| Receptor activity-modifying protein | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| Identifiers | |||||||||
| Symbol | RAMP | ||||||||
| Pfam | PF04901 | ||||||||
| InterPro | IPR006985 | ||||||||
| Membranome | 10 | ||||||||
| |||||||||
| Receptor activity-modifying protein 1 | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Symbol | RAMP1 | ||||||
| NCBI gene | 10267 | ||||||
| HGNC | 9843 | ||||||
| OMIM | 605153 | ||||||
| RefSeq | NM_005855 | ||||||
| UniProt | O60894 | ||||||
| Other data | |||||||
| Locus | Chr. 2q36-37.1 | ||||||
| |||||||
| Receptor activity-modifying protein 2 | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Symbol | RAMP2 | ||||||
| NCBI gene | 10266 | ||||||
| HGNC | 9844 | ||||||
| OMIM | 605154 | ||||||
| RefSeq | NM_005854 | ||||||
| UniProt | O60895 | ||||||
| Other data | |||||||
| Locus | Chr. 17q12-21.1 | ||||||
| |||||||
| Receptor activity-modifying protein 3 | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Symbol | RAMP3 | ||||||
| NCBI gene | 10268 | ||||||
| HGNC | 9845 | ||||||
| OMIM | 605155 | ||||||
| RefSeq | NM_005856 | ||||||
| UniProt | O60896 | ||||||
| Other data | |||||||
| Locus | Chr. 7q13-p12 | ||||||
| |||||||
Receptor activity-modifying proteins (RAMPs) are a class of protein that interact with and modulate the activities of several Class BG protein-coupled receptors including the receptors forsecretin,calcitonin (CT),glucagon, andvasoactive intestinal peptide (VIP).[1] There are three distinct types of RAMPs in mammals (though more in fish), designatedRAMP1,RAMP2, andRAMP3, each encoded by a separate gene.[2]
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Currently, the function of RAMPs is divided into classes of activities. When associated with theCalcitonin receptor (CTR) orCalcitonin receptor-like (CALCRL) (below), RAMPs can change the selectivity of the receptor for a specific hormone. In the cases of the other receptors mentioned, however, there is no evidence that they can do this, but instead function to regulate trafficking of receptors from theER /golgi to the membrane. These functions appear to be ones where there is redundancy, as neither RAMP1 nor RAMP3knockout mice (KO) have grossly abnormalphenotypes. The likelihood is that the phenotype of RAMP2 KO mice is more connected with the abolition of mostadrenomedullin (AM) signalling than effects on trafficking of other receptors, as those mice are almost identical to AM KO mice and mice lacking the Calcitonin-like receptor which are unable to form either AM1 or AM-2 adrenomedullin receptors (CLR/RAMP2 and CLR/RAMP3 respectively).
Association of RAMPs with either theCT orCALCRL proteins forms 6 different receptors from the calcitonin receptor family:[3][4][5]
| GPCR | RAMP isoform | resultant receptor |
|---|---|---|
| Calcitonin receptor-like | RAMP1 | CGRP receptor |
| RAMP2 | adrenomedullin (AM) receptor, designated AM1[6] | |
| RAMP3 | dual CGRP/AM receptor, designated AM2 | |
| Calcitonin receptor | RAMP1 | amylin receptor AMY1 |
| RAMP2 | amylin receptor AMY2 | |
| RAMP3 | amylin receptor AMY3 |
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