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Acts at E2F-responsive promoters to integrate signals provided by PHD- and/or bromodomain-containing transcription factors. Additionally we are shipping SERTA Domain Containing 1 Proteins (5) and and many more products for this protein.
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NEDD4-1 (show NEDD4 Antibodies) recognizes SERTA domain containing proline rich region of p34SEI-1. Residues of NEDD4-1 (show NEDD4 Antibodies) responsible for direct interaction with p34SEI-1 are identified by NMR titration experiments.
SEI1 up-regulation induces genomic instability by inhibiting DNA damage response in ovarian cancer cells.
Findings provide evidence that TRIP-Br1 functions as an oncogenic protein by providing cancer cells resistance to the hypoxia-induced cell death of breast cancer cells.
TRIP-Br1 confers resistance to serum starvation-induced cell deaths by stabilizing the XIAP (show XIAP Antibodies) protein and inhibiting cellular ROS (show ROS1 Antibodies) production.
Data demonstrate that p34SEI-1 induces the activation of either AKT (show AKT1 Antibodies) or ILK (show ILK Antibodies) signaling on HER2/neu (show ERBB2 Antibodies) expression status.
High SERTAD1 expression is associated with breast cancer.
These results suggest that p34 (show CCNH Antibodies) (SEI-1) inhibits ROS (show ROS1 Antibodies)-induced cell death through by indirectly inducing ubiquitination of ASK1 (show MAP3K5 Antibodies).
Translocation of small amount of NM23H1 (show NME1 Antibodies) into the nucleus induced by the overexpressions of SEI1/SET could increase the frequency of sister chromatid exchangein esophageal cancers.
p34SEI-1 strongly suppressed CREB (show CREB1 Antibodies)-mediated transcription, and this suppression was overcome by excess amount of CBP (show CREBBP Antibodies)
p34SEI1 fragment 30-160 can bind, activate, and inhibit cyclin-dependent kinase (show CDK1 Antibodies) CDK4 (show CDK4 Antibodies); fragment 30-132 binds and activates but does not inhibit CDK4 (show CDK4 Antibodies), while fragment 30-88 cannot bind, activate, or inhibit but retains LexA-mediated transactivation activity.
these data suggest that SERTAD1 acts as a SMAD1 transcriptional co-activator to promote the expression of BMP target genes during mouse cardiogenesis.
Sertad1 expression is required is required for developmental neuronal death in the cerebral cortex.
conclude that Sei1 plays an important role in pancreatic beta-cells, which supports a functional link between Sei1 and the core cell cycle regulators specifically in the context of the pancreas
Acts at E2F-responsive promoters to integrate signals provided by PHD- and/or bromodomain-containing transcription factors. Stimulates E2F-1/DP-1 transcriptional activity. Renders the activity of cyclin D1/CDK4 resistant to the inhibitory effects of p16(INK4a).
SERTA domain containing 1
, CDK4-binding protein p34SEI
, CDK4-binding protein p34SEI1
, SERTA domain-containing protein 1
, transcriptional regulator interacting with the PHD-bromodomain 1
, PHD zinc finger- and bromodomain-interacting protein 1