Related Experiment Video
Updated: Aug 5, 2026
11:03
Massively Parallel Reporter Assays in Cultured Mammalian Cells
Published on: August 17, 2014
Promiscuity among the MRAPs
1Centre for EndocrinologyWilliam Harvey Research Institute, Barts & the London School of Medicine & Dentistry, Queen Mary University of London, Charterhouse Square, London, UK a.j.clark@qmul.ac.uk.
Journal of Molecular Endocrinology
|February 19, 2017
Summary
Melanocortin 2 receptor accessory proteins (MRAP and MRAP2) are crucial for ACTH and melanocortin 4 receptor function. MRAP2 deletion in mice causes obesity, suggesting broader roles beyond melanocortin receptors.
Area of Science:
- Endocrinology
- Molecular Biology
- Neuroscience
Background:
- Melanocortin 2 receptor accessory protein (MRAP) is essential for ACTH receptor (MC2R) function, mediating trafficking and ligand binding.
- MRAP2, a related protein, is primarily found in the CNS and interacts with the melanocortin 4 receptor (MC4R).
Purpose of the Study:
- To investigate the broader roles of MRAP and MRAP2 beyond their known interactions with melanocortin receptors.
- To explore potential new receptor interactions and tissue distribution patterns of MRAP and MRAP2.
Main Methods:
- Gene deletion studies in mice (Mrap2 knockout).
- Phenotypic analysis of knockout mice, comparing with existing Mc4r knockout models.
- Literature review on functional interactions and tissue expression.
Main Results:
- Mice lacking Mrap2 exhibit a severe obesity phenotype, distinct from Mc4r-deleted mice.
- A functional interaction between MRAP2 and prokineticin receptors has been recently identified.
- MRAP and MRAP2 show varied tissue distribution, hinting at diverse functions.
Conclusions:
- MRAP and MRAP2 likely have roles extending beyond melanocortin receptors.
- MRAP2's involvement in obesity suggests complex regulatory functions in the CNS.
- Further research into MRAP/MRAP2 interactions with other receptors is warranted.
Related Concept Videos
01:36Mismatch Repair
Overview
01:25Rab Cascades
Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
01:25Mechanism of Antibiotic Resistance in MRSA
Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
01:25Clinical Significance of Antibiotic Resistance
Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...