
Thermo Fisher Scientific Human TL-1A, Animal-Free Recombinant Protein, PeproTech
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Applications
Tested Dilution
Publications
Functional Assay (Functional)
Assay-dependent
Product Specifications
Species
Human
Expression System
E. coli
Amino acid sequence
MQLRAQGEAS VQFQALKGQE FAPSHQQVYA PLRADGDKPR AHLTVVRQTP TQHFKNQFPA LHWEHELGLA FTKNRMNYTN KFLLIPESGD YFIYSQVTFR GMTSECSEIR QAGRPNKPDS ITVVITKVTD SYPEPTQLLM GTKSVCEVGS NWFQPIYLGA MFSLQEGDKL MVNVSDISLV DYTKEDKTFF GAFLL
Molecular weight
22.1 kDa
Class
Recombinant
Type
Protein
Purity
≥ 98% by SDS-PAGE gel and HPLC analyses.
Endotoxin concentration
<0.1 EU/µg
Activity
Determined by its ability to stimulate IFN-gamma production by human PBMC co-stimulated with Human IL-12 and Human IL-18.
Conjugate
Unconjugated Unconjugated Unconjugated
Form
Lyophilized
Purification
purified
Contains
no preservative
Storage conditions
-20°C
Shipping conditions
Ambient
Product Specific Information
Recombinant Human TL-1A is a 22.1 kDa polypeptide of 195 amino acid residues.
This product is shipped at ambient temperature. For storage, handling and reconstitution information, please see the lot-specific Certificate of Analysis
Target Information
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is abundantly expressed in endothelial cells, but is not expressed in either B or T cells. The expression of this protein is inducible by TNF and IL-1 alpha. This cytokine is a ligand for receptor TNFRSF25 and decoy receptor TNFRSF21/DR6. It can activate NF-kappaB and MAP kinases, and acts as an autocrine factor to induce apoptosis in endothelial cells. This cytokine is also found to inhibit endothelial cell proliferation, and thus may function as an angiogenesis inhibitor. An additional isoform encoded by an alternatively spliced transcript variant has been reported but the sequence of this transcript has not been determined.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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