Recombinant Human FGE protein (denatured) (ab115708)
Key features and details
- Expression system: Escherichia coli
- Purity: > 85% SDS-PAGE
- Tags: His tag N-Terminus
- Suitable for: SDS-PAGE
Description
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Product name
Recombinant Human FGE protein (denatured)
See all FGE proteins and peptides -
Purity
> 85 % SDS-PAGE. -
Expression system
Escherichia coli -
Accession
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Protein length
Protein fragment -
Animal free
No -
Nature
Recombinant -
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Species
Human -
Sequence
MGSSHHHHHHSSGLVPRGSHMVPIPAGVFTMGTDDPQIKQDGEAPARRVT IDAFYMDAYEVSNTEFEKFVNSTGYLTEAEKFGDSFVFEGMLSEQVKTNI QQAVAAAPWWLPVKGANWRHPEGPDSTILHRPDHPVLHVSWNDAVAYCTW AGKRLPTEAEWEYSCRGGLHNRLFPWGNKLQPKGQHYANIWQGEFPVTNT GEDGFQGTAPVDAFPPNGYGLYNIVGNAWEWTSDWWTVHHSVEETLNPKG PPSGKDRVKKGGSYMCHRSYCYRYRCAARSQNTPDSSASNLGFRCAADRL PTMD -
Predicted molecular weight
34 kDa including tags -
Amino acids
91 to 374 -
Tags
His tag N-Terminus
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Associated products
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Related Products
Specifications
Our Abpromise guarantee covers the use of ab115708 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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Applications
SDS-PAGE
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Form
Liquid -
Additional notes
This product was previously labelled as SUMF1
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Concentration information loading...
Preparation and Storage
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Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
pH: 8.00
Constituents: 12.01% Urea, 0.03% DTT, 0.32% Tris HCl, 20% Glycerol (glycerin, glycerine)
General Info
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Alternative names
- MGC150436
- AAPA3037
- C alpha formylglycine generating enzyme 1
see all -
Function
Using molecular oxygen and an unidentified reducing agent, oxidizes a cysteine residue in the substrate sulfatase to an active site 3-oxoalanine residue, which is also called C(alpha)-formylglycine. Known substrates include GALNS, ARSA, STS and ARSE. -
Tissue specificity
Ubiquitous. Highly expressed in kidney, pancreas and liver. Detected at lower levels in leukocytes, lung, placenta, small intestine, skeletal muscle and heart. -
Pathway
Protein modification; sulfatase oxidation. -
Involvement in disease
Defects in SUMF1 are the cause of multiple sulfatase deficiency (MSD) [MIM:272200]. MSD is a clinically and biochemically heterogeneous disorder caused by the simultaneous impairment of all sulfatases, due to defective post-translational modification and activation. It combines features of individual sulfatase deficiencies such as metachromatic leukodystrophy, mucopolysaccharidosis, chondrodysplasia punctata, hydrocephalus, ichthyosis, neurologic deterioration and developmental delay. Inheritance is autosomal recessive. -
Sequence similarities
Belongs to the sulfatase-modifying factor family. -
Post-translational
modificationsN-glycosylated. Contains high-mannose-type oligosaccharides. -
Cellular localization
Endoplasmic reticulum lumen. - Information by UniProt
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
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SDS download
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Datasheet download
References (0)
ab115708 has not yet been referenced specifically in any publications.