Cloning and characterization of Kir3.1 (GIRK1) C-terminal alternative splice variants

Cole S. Nelson, Jennifer L. Marino, Charles N. Allen

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Southern blot analysis of RT-PCR products from brain and heart revealed multiple products for a C-terminal region of Kir3.1. Sequencing yielded clones for wild-type Kir3.1 and three Kir3.1 C-terminal alternative splice variants, including a unique alternative exon. Two of these variants encoded truncated Kir3.1 molecules. Tissue distribution and electrophysiological characterization of a single truncated variant, Kir3.100 were then examined. Kir3.1 channels are gated by G-protein βγ-subunits binding to the C-terminal domain, thus, the truncation of Kir3.100 removes a major functional domain. When incorporated into heteromeric channels with other family members (Kir3.1, 3.2 or 3.4) several functional changes were observed: (1) Kir3.100 changes G-protein activation of Kir3 channels; (2) Kir3.100 is restricted in its ability to assemble with other channel subunits as heteromers; and (3) incorporation of Kir3.100 into heteromeric channel complexes alters the kinetics of channel re-activation.

Original languageEnglish (US)
Pages (from-to)185-196
Number of pages12
JournalMolecular Brain Research
Issue number1-2
StatePublished - Jun 1997


  • Dopamine
  • Dopamine receptor
  • G-protein
  • Inward rectifier
  • Kir3
  • Oocyte
  • Potassium channel

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience


Dive into the research topics of 'Cloning and characterization of Kir3.1 (GIRK1) C-terminal alternative splice variants'. Together they form a unique fingerprint.

Cite this