Target intelligence / Profile preview

Thyrotroph embryonic factor (TEF)

Target
TEF
Molecular classification
Transcription factor, Basic leucine zipper (bZIP) family, PAR (proline and acidic amino acid-rich) bZIP subfamily
01

Overview

Thyrotroph embryonic factor (TEF) is a member of the PAR (proline and acidic amino acid-rich) bZIP (basic region/leucine zipper) transcription factor family, closely related to DBP and HLF. TEF exhibits robust circadian expression in peripheral organs such as liver, where it activates key genes—most notably pyridoxal kinase, which is required for the synthesis of pyridoxal phosphate, a coenzyme central to neurotransmitter metabolism. TEF is necessary for maintaining brain pyridoxal phosphate, serotonin, and dopamine levels; mice lacking TEF (and related PAR bZIP factors) suffer from spontaneous and audiogenic epileptic seizures, likely due to metabolic disruption in neurotransmitter and vitamin B6 pathways. TEF acts as a nuclear transcription factor, predominantly via DNA-binding and regulation of gene expression, and does not function as a classic therapeutic "target" (enzyme, receptor, transporter), nor are there known drugs directly acting on it as of now[1][3][5].

Other names
TEFKIAA1655PAR bZIP transcription factorthyrotroph embryonic factorthyrotrophic embryonic factor
02

Biological functions

Regulation of circadian rhythmTranscriptional activation of target genes (notably pyridoxal kinase)Regulation of neurotransmitter homeostasisInvolvement in amino acid metabolism
03

Disease associations

Epilepsy (due to disruption of TEF and other PAR bZIP factors)Potential involvement in neurological dysfunction via effects on vitamin B6 metabolism
04

Safety considerations

Loss of TEF leads to reduced expression of pyridoxal kinase, loss of pyridoxal phosphate in brain, and increased risk of epilepsy[1]

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