SLC31A1/CTR1 Antibody (5E6.1B4) - Azide and BSA Free Summary
Immunogen |
Two synthetic peptides made to internal sequences of human SLC31A1/CTR1 protein (sequences found between amino acids 50-150) [UniProt# O15431] |
Isotype |
IgG2b Kappa |
Clonality |
Monoclonal |
Host |
Mouse |
Gene |
SLC31A1 |
Purity |
Protein G purified |
Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Applications/Dilutions
Dilutions |
- Immunocytochemistry/ Immunofluorescence 0.0763888888888889
- Immunohistochemistry 5 ug/ml
- Immunohistochemistry-Paraffin 5 ug/ml
- Western Blot 2 ug/ml
|
Packaging, Storage & Formulations
Storage |
Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles. |
Buffer |
PBS |
Preservative |
No Preservative |
Concentration |
1 mg/ml |
Purity |
Protein G purified |
Alternate Names for SLC31A1/CTR1 Antibody (5E6.1B4) - Azide and BSA Free
Background
SLC31A1/CTR1 (solute carrier family 31 member 1/copper transporter 1) is a homotrimeric high-affinity, saturable copper importer implicated in dietary copper uptake. Homeostasis of copper is tightly controlled by inter-regulatory circuitry containing copper, Sp1, and CTR1, wherein Sp1 transcription factor acts as a copper sensor in modulating CTR1 expression which in turn controls cellular copper and Sp1 levels in a 3-way mutual regulatory loop. CTR1 mediated copper uptake is time, temperature, and pH dependent and specific for reduced form of Cu (I) and copper reduction has been proposed to be caused by Steap protein family or Dcytb protein (Cybrd1) both of which are reported to possess cupric reductase activity. The intracellular localization of CTR1 is variable in different cell lines: CTR1 is localized at the plasma membrane in HEK293, CaCo-2, and A2780 cells, whereas, in other cells such as HeLa, it is predominantly localized to vesicular compartments, and variability in trafficking rates between vesicular and plasma membrane compartments has been suggested as the cause of this differential localization. Post-translational O-linked glycosylation of CTR1 protects it against proteolytic cleavage of N terminal 17-kD fragment and the biological function of this cleaved variant or protease responsible is largely unknown. Selective knockout of Ctr1 in murine intestinal epithelial cells results in severe systemic copper deficiency, ataxia, and death prior to weaning.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are
guaranteed for 1 year from date of receipt.
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