Target intelligence / Profile preview

Elongin A (ELOA)

Target
ELOA
Molecular classification
Transcription factor, Transcription elongation factor, Component of E3 ubiquitin ligase complex (via interaction with Cullin-RING ligases)
01

Overview

Elongin A (ELOA) is the transcriptionally active subunit of the heterotrimeric Elongin (also known as SIII) complex, composed of Elongin A (ELOA), Elongin B (ELOB), and Elongin C (ELOC)[1][2][3][4]. Elongin A stimulates the elongation phase of RNA polymerase II transcription by suppressing transient pausing and increasing the overall rate of transcript synthesis[1][3][4]. ELOA binds to the RPB2 subunit of Pol II, using specific domains—including a "latch" region that induces conformational changes near the polymerase’s active center, critical for its elongation-stimulatory activity[1][2]. In addition to its canonical role in transcription elongation, Elongin A participates in promoting Mediator complex loading during transcription initiation and can act as a substrate-recognition subunit in E3 ubiquitin ligases (via assembly with CUL5 and RBX2), directing ubiquitylation and proteasomal degradation of Pol II stalled at DNA lesions as part of the DNA damage response[1][3]. There are no approved drugs that directly target ELOA, and the protein does not serve as a common clinical biomarker[3]. However, dysregulation of the Elongin complex, including ELOA, is implicated in cancer, genome stability, and cellular stress responses[3].

Other names
Elongin-ATCEB3MSTP059EloASIIITCEB3AELOA1Elongin 110 kDa subunitRNA polymerase II transcription factor SIII subunit A1SIII p110Transcription elongation factor B polypeptide 3transcription elongation factor B alpha subunitelongin-A
02

Mechanism of action

Allosteric regulator of RNA polymerase II elongation; Adapter for E3 ubiquitin ligase complexes targeting Pol II

03

Biological functions

Stimulation of transcription elongation by RNA polymerase IIRegulation of RNA polymerase II pausingParticipation in transcription initiation (Mediator loading)Mediation of Pol II ubiquitylation and degradation (in complex with CUL5–RBX2)
04

Disease associations

Cancer (through role in transcription regulation and protein ubiquitylation)DNA damage response (by targeting Pol II for degradation)Potentially other stress-related and transcriptional disorders
05

Safety considerations

No direct therapeutic agents or clear safety issues described; manipulating ELOA function could broadly affect gene expression, potentially causing undesirable transcriptional dysregulation or impaired DNA damage response

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