Biology:HCN4

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Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

Potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4 is a protein that in humans is encoded by the HCN4 gene.[1][2][3][4]

There are four HCN channels. HCN4 is prominently expressed in the pace maker region of the mammalian heart.[5] Some humans with bradycardia and Sick sinus syndrome have been shown to have mutations in their HCN4 gene.[6][7][8] The role of HCN channels in autonomic control of heart rate is currently a matter of ongoing investigation.[9][10][11][12]

Interactions

HCN4 has been shown to interact with HCN2.[13]

See also

  • Cyclic nucleotide-gated ion channel
  • Funny current

References

  1. "Two pacemaker channels from human heart with profoundly different activation kinetics". The EMBO Journal 18 (9): 2323–9. May 1999. doi:10.1093/emboj/18.9.2323. PMID 10228147. 
  2. "Molecular characterization of a slowly gating human hyperpolarization-activated channel predominantly expressed in thalamus, heart, and testis". Proceedings of the National Academy of Sciences of the United States of America 96 (16): 9391–6. Aug 1999. doi:10.1073/pnas.96.16.9391. PMID 10430953. Bibcode1999PNAS...96.9391S. 
  3. "International Union of Pharmacology. LI. Nomenclature and structure-function relationships of cyclic nucleotide-regulated channels". Pharmacological Reviews 57 (4): 455–62. Dec 2005. doi:10.1124/pr.57.4.8. PMID 16382102. 
  4. "Entrez Gene: HCN4 hyperpolarization activated cyclic nucleotide-gated potassium channel 4". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=10021. 
  5. "Deep bradycardia and heart block caused by inducible cardiac-specific knockout of the pacemaker channel gene Hcn4". Proceedings of the National Academy of Sciences of the United States of America 108 (4): 1705–10. Jan 2011. doi:10.1073/pnas.1010122108. PMID 21220308. Bibcode2011PNAS..108.1705B. 
  6. Jou, Chuanchau J.; Arrington, Cammon B.; Barnett, Spencer M; Shen, Jiaxiang; Cho, Scott; Sheng, Xiaoming; McCullagh, Patrick C.; Bowles, Neil E. et al. (2017). "A Functional Assay for Sick Sinus Syndrome Genetic Variants" (in english). Cellular Physiology and Biochemistry 42 (5): 2021–2029. doi:10.1159/000479897. ISSN 1015-8987. PMID 28803248. https://www.karger.com/Article/FullText/479897. 
  7. "Pacemaker channel dysfunction in a patient with sinus node disease". The Journal of Clinical Investigation 111 (10): 1537–45. May 2003. doi:10.1172/JCI16387. PMID 12750403. 
  8. "A novel mutation in the HCN4 gene causes symptomatic sinus bradycardia in Moroccan Jews". Journal of Cardiovascular Electrophysiology 21 (12): 1365–72. Dec 2010. doi:10.1111/j.1540-8167.2010.01844.x. PMID 20662977. 
  9. "How is the heart rate regulated in the sinoatrial node? Another piece to the puzzle". The Journal of General Physiology 136 (3): 237–41. Sep 2010. doi:10.1085/jgp.201010506. PMID 20713549. 
  10. "cAMP sensitivity of HCN pacemaker channels determines basal heart rate but is not critical for autonomic rate control". Circulation: Arrhythmia and Electrophysiology 3 (5): 542–52. Oct 2010. doi:10.1161/CIRCEP.110.949768. PMID 20693575. 
  11. "Phosphorylation and modulation of hyperpolarization-activated HCN4 channels by protein kinase A in the mouse sinoatrial node". The Journal of General Physiology 136 (3): 247–58. Sep 2010. doi:10.1085/jgp.201010488. PMID 20713547. 
  12. "The Contribution of HCN4 to normal sinus node function in humans and animal models". Pacing and Clinical Electrophysiology 33 (1): 100–6. Jan 2010. doi:10.1111/j.1540-8159.2009.02563.x. PMID 19796353. 
  13. "Role of subunit heteromerization and N-linked glycosylation in the formation of functional hyperpolarization-activated cyclic nucleotide-gated channels". The Journal of Biological Chemistry 278 (44): 43781–6. Oct 2003. doi:10.1074/jbc.M306958200. PMID 12928435. 

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.