SLC30A1 KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 20 bp deletion in exon 1 and 3 bp deletion in exon 1.
SLC30 A1, SLC30A 1, SLC30A1, Solute carrier family 30 (zinc transporter), member 1, Solute carrier family 30 member 1, ZNT1_HUMAN, ZRC 1, Zinc transporter 1
SLC30A1 KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 20 bp deletion in exon 1 and 3 bp deletion in exon 1.
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Lysate preparation: Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10). This means that the protein of interest is denatured. If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions: Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
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.
ZnT1 also known as SLC30A1 is a critical protein responsible for the export of zinc ions out of cells. This transporter plays an important role in maintaining intracellular zinc homeostasis. The protein has a molecular mass of approximately 52 kDa. ZnT1 is expressed in a wide range of tissues including the brain liver and intestines indicating its significant role in various physiological processes. The protein is located in the cell plasma membrane which aligns with its function of mediating zinc efflux.
ZnT1 is essential for regulating the cellular zinc levels and protecting against zinc toxicity. It does not form part of a larger complex; instead it operates as an individual unit to ensure that excess zinc does not accumulate to harmful levels within the cell. By controlling zinc efflux ZnT1 influences processes such as cell signaling and apoptosis which rely on zinc as a cofactor or structural component.
Homeostasis of zinc ions in cells connects ZnT1 to the cellular zinc transport pathway and the metal ion transport pathway. ZnT1 coordinates with intracellular zinc-binding proteins like metallothioneins to modulate zinc availability and transportation within the cell. Proteins such as ZIP4 which facilitate zinc uptake operate in a complementary manner to ZnT1 balancing zinc influx and efflux to maintain cellular function.
Misregulation of ZnT1 has been linked to conditions such as cancer and neurodegenerative diseases. In cancer changes in zinc transport influence tumor growth and progression partly involving interactions with proteins like p53 a critical tumor suppressor modulated by zinc availability. In neurodegenerative diseases abnormal zinc levels can contribute to neuronal damage where ZnT1 interacts with Amyloid Beta plaques affecting the pathology of Alzheimer's disease.
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Allele-1: 20 bp deletion in exon 1
Allele-2: 3 bp deletion in exon 1
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