The purity of recombinant hTL1A was determined by SDS-PAGE of 6 µg reduced (+) and nonreduced (-) recombinant hTL1A and staining overnight with Coomassie Blue.Learn more about how we get our images
The viability of TF-1 cells treated with increasing amounts of hTL1A in the presence of 10 µg/ml cyclohexamide was determined. After a 24 hr treatment with hTL1A, cells were incubated with tetrazolium salt and the OD450 - OD650 was determined.Learn more about how we get our images
Recombinant Human TL1A Leu72-Leu251 (Accession #NP_095150) was expressed in E.coli at Cell Signaling Technology.
>95% as determined by SDS-PAGE of 6 μg reduced (+) and nonreduced (-) recombinant hTL1A. All lots are greater than 95% pure.
Recombinant hTL1A has a calculated MW of 20,0473. DTT-reduced protein migrates as a 21 kDa polypeptide. The nonreduced protein migrates as a 21 kDa monomer and 38 kDa cystine-linked homodimer. The expected amino terminus of recombinant hTL1A was verified by amino acid sequencing.
The bioactivity of hTL1A was determined in a TF-1 cell viability assay. The ED50 of each lot is between 2-15 ng/ml.
Less than 0.01 ng endotoxin/1 μg hTL1A.
With carrier: Lyophilized from a 0.22 μm filtered solution of hTL1A in 20 mM Tris, pH 7.2 containing 20 μg BSA per 1 μg hTL1A. Carrier free: Lyophilized from a 0.22 μm filtered solution of hTL1A in 20 mM Tris, pH 7.2.
Stable in lyophilized state at 4°C for 1 year after receipt. Sterile stock solutions reconstituted with carrier protein are stable at 4°C for 2 months and at -20°C for 6 months. Avoid repeated freeze-thaw cycles. Maintain sterility. Storage at -20°C should be in a manual defrost freezer.
TL1A (TNFSF15), a member of the TNF superfamily of proteins, is a splice variant of the TL1/VEGI gene (1). Endothelial cells, monocytes, macrophages, and dendritic cells express TL1A, which is upregulated by proinflammatory cytokines, microorganisms, and AMPK activation (1-4). TL1A activates the NF-κB and JNK pathways through its receptor, DR3 (1,5). TL1A may function as a costimulatory signal for T cell activation, specifically regulating Th17 cell development and proliferation (1,2,6). Mouse models suggest a role for TL1A as a driver for the inflammation and pathogenesis associated with inflammatory bowel disease (7,8).
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