Potentiation of estrogen receptor transcriptional activity by breast cancer amplified sequence 2

Proteomic profiling of rapid non-genomic and concomitant genomic effects of acute restraint stress on rat thymocytes

“…Several other proteins (RELA, RUVBL1, periredoxin, tubulin alpha, tubulin beta, cytokeratin 8, ACTB, ALBU and FETUA) were previously found to be part of cytosolic GR complexes in the liver [39]. Also PARK7, BCAS2 and EBP1 are known interaction partners of nuclear receptors such as the androgen receptor [40,41] and the estrogen receptor [42] both of which heterodimerize with the GR. The Hsp90 co-chaperone TERT (also p23, cPGES) is part of the basic GR complex [43] and showed a decrease in the cytosol after stress.…”

Breast Cancer Amplified Sequence 2, a Novel Negative Regulator of the p53 Tumor Suppressor

“…The BCAS2 gene maps to chromosome 1p13.3-21 region and contains 678 bp encoding 225 amino acids, with a predicted molecular mass of 26 kDa (2). BCAS2 was recently characterized as a transcriptional cofactor that enhances estrogen receptor-mediated gene expression (4). In this article, we found that BCAS2 associates with the tumor suppressor p53 protein; we have also probed the cellular and molecular effects of this interaction.…”

BCAS2 is essential for Drosophila viability and functions in pre-mRNA splicing

“…The rescue effect of hBCAS2-C is not as potent as fulllength hBCAS2, suggesting that there are other roles for BCAS2 in wing shape development, besides RNA splicing. Aside from RNA splicing, BCAS2 also has been reported to interact with estrogen receptor (ER) as a transcriptional cofactor (Qi et al 2005) and with p53 as a negative regulator (Kuo et al 2009). ER is known as a growth survivor and p53 as a tumor suppressor, both of these proteins are crucial for cell viability.…”