anti-MC3R (MC3R) Antikörper

Mouse (Murine) Melanocortin 3 Receptor (MC3R) Interaktionspartner

1. Replacing murine Mc3r with and double-mutant (C17A+G241A) human MC3R showed greater weight and fat mass, increased energy intake and feeding efficiency.

2. MC1-mediated effects were reduced, and MC3 anti-inflammatory circuits predominated. Mice bearing a nonfunctional MC1 displayed a transient exacerbation of neutrophil recruitment after global I/R, which diminished by 2 hours.

3. The minimum promoter region required for Mc3r expression has been identified, along with two binding sites for AP-1 (zeige JUN Antikörper) and ATF4 (zeige ATF4 Antikörper) and in the 5' upstream-flanking region of Mc3r that are essential for Mc3r expression.

4. 3' RACE experiments using hypothalamic RNA indicated the 3' UT (zeige UTS2R Antikörper)R terminates approximately 1286 bases after the translational stop codon, with a previously unknown 787 base splice between consensus splice donor and acceptor sites.

5. These data reveal novel protective properties of endogenous MC3 on periodontal status in health and disease

6. Data suggest that Mc3r (not Mc4r (zeige MC4R Antikörper)) is expressed in 1/3 of dopaminergic neurons in ventral tegmental area (VTA); global deletion of Mc3r in knockout mice increases VTA dopamine by 42% and decreases sucrose intake/preference in female (not male) mice.

7. Mutually opposite signal modulation by hypothalamic heterodimerization of ghrelin (zeige GHRL Antikörper) and melanocortin-3 receptors.

8. data suggest that the melanocortin-3 receptor is involved in the control of energy balance and the expression of rhythms anticipating nutrient intake.

9. MC(3) plays a subtle role in the regulation of food intake

10. Compared with WT, MC4R (zeige MC4R Antikörper)-/- showed no activation in area postrema but showed normal activation in paraventricular hypothalamus, whereas MC3R-/- showed reduced activation in PVN but not in AP.

Human Melanocortin 3 Receptor (MC3R) Interaktionspartner

1. Structural Insights into Selective Ligand-Receptor Interactions Leading to Receptor Inactivation Utilizing Selective Melanocortin 3 Receptor Antagonists.

2. Results show regulation of melanocortin receptors MC2R (zeige MC2R Antikörper), MC3R and MC4R (zeige MC4R Antikörper) gene expressions in CD8 (zeige CD8A Antikörper)(+) cytotoxic T-lymphocytes and CD19 (zeige CD19 Antikörper)(+) B lymphocytes in rheumatoid arthritis (RA) treated with tumor necrosis factor-alpha (TNF-alpha (zeige TNF Antikörper)) inhibitor (zeige ZFP36 Antikörper) adalimumab.

3. MC3R mutations are associated with Obesity.

4. findings support the role of MC3R genetic variants in adiposity gain during early childhood.

5. There is no evidence of any association between MC3R variations and obesity.

6. melanocortin receptors MC2R (zeige MC2R Antikörper), MC3R and MC5R (zeige MC5R Antikörper) are most abundantly expressed in glandular epithelium of the endometrium

7. Replacing murine Mc3r with and double-mutant (C17A+G241A) human MC3R showed greater weight and fat mass, increased energy intake and feeding efficiency.

8. the DPLIY motif and helix 8 was important for MC3R activation and signal transduction. The data led to a better understanding of the structure-function relationship of MC3R.

9. novel data about the structure-function relationship of MC3R, identifying residues important for receptor function; some studied mutations exhibited biased signaling, preferentially activating one intracellular signaling pathway.

10. propose three potential human candidate genes for voluntary physical exercise levels (MC3R, CYP24A1 (zeige CYP24A1 Antikörper), and GRM8 (zeige GRM8 Antikörper)).