Gene: maps to 5q31.3-q32.
mRNA: sizes: major transcripts of 0.7-0.85 kb in length and less abundant transcripts of 1.3-1.5 kb were detected in human multiple tissue northern blot (Lanz R.B. et al., 1999).
Protein: tentatives to generate protein encoded by SRA cDNAs were reported to be unsuccessful. In vitro translation of different SRA cDNAs did not result in detectable levels of protein (Lanz R.B. et al., 1999).
SRA was shown to enhance
progesterone receptor (PgR) transactivation but did not alter the activity of
PgR in the presence of the antagonist RU486. SRA also enhanced transactivation induced by
estrogen receptor (ER), glucocorticoid receptor, androgen receptor, thyroid hormone receptor, retinoid acid-(RAR and RXR) receptor, peroxisome proliferator-activated receptor, but not by various activators other than steroid receptors (CREB, Gal4,...). SRA appears to enhance transactivation through the N-terminal AF1 portion of steroid receptors.
Mutants of SRA containing single or multiple frameshift mutations along the core sequence, resulting in a "mosaic" organization of reading frames, were constructed. Most of them retained the ability to enhance
PgR transactivation, suggesting that the coactivation exerted by SRA on steroid receptor transcription was unlikely to be mediated by a translation product of the SRA gene (Lanz R.B. et al., 1999).
