Enhancer ID: | E_01_0739 |
Species: | human |
Position : | chr5:102751294-102753294 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Obesity, chronic inflammation |
Pubmed ID: | 30168706 |
Enhancer experiment: | Western blot, statistical analysis |
Enhancer experiment description: | In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. |
Target gene : | MC1R |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. ;In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.;In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8. |
TF name : | MYCBP2MC2R |
TF experiment: | western blot,???? |
TF experiment description: | In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. ;In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.;In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8. |
Enhancer function : | In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
---|---|---|---|
MYCBP2 | Hs_Integrated_Breast_Cancer_Pathway_WP1984_82941 | wikipathways | 122 |
MC2R | Corticotropin Activation of Cortisol Production | smpdb | 6 |
MC2R | G alpha (s) signalling events | reactome | 142 |
MC2R | Peptide ligand-binding receptors | reactome | 103 |
MC2R | Neuroactive ligand-receptor interaction | kegg | 272 |