Biology:Heteromer

From HandWiki

A heteromer is something that consists of different parts; the antonym of homomeric. Examples are:

Biology

Pharmacology

  • Ligand-gated ion channels such as the nicotinic acetylcholine receptor and GABAA receptor are composed of five subunits arranged around a central pore that opens to allow ions to pass through. There are many different subunits available that can come together in a wide variety of combinations to form different subtypes of the ion channel.[3][4][5] Sometimes the channel can be made from only one type of subunit, such as the α7 nicotinic receptor, which is made up from five α7 subunits, and so is a homomer rather than a heteromer, but more commonly several different types of subunit will come together to form a heteromeric complex (e.g., the α4β2 nicotinic receptor, which is made up from two α4 subunits and three β2 subunits). Because the different ion channel subtypes are expressed to different extents in different tissues, this allows selective modulation of ion transport and means that a single neurotransmitter can produce varying effects depending on where in the body it is released.[6][7][8]
  • G protein-coupled receptors are composed of seven membrane-spanning alpha-helical segments that are usually linked together into a single folded chain to form the receptor complex. However, research has demonstrated that a number of GPCRs are also capable of forming heteromers from a combination of two or more individual GPCR subunits under some circumstances, especially where several different GPCRs are densely expressed in the same neuron. Such heteromers may be between receptors from the same family (e.g., adenosine A1/A2A heteromers[9][10] and dopamine D1/D2[11] and D1/D3 heteromers[12]) or between entirely unrelated receptors such as CB1/A2A,[13] glutamate mGluR5 / adenosine A2A heteromers,[14] cannabinoid CB1 / dopamine D2 heteromers,[15] and even CB1/A2A/D2 heterotrimers where three different receptors have come together to form a heteromer.[16][17] The ligand binding properties and intracellular trafficking pathways of GPCR heteromers usually show elements from both parent receptors, but may also produce quite unexpected pharmacological effects, making such heteromers an important focus of current research.[18][19][20][21][22]

See also

References

  1. ↑ Medical dictionary
  2. ↑ Merriam-Webster Dictionary
  3. ↑ "Heterogeneity and complexity of native brain nicotinic receptors". Biochemical Pharmacology 74 (8): 1102–11. October 2007. doi:10.1016/j.bcp.2007.05.023. PMID 17597586. 
  4. ↑ "Diversity of vertebrate nicotinic acetylcholine receptors". Neuropharmacology 56 (1): 237–46. January 2009. doi:10.1016/j.neuropharm.2008.07.041. PMID 18723036. https://zenodo.org/record/3443542. 
  5. ↑ "The road to discovery of neuronal nicotinic cholinergic receptor subtypes". Nicotine Psychopharmacology. Handbook of Experimental Pharmacology. 192. 2009. pp. 85–112. doi:10.1007/978-3-540-69248-5_4. ISBN 978-3-540-69246-1. 
  6. ↑ "Human brain nicotinic receptors, their distribution and participation in neuropsychiatric disorders". Current Drug Targets. CNS and Neurological Disorders 1 (4): 387–97. August 2002. doi:10.2174/1568007023339283. PMID 12769611. 
  7. ↑ Nutt D (April 2006). "GABAA receptors: subtypes, regional distribution, and function". Journal of Clinical Sleep Medicine 2 (2): S7–11. doi:10.5664/jcsm.26525. PMID 17557501. 
  8. ↑ "Forebrain and midbrain distribution of major benzodiazepine–sensitive GABAA receptor subunits in the adult C57 mouse as assessed with in situ hybridization". Neuroscience 150 (2): 370–85. December 2007. doi:10.1016/j.neuroscience.2007.09.008. PMID 17950542. 
  9. ↑ "Presynaptic control of striatal glutamatergic neurotransmission by adenosine A1-A2A receptor heteromers". Journal of Neuroscience 26 (7): 2080–7. February 2006. doi:10.1523/JNEUROSCI.3574-05.2006. PMID 16481441. 
  10. ↑ "Adenosine A1-A2A receptor heteromers: new targets for caffeine in the brain". Frontiers in Bioscience 13 (13): 2391–9. 2008. doi:10.2741/2852. PMID 17981720. http://www.bioscience.org/2008/v13/af/2852/fulltext.htm. 
  11. ↑ "D1–D2 dopamine receptor heterooligomers with unique pharmacology are coupled to rapid activation of Gq/11 in the striatum". Proceedings of the National Academy of Sciences of the United States of America 104 (2): 654–9. January 2007. doi:10.1073/pnas.0604049104. PMID 17194762. Bibcode: 2007PNAS..104..654R. 
  12. ↑ "Identification of Dopamine D1–D3 Receptor Heteromers: INDICATIONS FOR A ROLE OF SYNERGISTIC D1–D3 RECEPTOR INTERACTIONS IN THE STRIATUM". The Journal of Biological Chemistry 283 (38): 26016–25. September 2008. doi:10.1074/jbc.M710349200. PMID 18644790. 
  13. ↑ "Striatal adenosine A2A and cannabinoid CB1 receptors form functional heteromeric complexes that mediate the motor effects of cannabinoids". Neuropsychopharmacology 32 (11): 2249–59. 2007. doi:10.1038/sj.npp.1301375. PMID 17356572. 
  14. ↑ "The A2A-adenosine receptor: a GPCR with unique features?". British Journal of Pharmacology 153 Suppl 1 (S1): S184–90. March 2008. doi:10.1038/sj.bjp.0707674. PMID 18246094. 
  15. ↑ "Antagonistic cannabinoid CB1/dopamine D2 receptor interactions in striatal CB1/D2 heteromers. A combined neurochemical and behavioral analysis". Neuropharmacology 54 (5): 815–23. April 2008. doi:10.1016/j.neuropharm.2007.12.011. PMID 18262573. 
  16. ↑ "Detection of heteromerization of more than two proteins by sequential BRET-FRET". Nature Methods 5 (8): 727–33. 2008. doi:10.1038/nmeth.1229. PMID 18587404. 
  17. ↑ "Looking for the role of cannabinoid receptor heteromers in striatal function". Neuropharmacology 56 Suppl 1 (Suppl 1): 226–34. 2009. doi:10.1016/j.neuropharm.2008.06.076. PMID 18691604. 
  18. ↑ "G-protein-coupled receptor heteromers: function and ligand pharmacology". British Journal of Pharmacology 153 Suppl 1 (S1): S90–8. March 2008. doi:10.1038/sj.bjp.0707571. PMID 18037920. 
  19. ↑ "Receptor-receptor interactions within receptor mosaics. Impact on neuropsychopharmacology". Brain Research Reviews 58 (2): 415–52. August 2008. doi:10.1016/j.brainresrev.2007.11.007. PMID 18222544. 
  20. ↑ "Novel pharmacological targets based on receptor heteromers". Brain Research Reviews 58 (2): 475–82. August 2008. doi:10.1016/j.brainresrev.2008.06.002. PMID 18620000. 
  21. ↑ "Integrated signaling in heterodimers and receptor mosaics of different types of GPCRs of the forebrain: relevance for schizophrenia". Journal of Neural Transmission 116 (8): 923–39. January 2009. doi:10.1007/s00702-008-0174-9. PMID 19156349. 
  22. ↑ "Building a new conceptual framework for receptor heteromers". Nature Chemical Biology 5 (3): 131–4. March 2009. doi:10.1038/nchembio0309-131. PMID 19219011. 



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