Steroid receptor RNA activator 1 (SRA1)

Steroid receptor RNA activator 1 (SRA1) encodes both a long noncoding RNA (SRA) and an endogenous protein (SRAP).[1][2][3][4] The SRA lncRNA acts as a transcriptional coactivator, selectively enhancing the activity of class I nuclear steroid receptors—including androgen receptor, estrogen receptor alpha (but not beta), glucocorticoid receptor, and progesterone receptor—by facilitating interactions within transcriptional complexes and influencing gene transcription in a binding- and structure-dependent manner.[1][3] Recent studies show that SRA gene transcripts can be translated into SRAP, a protein that may regulate estrogen and androgen receptor activity, although its precise molecular mechanism and biological role remain less well defined.[2] Both SRA and SRAP are implicated in the development and progression of hormone-dependent cancers, notably breast and prostate cancer; the ratio of their expression may be an indicator of cancer cell aggressiveness.[2] SRA1 functions within a multi-protein regulatory network, interacting with other coactivators (SRC-1), RNA helicases (p68/p72), pseudouridine synthases (Pus1p/Pus3p), and RNA-binding proteins (SLIRP, SHARP), and is subject to structural and post-transcriptional modifications that can shift its role between coactivation and repression.[1][2] There are currently no approved drugs directly targeting SRA1 or SRAP, and therapeutic strategies may be challenged by their broad roles in nuclear receptor signaling.

Other names

SRASRAPPP7684STRAA1Steroid receptor RNA activator proteinlncRNA SRASteroid receptor coactivatorSRA1

Acts primarily as a transcriptional coactivator: modulates activity of nuclear steroid receptors (androgen, estrogen, glucocorticoid, progesterone receptors), enhancing or modifying gene transcription based on coregulator and post-transcriptional modifications. SRAP isoform may influence assembly of transcriptional complexes or splicing, but its mechanism is not fully defined.