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Anti-Ac-6-FP T cell receptor (TRBV6-1), pCDTCR1 (TCR-YC0058)

 Datasheet

All products and services are For Research Use Only and CANNOT be used in the treatment or diagnosis of disease.

Mucosal-associated invariant T (MAIT) cells express an invariant T cell receptor (TCR) α-chain (TRAV1-2 joined to TRAJ33, TRAJ20, or TRAJ12 in humans), which pairs with an array of TCR β-chains. MAIT TCRs can bind folate- and riboflavin-based metabolites restricted by the major histocompatibility complex (MHC)-related class I−like molecule, MR1. The TCR is specific for Acetyl-6-FP in the context of human MR1.

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Details

  • Target
  • Ac-6-FP
  • Epitope
  • Acetyl-6-FP
  • Format
  • Non-Modified TCR
  • Allele
  • MR1
  • Vector Name
  • pCDTCR1
  • Vector Length
  • ~ 8 kb
  • Vector Type
  • Lentiviral vector
  • TCR Clone
  • TRBV6-1
  • Host Species
  • Human

Target

  • Introduction
  • The MAIT TCR is restricted by the MHC class I–related molecule MR1. MR1 is a monomorphic Ag-presenting molecule that is highly conserved across mammals. Although the MR1 transcript is expressed widely, cell surface expression of MR1 is very low/absent, thereby indicating that other factors, including Ag supply, can determine the level of MR1 that egresses to the cell membrane. Recently, it has been established that MR1 can bind vitamin B–based precursors and derivatives that originate from folic acid (vitamin B9) and riboflavin (vitamin B2) biosynthesis. Specifically, MR1 can present 6-formylpterin (6-FP), a naturally occurring photo-degradation product of folic acid, and a series of ribityllumazines, including 6,7-dimethyl-8-d-ribityllumazine (RL-6,7-DiMe), 6-methyl-7-hydroxy-8-d-ribityllumazine (RL-6-Me-7-OH), 5-(2-oxoethylideneamino)-6-d-ribitylaminouracil (5-OE-RU), and 5-(2-oxopropylideneamino)-6-d-ribitylaminouracil (5-OP-RU). The MR1 Ag-binding cleft is ideally disposed to bind to these small organic metabolites, with the ligands being closely sequestered by an aromatic cradle within MR1, whereupon some of the ligands can form a covalent bond (Schiff base) with MR1. Although the 6-FP ligand up-regulated MR1 cell surface expression, it did not stimulate MAIT cells. However, the ribityllumazines were stimulatory, with the extent of MAIT cell potency varying markedly, such that synthetic rRL-6-CH2OH (reduced 6-hydroxymethyl-8-d-ribityllumazine) is ∼1,000 times more potent than the weak agonists RL-6,7-DiMe and RL-6-Me-7-OH. We recently traced the high potency of rRL-6-CH2OH to MR1 trapping and presentation of a relatively unstable pyrimidine-based transitory derivative (5-OP-RU), with similar high potency also found for a homologue with one carbon less (5-OE-RU) but no activity for another homologue with one extra carbon, 5-(1-methyl-2-oxopropylideneamino)-6-d-ribitylaminouracil (5-MOP-RU).

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For research use only. Not intended for any clinical use. No products from Creative Biolabs may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative Biolabs.

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