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Cat.No.: F4553
| Dilution |
|---|
|
| Application |
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| WB |
| Reactivity |
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| Human |
| Source |
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| Mouse Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Observed MW |
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| 47.7 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. |
| Specificity |
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| TDO2 Antibody [L23B14] detects endogenous levels of total TDO2 protein. |
| Clone |
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| L23B14 |
| Synonym(s) |
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| chky; TDO; TDO2; TDOTO; TO; TPH2EC 1.13.11.11; TRPO; TRPOtryptophanase; Tryptamin 2,3-dioxygenase; tryptophan 2,3-dioxygenase; Tryptophan Oxygenase; Tryptophan Pyrrolase; Tryptophanase |
| Background |
|---|
| TDO2 (tryptophan 2,3-dioxygenase), encoded by the TDO2 gene, functions as a heme-dependent homotetrameric enzyme catalyzing the initial, rate-limiting step of the kynurenine pathway by oxidizing L-tryptophan to N-formylkynurenine (hydrolyzed to kynurenine), thereby controlling systemic tryptophan catabolism predominantly in the liver with inducible expression in brain and tumors. It comprises four ~47 kDa subunits (406 aa each) in a dimer-of-dimers assembly featuring an all-α-helical fold; each monomer harbors a protoporphyrin IX heme bidentally coordinated by proximal His328 in a four-helix bundle active site, with substrate docking enabled by Arg144 (polarizes indole), Phe72/His76 (hydrophobic clamp), and N-terminal loops mediating positive cooperativity. TDO2 homotropically activates via Trp-induced conformational shifts propagating across interfaces, depleting local Trp to curb serotonin/melatonin while channeling flux to NAD+ biosynthesis and immunoregulatory kynurenines, Kyn binds/dimerizes AhR, translocating it to induce IDO1, TGF-β, IL-10 for T-cell anergy, Treg expansion, and M2 macrophage polarization; disease-wise, TDO2 overexpression in gliomas, breast, and colorectal cancers exploits this axis for tumor immune evasion (correlating with poor survival), while in neurodegeneration (Alzheimer's, schizophrenia), excess quinolinic acid drives NMDA-mediated excitotoxicity. |
| References |
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