Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Kcna5. (This text reflects annotations as of Tuesday, May 21, 2013.)

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] Potassium channels represent the most complex class of voltage-gated ino channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily. This member contains six membrane-spanning domains with a shaker-type repeat in the fourth segment. It belongs to the delayed rectifier class, the function of which could restore the resting membrane potential of beta cells after depolarization and thereby contribute to the regulation of insulin secretion. This gene is intronless, and the gene is clustered with genes KCNA1 and KCNA6 on chromosome 12. Defects in this gene are a cause of familial atrial fibrillation type 7 (ATFB7). [provided by RefSeq, May 2012]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Kcna5
  • participates in the following biological processes:
    • negative regulation of potassium ion transport ^[2]
    • potassium ion transport ^[2]
    • regulation of ion transmembrane transport ^[2]
  • performs the following molecular functions:
    • potassium channel inhibitor activity ^[2]
    • voltage-gated potassium channel activity ^[2]
  • is located in the following cellular components:
    • integral to plasma membrane ^[2]
    • intercalated disc ^[4]
    • membrane ^[4]
    • plasma membrane ^[3]
• The gene product of Kcna5 has been shown to bind to the gene products of Cav3, Dlg1, Kcne2. ^{[3, 4]}
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Kcna5
  • participates in the following biological processes:
    • regulation of vasoconstriction ^[1]
• Researchers have inferred, based on genetic interactions, that the gene product of Kcna5
  • participates in the following biological processes:
    • regulation of membrane potential based on interactions with Cav3, Dlg1 ^[3]
• Based on the experimental annotations above, MGI curators have inferred, that the gene product of Kcna5
  • is located in the following cellular components:
    • integral to plasma membrane ^[2]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Kcna5:
  • participates in the following biological processes:
    • membrane hyperpolarization
    • positive regulation of G1/S transition of mitotic cell cycle
    • positive regulation of myoblast proliferation
    • potassium ion export
    • potassium ion homeostasis
    • potassium ion transport
    • protein oligomerization
    • reduction of cytosolic calcium ion concentration
    • regulation of atrial cardiac muscle cell action potential
    • regulation of atrial cardiac muscle cell membrane repolarization
    • regulation of heart rate by cardiac conduction
    • regulation of membrane potential
    • regulation of potassium ion transport
  • performs the following molecular functions:
    • alpha-actinin binding
    • delayed rectifier potassium channel activity
    • outward rectifier potassium channel activity
    • protein kinase binding
    • receptor binding
    • scaffold protein binding
    • voltage-gated potassium channel activity involved in atrial cardiac muscle cell action potential repolarization
  • is located in the following cellular components:
    • endoplasmic reticulum
    • Golgi apparatus
    • intercalated disc
    • intracellular canaliculus
    • membrane raft
    • perinuclear region of cytoplasm
    • plasma membrane
    • voltage-gated potassium channel complex
    • Z disc

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Summary text based on GO annotations supported by structural data

• Kcna5 encodes a protein or proteins that contain the following InterPro domains: BTB/POZ fold, BTB/POZ-like, Ion transport domain, Potassium channel tetramerisation-type BTB domain, Potassium channel, voltage dependent, Kv, Potassium channel, voltage dependent, Kv1, Potassium channel, voltage dependent, Kv1.5, Voltage-dependent potassium channel, indicating that the gene product:
  • participates in the following biological processes:
    • ion transport
    • protein homooligomerization
    • transmembrane transport
  • performs the following molecular functions:
    • ion channel activity

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Kcna5 indicates that it:
  • participates in the following biological processes:
    • ion transport
    • potassium ion transmembrane transport
    • transport
  • performs the following molecular functions:
    • potassium channel activity
    • voltage-gated ion channel activity
  • is located in the following cellular components:
    • integral to membrane

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References

1. Archer SL et al. (2001) Impairment of hypoxic pulmonary vasoconstriction in mice lacking the voltage-gated potassium channel Kv1.5. FASEB J, 15:1801-3. (PubMed:11481235)
2. Attali B et al. (1993) Multiple mRNA isoforms encoding the mouse cardiac Kv1-5 delayed rectifier K+ channel. J Biol Chem, 268:24283-9. (PubMed:8226976)
3. Folco EJ et al. (2004) Caveolin-3 and SAP97 form a scaffolding protein complex that regulates the voltage-gated potassium channel Kv1.5. Am J Physiol Heart Circ Physiol, 287:H681-90. (PubMed:15277200)
4. Roepke TK et al. (2008) Targeted deletion of kcne2 impairs ventricular repolarization via disruption of I(K,slow1) and I(to,f). FASEB J, 22:3648-60. (PubMed:18603586)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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