UCK1 KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon1 and 1 bp deletion in exon1.
Cytidine monophosphate kinase, Cytidine monophosphokinase 1, Cytidylate kinase, Deoxycytidylate kinase, FLJ12255, OTTHUMP00000022400, OTTHUMP00000022401, OTTHUMP00000022403, OTTHUMP00000022404, RP11-334J6.5, UCK1_HUMAN, UMP-CMP kinase, URK1, Uridine monophosphokinase 1, Uridine-cytidine kinase 1, Uridine/cytidine kinase 1
UCK1 KO cell lysate available now. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon1 and 1 bp deletion in exon1.
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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.
Uridine-cytidine kinase (UCK) also known as uridine monophosphate kinase catalyzes the phosphorylation of uridine and cytidine to form uridine monophosphate (UMP) and cytidine monophosphate (CMP) respectively. This enzyme weighs about 30 kilodaltons. UCK expresses mostly in the cytoplasm with notable activity in tissues like the liver pancreas and kidney. Its function hinges on its ability to regulate nucleotide levels which are essential for nucleic acid metabolism.
Uridine-cytidine kinase supports nucleotide homeostasis in cells. It does not form part of a larger enzymatic complex. This enzyme facilitates the salvage pathway converting nucleosides back into nucleotides. Such activity ensures sufficient nucleotide precursors for DNA and RNA synthesis which is critical during cell division and repair. Therefore disruptions in UCK function can severely impact cellular metabolism and proliferation.
Nucleoside and nucleotide metabolism are key areas where uridine-cytidine kinase plays a prominent role. It particularly influences the pyrimidine salvage pathway an important process that helps recycle nucleotides within the cell. UCK interacts with other enzymes such as cytidine monophosphate kinase (CMP kinase) which further phosphorylates CMP into cytidine diphosphate (CDP). Proper functioning of these pathways ensures cellular nucleotide balance and genome integrity.
Abnormalities in uridine-cytidine kinase activity link to certain cancers and metabolic disorders. For example altered UCK activity has connections to cancer types where fast-proliferating cells show increased demand for nucleotides. Furthermore UCK changes have been associated with mitochondrial neurogastrointestinal encephalopathy (MNGIE). This disorder connects with dysfunctional thymidine phosphorylase highlighting the importance of nucleotide metabolism coordination. These insights help target UCK in therapeutic strategies for such diseases.
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Allele-2: 1 bp deletion in exon1
Allele-1: 10 bp deletion in exon1
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