Target intelligence / Profile preview

Ubiquitously expressed prefoldin-like chaperone (UXT)

Target
UXT
Molecular classification
Prefoldin-like molecular chaperone, cofactor, nuclear chaperone, other
01

Overview

Ubiquitously expressed prefoldin-like chaperone (UXT) is a small, highly conserved protein involved in the regulation of androgen receptor-dependent transcription, apoptosis, autophagy, and immune signaling[3][4][6]. UXT acts as a nuclear and cytoplasmic chaperone, regulating transcriptional complexes—including those for NF-κB and androgen receptor—and interacting with key factors in programmed cell death, cellular proteostasis (including autophagy via p62/SQSTM1), and the maintenance of centrosome structure[1][2][4][6]. UXT is widely expressed, with enhanced or altered expression implicated in tumorigenesis and neurodegenerative pathologies[1][3][4]. Multiple isoforms exist, with distinct cellular locations and functions in death receptor signaling and gene regulation[3][4]. There are currently no clinically validated drugs that directly target UXT, and its essential cellular roles indicate safety challenges if it were considered for therapeutic targeting[1][3][4].

Other names
Protein UXTHSPC024ART-27STAP1SKP2-associated alpha PFD 1Androgen receptor trapped clone 27 proteinUbiquitously expressed transcript proteinandrogen receptor trapped clone 27
02

Biological functions

Modulation of androgen receptor-dependent transcriptionregulation of apoptosisregulation of autophagymodulation of NF-κB signalingcell proliferation controlprotein chaperoningcellular proteostasisimmune responsemaintenance of centrosome structure
03

Disease associations

Cancer (tumorigenesis and progression)Neurodegenerative diseaseRetinitis pigmentosaInflammationImmune regulation
04

Safety considerations

Potential therapeutic challenges in targeting an essential and ubiquitously expressed protein; role in fundamental cell survival processes may limit druggability due to toxicity[1][3][4]
05

Biomarkers

Potential biomarker for tumorigenesis (overexpressed in certain cancers)decreased in prostate cancer progression

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