydroxyacetone phosphate playing an important role in energy metabolism by participating in the glycerol phosphate shuttle. This shuttle facilitates the transfer of reducing equivalents across the mitochondrial membrane.
GPD2 plays a role in cellular energy production by linking lipid metabolism to carbohydrate metabolism. It forms part of a complex system supporting oxidative phosphorylation by transferring electrons to the mitochondrial electron transport chain. The activity of GPD2 helps sustain the NAD+/NADH balance which is essential for maintaining cellular redox states. Through its function GPD2 contributes to metabolic flexibility allowing cells to adapt to changes in fuel availability.
GPD2 is involved in important energy production pathways such as the glycerol phosphate shuttle and the oxidative phosphorylation pathway. These pathways are important for efficient ATP production in eukaryotic cells. GPD2 interacts with other metabolic proteins like cytosolic glycerol-3-phosphate dehydrogenase (GPD1) which works in tandem to facilitate the shuttle of reducing equivalents between cytosol and mitochondria. Such processes ensure continuous energy supply necessary for cellular functions especially under conditions where carbohydrates and lipids serve interchangeably as energy sources.
GPD2 associates with conditions such as obesity and type 2 diabetes where energy metabolism is often disrupted. Altered GPD2 activity can lead to impaired mitochondrial function contributing to the pathogenesis of these metabolic disorders. Furthermore GPD2 links to proteins implicated in these diseases such as insulin receptor substrates and oxidative stress markers which further influence glucose and lipid homeostasis. Understanding GPD2's interaction with these elements helps in uncovering potential therapeutic targets for such diseases.
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Knockout achieved by CRISPR/Cas9; X = 32 bp deletion, 31 bp deletion, 4 bp deletion; Frameshift: 100%
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