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HCN4 - Wikipedia, the free encyclopedia

HCN4

From Wikipedia, the free encyclopedia


Hyperpolarization activated cyclic nucleotide-gated potassium channel 4
PDB rendering based on 1q3e.
Available structures: 1q3e, 1q43, 1q5o
Identifiers
Symbol(s) HCN4;
External IDs OMIM: 605206 MGI1298209 HomoloGene3997
RNA expression pattern

More reference expression data

Orthologs
Human Mouse
Entrez 10021 330953
Ensembl ENSG00000138622 ENSMUSG00000032338
Uniprot Q9Y3Q4 O70507
Refseq NM_005477 (mRNA)
NP_005468 (protein)
XM_287905 (mRNA)
XP_287905 (protein)
Location Chr 15: 71.4 - 71.45 Mb Chr 9: 58.62 - 58.66 Mb
Pubmed search [1] [2]

Hyperpolarization activated cyclic nucleotide-gated potassium channel 4, also known as HCN4, is a human gene.[1]


Contents

[edit] See also

[edit] References

[edit] Further reading

  • Hofmann F, Biel M, Kaupp UB (2006). "International Union of Pharmacology. LI. Nomenclature and structure-function relationships of cyclic nucleotide-regulated channels.". Pharmacol. Rev. 57 (4): 455–62. doi:10.1124/pr.57.4.8. PMID 16382102. 
  • Ludwig A, Zong X, Stieber J, et al. (1999). "Two pacemaker channels from human heart with profoundly different activation kinetics.". EMBO J. 18 (9): 2323–9. doi:10.1093/emboj/18.9.2323. PMID 10228147. 
  • Seifert R, Scholten A, Gauss R, et al. (1999). "Molecular characterization of a slowly gating human hyperpolarization-activated channel predominantly expressed in thalamus, heart, and testis.". Proc. Natl. Acad. Sci. U.S.A. 96 (16): 9391–6. PMID 10430953. 
  • Qu J, Altomare C, Bucchi A, et al. (2003). "Functional comparison of HCN isoforms expressed in ventricular and HEK 293 cells.". Pflugers Arch. 444 (5): 597–601. doi:10.1007/s00424-002-0860-7. PMID 12194012. 
  • Schulze-Bahr E, Neu A, Friederich P, et al. (2003). "Pacemaker channel dysfunction in a patient with sinus node disease.". J. Clin. Invest. 111 (10): 1537–45. PMID 12750403. 
  • Stieber J, Thomer A, Much B, et al. (2003). "Molecular basis for the different activation kinetics of the pacemaker channels HCN2 and HCN4.". J. Biol. Chem. 278 (36): 33672–80. doi:10.1074/jbc.M305318200. PMID 12813043. 
  • Decher N, Bundis F, Vajna R, Steinmeyer K (2004). "KCNE2 modulates current amplitudes and activation kinetics of HCN4: influence of KCNE family members on HCN4 currents.". Pflugers Arch. 446 (6): 633–40. doi:10.1007/s00424-003-1127-7. PMID 12856183. 
  • Much B, Wahl-Schott C, Zong X, et al. (2003). "Role of subunit heteromerization and N-linked glycosylation in the formation of functional hyperpolarization-activated cyclic nucleotide-gated channels.". J. Biol. Chem. 278 (44): 43781–6. doi:10.1074/jbc.M306958200. PMID 12928435. 
  • Ueda K, Nakamura K, Hayashi T, et al. (2004). "Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac arrhythmia.". J. Biol. Chem. 279 (26): 27194–8. doi:10.1074/jbc.M311953200. PMID 15123648. 
  • Michels G, Er F, Khan I, et al. (2005). "Single-channel properties support a potential contribution of hyperpolarization-activated cyclic nucleotide-gated channels and If to cardiac arrhythmias.". Circulation 111 (4): 399–404. doi:10.1161/01.CIR.0000153799.65783.3A. PMID 15687126. 
  • Milanesi R, Baruscotti M, Gnecchi-Ruscone T, DiFrancesco D (2006). "Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel.". N. Engl. J. Med. 354 (2): 151–7. doi:10.1056/NEJMoa052475. PMID 16407510. 
  • Elinder F, Männikkö R, Pandey S, Larsson HP (2006). "Mode shifts in the voltage gating of the mouse and human HCN2 and HCN4 channels.". J. Physiol. (Lond.) 575 (Pt 2): 417–31. doi:10.1113/jphysiol.2006.110437. PMID 16777944. 
  • Nof E, Luria D, Brass D, et al. (2007). "Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia.". Circulation 116 (5): 463–70. doi:10.1161/CIRCULATIONAHA.107.706887. PMID 17646576. 

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


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