Product Name
Rat Divalent Metal Transporter 1 (DMT1) ELISA Kit
Product Alternative Names
DCT1; NRAMP2; Natural resistance-associated macrophage protein 2; Solute Carrier Family 11 Member 2,Proton-Coupled Divalent Metal Ion Transporters; divalent metal transporter 1; solute carrier family
Reactivity
Rat
Sensitivity
0.117 ng/mL
Detection Range
0.312-20 ng/ml
Assay Type
Sandwich
Description
The product is designed for analyse the presence of the target Divalent Metal Transporter 1 (DMT1) in Rat biological samples using enzyme-linked immunosorbent assay technology.
Sample Type
Tissue Homogenates, Cell Lysates and Other Biological Fluids.
Components
Pre-coated, ready to use 96 Well strip plate 1
Plate sealer for 96 wells 4
Standard 2
Standard Diluent 20 mL
Detection Reagent A 120 µL
Assay Diluent A 12 mL
Detection Reagent B 120 µL
Assay Diluent B 12 mL
TMB Substrate 9 mL
Stop Solution 6 mL
Wash Buffer
Instruction manual 1
Notes
For research use only.
Applications
ELISA
Gene Symbol
SLC11A2
Related Gene ID
Gene Name
solute carrier family 11 member 2
Alias Symbols
DMT1; slc11a2; cb426; fa07b10; wu:fa07b10; zgc:136699
Protein Name
Divalent metal transporter 1
Related Uniprot ID
Molecular Weight
62.2 kDa
Sequence Similarities
Belongs to the NRAMP family.
Tissue Specificity
Ubiquitously expressed. Expressed in erythroid progenitors.
Cellular Localization
Cell membrane, Endosome, Golgi apparatus, Lysosome and Membrane.
Function
Essential for maintenance of iron homeostasis by modulating intestinal absorption of dietary Fe2+ and TF-associated endosomal Fe2+ transport in erythroid precursors and other cells (By similarity).
Enables Fe2+ and Mn2+ ion entry into mitochondria, and is thus expected to promote mitochondrial heme synthesis, iron-sulfur cluster biogenesis and antioxidant defense (PubMed:24448823) (By similarity).
Can mediate uncoupled fluxes of either protons or metal ions.
Disease Area
Anemia, hypochromic microcytic, with iron overload 1 (AHMIO1), a hematologic disease characterized by abnormal hemoglobin content in the erythrocytes which are reduced in size. The disorder is due to an error of iron metabolism that results in high serum iron, massive hepatic iron deposition, and absence of sideroblasts and stainable bone marrow iron store. Despite adequate transferrin-iron complex, delivery of iron to the erythroid bone marrow is apparently insufficient for the demands of hemoglobin synthesis.