Summary of OPRM1
The OPRM1 gene codes for the mu opioid receptor. This receptor is activated by your body’s natural opioids (such as beta-endorphins) and by opioid medications (such as morphine) [R].
OPRM1 promotes pain relief. OPRM1 activation also leads to the release of dopamine, a chemical messenger that promotes feelings of pleasure. This process is involved in reward-seeking and addictive behaviors [R, R, R].
OPRM1 variants have been linked to opioid addiction and heavy alcohol intake [R, R, R, R].
Protein names
Recommended name:
Mu-type opioid receptorShort name:
MOPAlternative name(s):
M-OR-1MOR-1
Mu opiate receptor
Mu opioid receptor
hMOP
- RS10485057 (OPRM1) ??
- RS1799971 (OPRM1) ??
- RS1799972 (OPRM1) ??
- RS2075572 (OPRM1) ??
- RS2236256 (OPRM1) ??
- RS3778151 (OPRM1) ??
- RS3823010 (OPRM1) ??
- RS495491 (OPRM1) ??
- RS538174 (OPRM1) ??
- RS540825 (OPRM1) ??
- RS563649 (OPRM1) ??
- RS609148 (OPRM1) ??
- RS675026 (OPRM1) ??
- RS9384179 (OPRM1) ??
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Top Gene-Substance Interactions
OPRM1 Interacts with These Diseases
| Disease | Score |
Fixes
Natural Ways to Increase Opioid Activity
All of these give us a positive feeling, and at least some of it is because of the opioid system in our body. The following either increase activation of our mu opioid receptors, increase endorphins, which naturally activate our mu-opioid receptors, or make our receptors more sensitive.
Substances That Increase OPRM1
| Substances | Interaction | Organism | Category |
Substances That Decrease OPRM1
| Substances | Interaction | Organism | Category |
Advanced Summary
Activation of the mu receptor by a substance such as morphine causes sedation, euphoria and decreased respiration (R). Although morphine increases sedation, it decreases the total amount of deep sleep and rapid eye movement sleep in humans. (R).
Individual differences in the function of the mu-receptor system predict personality traits that confer vulnerability to or resiliency against risky behaviors such as the predisposition to develop substance use disorders (R).
Activating opioid receptors promote eating and weight gain, at least in the short term (R). When fed a high-fat diet, mice without mu-opioid receptors were resistant to obesity, despite having similar calorie intake to normal mice fed a high-fat diet. This resistance to obesity with the mutant mouse without mu-opioid receptors was associated with increased fatty acid oxidation within muscles (R).
When food proteins are digested, they produce peptides that block mu-opioid activity. These peptides are released in the vein that brings blood flow to the gut.
The vagus nerves communicate with the brain initiate satiety as a result of the mu-opioid blocking (as a result of sensing gut gluconeogenesis) (R). This is one reason why a protein rich diet aids in weight loss.
When the mice were switched from a starch- to a protein-enriched diet, mice reduced their food intake by about 20%, but no such effect occurred in the mice lacking the mu-opioid receptors (R).
Conditions with Increased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
|---|
Conditions with Decreased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
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Technical
The following transcription factors affect gene expression:
Tissue specificity:
Expressed in brain. Isoform 16 and isoform 17 are detected in brain.
Gene Pathways:
Molecular Function:
- G-Protein Alpha-Subunit Binding
- G-Protein Coupled Receptor Activity
- Beta-Endorphin Receptor Activity
- Voltage-Gated Calcium Channel Activity
- G-Protein Beta-Subunit Binding
- Morphine Receptor Activity
- Neuropeptide Binding
Biological Processes:
- Acute Inflammatory Response To Antigenic Stimulus
- G-Protein Coupled Receptor Signaling Pathway, Coupled To Cyclic Nucleotide Second Messenger
- Adenylate Cyclase-Activating Dopamine Receptor Signaling Pathway
- Negative Regulation Of Adenylate Cyclase Activity
- Phospholipase C-Activating G-Protein Coupled Receptor Signaling Pathway
- Positive Regulation Of Cytosolic Calcium Ion Concentration
- Chemical Synaptic Transmission
- Sensory Perception
- Locomotory Behavior
- Negative Regulation Of Cell Proliferation
- Response To Radiation
- Sensory Perception Of Pain
- Adenylate Cyclase-Inhibiting Opioid Receptor Signaling Pathway
- Response To Food
- Positive Regulation Of Appetite
- Response To Lipopolysaccharide
- Cellular Response To Stress
- Wound Healing
- Response To Cocaine
- Eating Behavior
- Positive Regulation Of Camp-Mediated Signaling
- Negative Regulation Of Camp-Mediated Signaling
- Estrous Cycle
- Negative Regulation Of Nitric Oxide Biosynthetic Process
- Positive Regulation Of Nitric Oxide Biosynthetic Process
- Behavioral Response To Ethanol
- Positive Regulation Of Neurogenesis
- Negative Regulation Of Cytosolic Calcium Ion Concentration
- Regulation Of Sensory Perception Of Pain
- Excitatory Postsynaptic Potential
- Negative Regulation Of Wnt Protein Secretion
- Positive Regulation Of Erk1 And Erk2 Cascade
- Response To Growth Factor
- Cellular Response To Morphine
- Regulation Of N-Methyl-D-Aspartate Selective Glutamate Receptor Activity
Drug Bank:
- Levomethadyl Acetate
- Alvimopan
- Amitriptyline
- Anileridine
- Butorphanol
- Codeine
- Dextromethorphan
- Dextropropoxyphene
- Dezocine
- Diphenoxylate
- Ethylmorphine
- Fentanyl
- Heroin
- Hydrocodone
- Hydromorphone
- Ketamine
- Levallorphan
- Levorphanol
- Loperamide
- Methadone
- Methadyl Acetate
- Pethidine
- Naloxegol
- Naloxone
- Naltrexone
- Ondansetron
- Oxymorphone
- Pentazocine
- Remifentanil
- Sufentanil
- Tapentadol
- Methylnaltrexone
- Alfentanil
- Buprenorphine
- Eluxadoline
- Ketobemidone
- Morphine
- Nalbuphine
- Oxycodone
- Tramadol