UXT Proteine (UXT)

Zebrafish Ubiquitously-Expressed, Prefoldin-Like Chaperone (UXT) Interaktionspartner

1. data presented in this study characterize UXT as a novel repressor of Notch signaling, shedding new light on the molecular regulation of angiogenesis.

Mouse (Murine) Ubiquitously-Expressed, Prefoldin-Like Chaperone (UXT) Interaktionspartner

1. Our study has revealed the first in vivo function for UXT in the mammalian germline as a regulator of distinct transcriptional programs in SSCs and differentiating spermatogonia.

2. UXT Is a LOX-PP Interacting Protein That Modulates Estrogen Receptor Alpha Activity in Breast Cancer Cells.

3. UXT-V1 represents a novel integral component of the MAVS signalosome on mitochondria, mediating the innate antiviral signal transduction.

4. these results suggest that Als2 is a binding partner of Uxt and Als2/Uxt interaction could be important for the activation of Nf-kappaB pathway.

5. Ubiquitously expressed transcript, UXT-V1, is a novel regulator of TNF-induced apoptosis. It protects cells against TNF-induced apoptosis through modulating complex II formation.

6. Uxt is a novel and essential cofactor in the NF-kappa B transcriptional enhanceosome.

Human Ubiquitously-Expressed, Prefoldin-Like Chaperone (UXT) Interaktionspartner

1. UXT Is a LOX-PP Interacting Protein That Modulates Estrogen Receptor Alpha Activity in Breast Cancer Cells.

2. EZH1, SUZ12 and UXT work synergistically to regulate pathway activation in the nucleus.

3. we describe the identification of UXT as a novel MDMX-interacting protein

4. UXT is a binding protein of PIAS2, and interaction between PIAS2 and UXT may be important for the transcriptional activation of AR.

5. Art27 interacts with GATA4, FOG2 and NKX2.5 and is a novel co-repressor of cardiac genes.

6. Knockdown of UXT expression in Treg cells results in a less-suppressive phenotype.

7. VHL-UXT interaction and VHL-induced ubiquitination of androgen receptor(AR) regulate transcriptional activation of the AR.

8. Data found that the UXT isoforms elicit dual opposing regulatory effects on SARM-induced apoptosis.

9. Epstein-Barr virus BGLF4 kinase downregulates NF-kappaB transactivation through phosphorylation of coactivator UXT

10. Loss of ART-27 enhances expression of many androgen-regulated genes, suggesting that ART-27 inhibits gene expression, and nuclear ART-27 expression was lost in the majority of AR-positive recurrent prostate cancers.

11. UXT-V1 represents a novel integral component of the MAVS signalosome on mitochondria, mediating the innate antiviral signal transduction.

12. these results suggest that Als2 is a binding partner of Uxt and Als2/Uxt interaction could be important for the activation of Nf-kappaB pathway.

13. Data show that while Art-27 can bind AR directly, URI is bound to chromatin prior to hormone-dependent recruitment of AR, suggesting a role for URI in modulating AR recruitment to target genes.

14. Ubiquitously expressed transcript, UXT-V1, is a novel regulator of TNF-induced apoptosis. It protects cells against TNF-induced apoptosis through modulating complex II formation.

15. decreased levels of ART-27 protein in prostate cancer tissue may occur as a result of de-differentiation, and indicate that ART-27 is likely to regulate a subset of AR-responsive genes important to prostate growth suppression and differentiation.

16. UXT is a component of centrosome and is essential for cell viability and may facilitate transformation by corrupting regulated centrosome functions.

17. Increasing concentrations of UXT contributes to progressive aggregation of mitochondria.

18. UXT is a novel and essential cofactor in the NF-kappa B transcriptional enhanceosome.

19. UXT suppresses cell transformation and might mediate this function by interaction and inhibition of the biological activity of cell proliferation and survival stimulatory factors like ecotropic viral integration site 1

20. propose a transcriptional regulatory circuit for the developmental expression of ART-27 that includes repression by chromatin modification through a trichostatin A-sensitive factor and activation upon growth factor stimulation via CREB