γ-Melanocyte-stimulating hormone
Names
IUPAC name
L-Tyrosyl-L-valyl-L-methionylglycyl-L-histidyl-L-phenylalanyl-L-arginyl-L-tryptophyl-L-α-aspartyl-L-arginyl-L-phenylalaninamide
Other names
gamma-MSH, γ-melanotropin, γ-melanocortin, γ-intermedin
Identifiers
3D model (JSmol)
ChemSpider
  • InChI=1S/C74H99N21O16S/c1-41(2)62(95-63(102)49(75)30-44-22-24-47(96)25-23-44)72(111)90-53(26-29-112-3)64(103)84-38-59(97)87-57(34-46-37-80-40-86-46)70(109)92-55(32-43-16-8-5-9-17-43)68(107)88-52(21-13-28-82-74(78)79)67(106)93-56(33-45-36-83-50-19-11-10-18-48(45)50)69(108)94-58(35-60(98)99)71(110)89-51(20-12-27-81-73(76)77)66(105)91-54(65(104)85-39-61(100)101)31-42-14-6-4-7-15-42/h4-11,14-19,22-25,36-37,40-41,49,51-58,62,83,96H,12-13,20-21,26-35,38-39,75H2,1-3H3,(H,80,86)(H,84,103)(H,85,104)(H,87,97)(H,88,107)(H,89,110)(H,90,111)(H,91,105)(H,92,109)(H,93,106)(H,94,108)(H,95,102)(H,98,99)(H,100,101)(H4,76,77,81)(H4,78,79,82)/t49-,51-,52+,53-,54-,55-,56-,57-,58-,62-/m0/s1
    Key: GZWUQPQBOGLSIM-XEMHBVLISA-N
  • CC(C)[C@@H](C(=O)N[C@@H](CCSC)C(=O)NCC(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](CC2=CC=CC=C2)C(=O)N[C@H](CCCNC(=N)N)C(=O)N[C@@H](CC3=CNC4=CC=CC=C43)C(=O)N[C@@H](CC(=O)O)C(=O)N[C@@H](CCCNC(=N)N)C(=O)N[C@@H](CC5=CC=CC=C5)C(=O)NCC(=O)O)NC(=O)[C@H](CC6=CC=C(C=C6)O)N
Properties
C74H99N21O16S
Molar mass 1570.80 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Infobox references

γ-Melanocyte-stimulating hormone (γ-MSH) is an endogenous peptide hormone and neuropeptide.[1] It is a melanocortin, specifically, one of the three types of melanocyte-stimulating hormone (MSH), and is produced from proopiomelanocortin (POMC).[1] It is an agonist of the MC1, MC3, MC4, and MC5 receptors.[1] It exists in three forms, γ1-MSH, γ2-MSH, and γ3-MSH.[2]

γ-MSH regulated cardiovascular functions. γ-MSH effects are measured through the effects it has on the central neural pathway dispersed throughout the kidney.[3] It is not moderated based on tubular sodium transport. Gamma-MSH activates MC3R in renal tubular cells by limiting sodium absorption by inhibiting the central neural pathway.[3] This regulates sodium balance and blood pressure. If MC3R is absent then there is resistance in γ-MSH which results in hypertension on HSD.[4]

See also

References

  1. 1 2 3 Kastin A (26 January 2013). Handbook of Biologically Active Peptides. Academic Press. pp. 838–844. ISBN 978-0-12-385096-6.
  2. Jakubke HD, Sewald N (8 September 2008). Peptides from A to Z: A Concise Encyclopedia. John Wiley & Sons. pp. 216–. ISBN 978-3-527-62117-0.
  3. 1 2 Kathpalia PP, Charlton C, Rajagopal M, Pao AC (May 2011). "The natriuretic mechanism of Gamma-Melanocyte-Stimulating Hormone". Peptides. 32 (5): 1068–1072. doi:10.1016/j.peptides.2011.02.006. PMC 3112371. PMID 21335042.
  4. Reudelhuber TL (April 2003). "Salt-sensitive hypertension: if only it were as simple as rocket science". The Journal of Clinical Investigation. 111 (8): 1115–1116. doi:10.1172/jci200316993. PMC 152948. PMID 12697727.
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