anti-Nuclear Receptor Subfamily 1, Group D, Member 2 (NR1D2) Antikörper

Human Nuclear Receptor Subfamily 1, Group D, Member 2 (NR1D2) Interaktionspartner

1. A GBM-promoting role of NR1D2.

2. Rev-erbalpha regulates Cyp7a1 and cholesterol metabolism through its repression of the Lrh-1 receptor.

3. Data show that miR-210 inhibits the expression of nuclear receptor subfamily 1, group D, member 2 (NR1D2), particularly in cryptorchidic tissues.

4. These results demonstrate the importance of the Rev-erbbeta HRM in regulating interactions with heme and NCoR1 and advance our understanding of how signaling through HRMs affects the major cellular processes of circadian rhythm maintenance and metabolism.

5. heme is involved in regulating the degradation of Rev-erbbeta in a manner consistent with its role in circadian rhythm maintenance

6. Together, the findings demonstrate an anti-inflammatory effect, downregulating of MMP-9 and CCL2 transcription, of astroglial REV-ERBs activation through HDAC3-dependent and HDAC3-independent mechanisms.

7. REV-ERBbeta plays a role in supporting cancer cell viability when autophagy is compromised.

8. REV-ERB-ALPHA circadian gene variant associates with obesity in two independent populations: Mediterranean and North American.

9. Cobalt protoporphyrin IX (CoPP) and zinc protoporphyrin IX (ZnPP) are ligands that bind directly to the REV-ERBs. However, instead of mimicking the agonist action of heme, CoPP and ZnPP function as antagonists of REV-ERB function.

10. Our results suggest that the REV-ERBalpha rs2071427 polymorphism modulates body fat mass in both adult and young people.

11. oxidative stress leads to oxidation of cysteine(s), thus releasing heme from Rev-erbbeta and altering its transcriptional activity.

12. Nuclear receptor rev-erb-{alpha} circadian gene variants have a role in response to lithium carbonate in bipolar affective disorder

13. Rev-erbbeta modulates the apoCIII gene expression by recruiting different transcription co-activator or co-repressor.

14. heme regulation of REV-ERBs may link the control of metabolism and the mammalian clock

Mouse (Murine) Nuclear Receptor Subfamily 1, Group D, Member 2 (NR1D2) Interaktionspartner

1. Rev-erbalpha is a pharmacologically accessible link between the circadian clock and neuroinflammation.

2. results proved that the REV-ERB agonism inhibited osteoclastogenesis partially via FABP4 up-regulation.

3. REV-ERBbeta is involved in the maintenance of wakefulness during the activity period of the circadian rhythm.

4. REV-ERBbeta drives mitochondrial biogenesis and the expression of genes involved in fatty acid oxidation. REV-ERBbeta-deficient mice exhibited an altered metabolic phenotype compared to wild-type littermates. REV-ERBbeta plays a role in the control of skeletal muscle metabolism and energy expenditure

5. Loss of REV-ERB-BETA leads to de-repression of orexinergic genes.

6. In conclusion, the present study demonstrates that KK-S6 functions as a novel modulator of the amplitude of molecular circadian rhythms by influencing RORE-mediated BMAL1 expression.

7. Genetic deletion of the Rev-erbalpha gene or pharmacological inhibition of REV-ERBalpha activity in the ventral midbrain induced mania-like behavior in association with a central hyperdopaminergic state.

8. data now unite REV-ERB-alpha and REV-ERB-beta with PER, CRY and other components of the principal feedback loop that drives circadian expression and indicate a more integral mechanism for the coordination of circadian rhythm and metabolism

9. In mouse livers, Rev-erbbeta mRNA and protein levels oscillate with a diurnal pattern similar to that of Rev-erbalpha, and both Rev-erbs are recruited to a remarkably similar set of binding sites across the genome, enriched near metabolic genes

10. The results suggest that heme, functioning as a REV-ERB ligand, is an important signaling molecule for induction of adipogenesis. Synthetic small molecule ligands for REV-ERB are effective modulators of adipogenesis.

11. oscillation of p21WAF1/CIP1 gene transcription is regulated by the antagonistic activities of the orphan nuclear receptors REV-ERBalpha/beta and RORalpha4/gamma, which are core clock regulators

12. examined cell-autonomous circadian oscillations using combined gene knockout and RNA interference and demonstrated that REV-ERBalpha and beta are functionally redundant and are required for rhythmic Bmal1 expression

13. These data suggest that Rev-erb beta has the potential to activate gene expression, and is a positive regulator of Srebp-1c, a regulator of lipogenesis.