Introduction of KCNJ3
G protein-activated inward rectifier potassium channel 1 (GIRK-1) is also known as inward rectifier potassium channel 2 (KCNJ3, Kir3.1), which is encoded by the gene KCNJ3. KCNJ3 is a member of G protein-coupled inwardly rectifying potassium (GIRK/Kir3) channels family, composed of at least five members, Kir3.1~Kir 3.5. Kir3.1 must combine with Kir3.2, Kir3.4, or Kir3.5 to form functional heteropolymer. Containing three exons separated by two introns, gene KCNJ3 was mapped to chromosome 2q24.1. Similar to other members of the Kir family, KCNJ3 also comprises two transmembrane helix domains (M1 and M2), an ion-selective P-loop between M1 and M2, and cytoplasmic N- and C-terminal domains. KCNJ3 is widely expressed in different tissues and cells, i.e., cardiac atrial myocytes and various neuronal cells, where KCNJ3 functions as G-protein effectors in the plasma membrane and regulates cellular excitability and activity via neurotransmitters and hormones.
|Basic Information of KCNJ3|
|Protein Name||Inward rectifier potassium channel 3|
|Organism||Homo sapiens (Human)|
Function of KCNJ3 Membrane Protein
KCNJ3 is a member of GIRKs, which have a wide range of physiological roles, including the regulation of heartbeat, reward mechanisms, learning and memory functions, blood platelet aggregation, insulin secretion, and lipid metabolism, etc. Most importantly, the foregone function of KCNJ3 is the correlation of increased KCNJ3 expression levels with breast cancer progression and patient’s prognosis. In primary invasive breast carcinomas, KCNJ3 mRNA is significantly incremental, which is positively correlated with the number of metastatic lymph nodes. Moreover, strong evidence showed that the motility, invasiveness and angiogenesis of KCNJ3 overexpressing MCF-7 breast cancer cells are enhancive when compared with controls. So, it is suggested that KCNJ3 can be recognized as a potential new prognostic biomarker in invasive breast carcinoma. Substantial researches have revealed the potential role of KCNJ3 in non-small cell lung cancer and pancreatic adenocarcinomas, during the disease’s progression process, KCNJ3 gene is always upregulated. In addition, it has been well documented that KCNJ3 is responsible for the etiology of juvenile myoclonic epilepsy and sinus node dysfunction.
Fig.1 Schematic association between inward-rectifier K+ current (IK, ACh) and KCNJ3. (Morishima, 2016)
Application of KCNJ3 Membrane Protein in Literature
In this article, the authors used gene expression data from the TCGA to study KCNJ3 levels in different breast cancer subtypes and to study the prognostic value of KCNJ3 using survival analysis. They validated that KCNJ3 expression was upregulated in tumor tissue, which was coincident with the proportion of positive estrogen receptor (ER).
This article established a protocol for the detection of KCNJ3 in formalin-fixed, paraffin-embedded (FFPE) breast cancer tissue. Besides the western blot, optimization of the immunohistochemistry (IHC) procedure, the authors recommended the establishment of KCNJ3 mRNA in situ hybridization (ISH), which had better sensitivity and specificity.
This article performed a gene-centric association study of KCNJ3 gene with schizophrenia by genotyping 38 tagSNPs in the Chinese population, and they detected significantly lower KCNJ3 expression in postmortem brains in schizophrenic patients.
This article verified that genetic mutations in KCNJ3 and KCNJ5 encoding the subunits of the acetylcholine-activated K(+) (KACh) channels did not participate in the pathogenesis of sinus node dysfunction (SND).
The authors found that overexpression of different KCNJ3 gene splice affected vital parameters of malignancy level in breast cancer, i.e. wound healing, chemoinvasion, cellular velocities/motilities and angiogenesis.
KCNJ3 Preparation Options
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