anti-Spen Homolog, Transcriptional Regulator (Drosophila) (SPEN) Antikörper

Human Spen Homolog, Transcriptional Regulator (Drosophila) (SPEN) Interaktionspartner

1. our data demonstrate a role for SPEN in the regulation of primary cilia formation and cell migration in breast cancer cells, which may collectively explain why its expression is associated with time to metastasis in cohorts of patients with ERalpha (zeige ESR1 Antikörper)-negative breast cancers.

2. SPEN is a novel tumor-suppressor gene that may be clinically useful as a predictive biomarker of tamoxifen response in ERalpha (zeige ESR1 Antikörper)-positive breast cancers.

3. SPEN mutations were associated with diffuse large B-cell lymphoma with hepatitis C virus infection.

4. Phosphorylation of the CK2 site on SMRT significantly increased affinity for SHARP.

5. These results demonstrate a role for the inactivation of SHARP transcription in DM1 biology.

6. MINT3 (zeige APBA3 Antikörper) and MINT17 were informative for patient grouping to predict local recurrence in rectal cancer patients

7. SHARP is a novel component of the HDAC (zeige HDAC3 Antikörper) corepressor complex, recruited by RBP (zeige RBP4 Antikörper)-Jkappa to repress transcription of target genes in the absence of activated Notch (zeige NOTCH1 Antikörper).

8. the conserved function of the SPOC domain of SHARP is to mediate interaction with SMRT/NCoR (zeige NCOR1 Antikörper) corepressors, and that Spen proteins play an essential role in the repression complex

9. both the androgen receptor (zeige AR Antikörper) interacting domains of the coactivator SRC1 (zeige SRC Antikörper) and of the corepressor SMRT compete for interaction with the androgen receptor (zeige AR Antikörper) N-terminus

10. Pak1 (zeige PAK1 Antikörper)-SHARP interaction plays an essential role in enhancing the corepressor functions of SHARP, thereby modulating Notch (zeige NOTCH1 Antikörper) signaling in human cancer cells.

Mouse (Murine) Spen Homolog, Transcriptional Regulator (Drosophila) (SPEN) Interaktionspartner

1. Spenito (zeige RBM15 Antikörper), a small Spen family member, counteracted Spen function in fat regulation. Finally, mouse Spen and Spenito (zeige RBM15 Antikörper) transcript levels scaled directly with body fat in vivo, suggesting a conserved role in fat liberation and catabolism. This study demonstrates that Spen is a key regulator of energy balance and provides a molecular context to understand the metabolic defects that arise from Spen dysfunction.

2. Spen is required for gene repression by Xist. Spen is not required for Xist RNA localization and the recruitment of chromatin modifications.

3. Spen is required for Xist-mediated silencing.

4. results suggest that Xist silences transcription by directly interacting with SHARP, recruiting SMRT, activating HDAC3 (zeige HDAC3 Antikörper), and deacetylating histones to exclude Pol II (zeige 0 Antikörper) across the X chromosome

5. MINT forms a high affinity complex with CSL (zeige SMPX Antikörper); the domains of MINT and CSL (zeige SMPX Antikörper) that are necessary and sufficient for complex formation are delineated

6. MINT plays an important role in tooth development, in particular, epithelial morphogenesis

7. Notch1 (zeige NOTCH1 Antikörper) in concert with Notch2 (zeige NOTCH2 Antikörper) contributes to the morphogenesis of renal vesicles into S-shaped bodies in a RBP-J (zeige RBPJ Antikörper)-dependent manner.

8. Msx2-interacting nuclear target protein (MINT) competed with the intracellular region of Notch (zeige NOTCH1 Antikörper) for binding to a DNA binding protein (zeige HSF4 Antikörper) RBP-J (zeige RBPJ Antikörper) and suppressed the transactivation activity of Notch (zeige NOTCH1 Antikörper) signaling.

9. Stra13, Dec and Sharp (Mint) bHLH repressors are dynamically regulated during mammary gland development and may function to regulate apoptosis

10. MINT enhances Runx2 (zeige RUNX2 Antikörper) activation of multiprotein complexes assembled by the OCFRE