DLAT Human Pre-designed siRNA Set A
DLAT Human Pre-designed siRNA Set A contains three designed siRNAs for DLAT gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
DLAT Human Pre-designed siRNA Set A contains three designed siRNAs for DLAT gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Components
DLAT siRNA-1: 5 nmol (HPLC)
DLAT siRNA-2: 5 nmol (HPLC)
DLAT siRNA-3: 5 nmol (HPLC)
siRNA Negative Control: 5 nmol (HPLC)
FAM-labeled siRNA Negative Control: 5 nmol (HPLC)
GAPDH siRNA Positive Control: 5 nmol (HPLC)
Gene ID
Gene Information
DLAT - dihydrolipoamide S-acetyltransferase Gene (Human)
Also Known as
E2; PBC; DLTA; PDCE2; PDC-E2
Chemical Information
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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RNA interference technology
RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing gene transcription or activating RNA degradation. This mechanism was discovered in plants in 1998 by Andrew Fire and Craig Mello. Today, this phenomenon can be observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals.
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Cuproptosis Solutions
Cuproptosis is a copper-dependent regulated cell-death pathway in which intracellular copper binds lipoylated tricarboxylic acid cycle proteins, especially DLAT-containing pyruvate dehydrogenase complex components, causing lipoylated protein aggregation, iron-sulfur cluster protein loss, proteotoxic stress, and cell death. The pathway is functionally linked to mitochondrial respiration because copper-ionophore sensitivity is higher in cells dependent on oxidative phosphorylation, and FDX1 and protein lipoylation machinery are required for copper-ionophore-induced death. Elesclomol-Cu and related copper-loading strategies are widely used experimental tools to induce cuproptosis, whereas copper chelation with tetrathiomolybdate or genetic suppression of FDX1, LIAS, LIPT1, or DLAT can test pathway dependence. The major unresolved questions are how disease context determines cuproptosis sensitivity, how copper transporters such as SLC31A1/CTR1 and ATP7A/ATP7B regulate the pathway, and whic
Purity & Documentation
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)