KCNJ3

Official Full Name

potassium inwardly rectifying channel subfamily J member 3

Organism

Homo sapiens

GeneID

3760

Background

Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins and plays an important role in regulating heartbeat. It associates with three other G-protein-activated potassium channels to form a heteromultimeric pore-forming complex that also couples to neurotransmitter receptors in the brain and whereby channel activation can inhibit action potential firing by hyperpolarizing the plasma membrane. These multimeric G-protein-gated inwardly-rectifying potassium (GIRK) channels may play a role in the pathophysiology of epilepsy, addiction, Down's syndrome, ataxia, and Parkinson's disease. Alternative splicing results in multiple transcript variants encoding distinct proteins. [provided by RefSeq, May 2012]

Synonyms

KGA; GIRK1; KIR3.1;

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Detailed Information

Recent Research

KCNJ3 is an inwardly rectifying potassium channel, subfamily J, member 3. It is also known as GIRK1 and Kir3.1. It belongs to a G protein-gated inwardly rectifying potassium (GIRK) channel family that plays a crucial role in controlling neuronal excitability by hyperpolarizing the membrane and generating slow post synaptic inhibitory potentials. GIRK channel is formed by the diversity of the four subunits expressed in mammals (GIRK1-GIRK4), of which only the first three are commonly expressed in the brain.

GIRK is a G protein effector that regulates cell excitability and activity through neurotransmitters and hormones. GIRK loss-of-function can lead to excessive neuronal excitation, such as in epilepsy, whereas gain-of-function can substantially reduce neuronal activity, such as when GIRK2 is triplicated in a mouse model of Down syndrome. In humans, changes in the expression level of KCNJ3 gene are associated with schizophrenia, developmental delays, epilepsy and language impairment, and mental retardation in children.

Several studies have demonstrated a closely correlation of increased KCNJ3 expression levels, breast cancer progression and patient’s prognosis. Stringer et al observed increased levels of KCNJ3 mRNA in primary invasive breast carcinomas when compared with corresponding normal breast tissue and found KCNJ3 mRNA levels positively correlating with the amount of metastatic lymph nodes. These results were supported by a study by Brevet et al that showed a correlation between GIRK1 protein expression and lymph node metastasis, as well as reduced overall survival in patients with tumors with high GIRK1 expression. In addition, the relevance of KCNJ3 in breast cancer is further underscored by Rezania et al, who demonstrated increased motility, invasiveness and angiogenesis of KCNJ3 over-expressing MCF-7 breast cancer cells compared with controls. Ko et al performed ion channel profiling in breast cancer, they found that KCNJ3 to be down-regulated in p53 mutant breast cancer samples and up-regulated in oestrogen receptor (ER) positive tumours.

References:

Amaral A C, et al. Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex. Neuroscience, 2015, 286:79-86.
Kammerer S, et al. Critical evaluation of KCNJ3 gene product detection in human breast cancer: mRNA in situ hybridisation is superior to immunohistochemistry. Journal of Clinical Pathology, 2016, 69(12):1116.
Rezania S, et al. Overexpression of KCNJ3 gene splice variants affects vital parameters of the malignant breast cancer cell line MCF-7 in an opposing manner. BMC Cancer, 2016, 16(1):628.

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