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Elongin-A2 (ELOA2) is the transcriptionally active subunit of the SIII (elongin) transcription elongation factor complex, which also comprises the regulatory subunits Elongin-B and Elongin-C[5]. This complex stimulates the rate of transcription elongation by RNA polymerase II, largely by suppressing transient polymerase pausing at many sites along the DNA template[1][3][5][6]. ELOA2 binds to the RPB2 side of RNA polymerase II and anchors the ELOB–ELOC subunit heterodimer[1]. When induced by DNA damage or other cellular stresses, ELOA2 can participate as an adaptor in the assembly of an E3 ubiquitin ligase complex (with CUL5–RBX2), facilitating ubiquitylation and degradation of stalled RNA polymerase II, thereby promoting transcriptional clearance and DNA repair[6]. Additionally, Elongin (including ELOA2) has roles in transcriptional induction in response to cellular stimuli, including ER stress where it acts as a loading factor for the Mediator complex at stress response gene promoters[2]. Recent evidence suggests that Elongin-A2 may also function at potential enhancer regions and is highly enriched at transcriptionally active genomic sites[4]. There are no known drugs currently targeting ELOA2, and it is not validated as a patient biomarker or a direct therapeutic target.
Not applicable (no drugs targeting this molecule; mechanistically, ELOA2 modulates transcription by allosteric regulation and, in complex, can participate in E3 ligase formation for ubiquitylation of stalled RNA polymerase II)
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