Target intelligence / Profile preview

Peroxiredoxin-like 2C (PRXL2C)

Target
PRXL2C
Molecular classification
Enzyme, AhpC/Prx1 subgroup, Antioxidant enzyme, Thioredoxin-like (contains thioredoxin domain)
01

Overview

Peroxiredoxin-like 2C (PRXL2C) is a member of the peroxiredoxin-like antioxidant enzyme family, lacking selenium and instead containing cysteine residues in a CxxC motif similar to canonical peroxiredoxins[1]. It acts as a regulator of oxidative stress and positively influences cell signaling cascades such as ERK1/2 and AKT1, resulting in increased expression of HIF1A and glycolytic genes, and promoting glycolytic metabolism[7][2][5]. PRXL2C is structurally related to selenoprotein U orthologs, but categorized as a non-selenoprotein peroxiredoxin-like molecule[1]. Although not extensively characterized as a therapeutic target or biomarker, its involvement in critical cell proliferation and survival signaling pathways, notably those active in cancer and metabolism, make it a molecule of emerging interest[7][2][5]. There is no current evidence of direct drug interactors or FDA-approved therapeutics targeting PRXL2C.

Other names
Peroxiredoxin-like 2CPRXL2CAAED1C9orf21AhpC/TSA antioxidant enzyme domain-containing protein 1Thioredoxin-like protein AAED1UPF0308 protein C9orf21
02

Mechanism of action

Drugs targeting PRXL2C would likely modulate oxidative stress response, ERK/AKT/HIF1A signaling, or glycolysis

03

Biological functions

Positive regulation of ERK1/ERK2 signaling cascadePositive regulation of AKT1 activityUpregulation of HIF1A (Hypoxia-inducible factor 1-alpha)Enhancement of expression of glycolysis genes and glycolytic processAntioxidant activityProtein-protein interaction regulation
04

Disease associations

Cancer (potential involvement via glycolytic pathway upregulation and ERK/AKT signaling modulation)Other (ERK/AKT regulation suggests possible relevance in metabolic or proliferative disorders)
05

Safety considerations

Modulating ERK/AKT/HIF1A/glycolytic pathways may risk unintended cell proliferation, metabolic dysregulation, or cancer

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