Cloning and characterisation of GIRK1 variants resulting from alternative RNA editing of the KCNJ3 gene transcript in a human breast cancer cell line

@article{Wagner2010CloningAC,
  title={Cloning and characterisation of GIRK1 variants resulting from alternative RNA editing of the KCNJ3 gene transcript in a human breast cancer cell line},
  author={Valerie A Wagner and Elke Stadelmeyer and Monika Riederer and Peter Regitnig and Astrid Gorischek and Trevor T. J. Devaney and Kurt Schmidt and Helmut A. Tritthart and Koret Hirschberg and Thomas Bauernhofer and Wolfgang Schreibmayer},
  journal={Journal of Cellular Biochemistry},
  year={2010},
  volume={110},
  url={https://api.semanticscholar.org/CorpusID:930096}
}
The very high abundance of mRNA's encoding GirK1 together with the presence of GIRK1 protein suggests a pathophysiological role in breast cancer.

Overexpression of KCNJ3 gene splice variants affects vital parameters of the malignant breast cancer cell line MCF-7 in an opposing manner

In insight into the cellular and molecular consequences of KCNJ3 overexpression in breast cancer cells and the mechanism upon clinical outcome in patients suffering from breast cancer, it is concluded that GIRK1d acts as a dominant negative constituent of functional G IRK complexes present in the plasma membrane of MCF-7 cells.

Consequences of somatic mutations of GIRK1 detected in primary malign tumors on expression and function of G-protein activated, inwardly rectifying, K+ channels

It is concluded that gain of function mutations, identical or similar to categories (ii) and (iii), may potentially be involved in genesis and progression of malignancies in tissues that exert a high rate of occurrence of somatic mutations of KCNJ3.

Alternatively Spliced Isoforms of KV10.1 Potassium Channels Modulate Channel Properties and Can Activate Cyclin-dependent Kinase in Xenopus Oocytes

Short splice variants of KV10.1 resulting from exon-skipping events (E65 and E70) in human brain and cancer cell lines are identified, highlighting the relevance of noncanonical functions for the oncogenicity of Kv10.

The Polarization of the G-Protein Activated Potassium Channel GIRK5 to the Vegetal Pole of Xenopus laevis Oocytes Is Driven by a Di-Leucine Motif

It is concluded that the N-terminal acidic di-leucine motif of GIRK5 determines its retention and polarized trafficking within Xl oocytes, and Y16 and I22 contributed to functional expression and were dominant in the polarization of GirK5.

Four and a Half LIM Protein 1C (FHL1C): A Binding Partner for Voltage-Gated Potassium Channel Kv1.5

It is found that functional FHL1A protein is completely absent in patient myoblasts and coexpression of Kv1.5 with FHL 1C in Xenopus laevis oocytes markedly reduced K+ currents when compared to oocytes expressing Kv 1.5 only.

GIRK1 triggers multiple cancer-related pathways in the benign mammary epithelial cell line MCF10A

According to transcriptome analysis, cellular migration was promoted while wound healing and extracellular matrix interactions were impaired and GIRK1 regulated cellular pathways in mammary epithelial cells are likely to contribute to the development and progression of breast cancer.

KCNJ3 is a new independent prognostic marker for estrogen receptor positive breast cancer patients

The data suggest that patients with ER positive breast cancer might be stratified into high risk and low risk groups based on the KC NJ3 levels in the tumor, whereby KCNJ3 is an independent prognostic factor.

Evaluation of Salivary KCNJ3 mRNA Levels in Breast Cancer: A Case–control Study and in silico Analysis

Salivary levels of KCNJ3 could be considered a potential diagnostic biomarker with high sensitivity and specificity for BC detection.

Cloning and characterization of G protein-gated inward rectifier K+ channel (GIRK1) isoforms from heart and brain

The cloning of three additional novel isoforms of GIRK1a from rat atria and and one from human brain are reported, indicating that isoforms were generated by alternative splicing and partial genomic analysis confirmed the presence of exons and introns in the rat GirK1 gene.

Expression of G-protein inwardly rectifying potassium channels (GIRKs) in lung cancer cell lines

Stimulation of GIRK channels and β-adrenergic signaling may activate similar signaling pathways in both SCLC and breast cancer, but lead to different results.

G-protein inwardly rectifying potassium channel 1 (GIRK 1) gene expression correlates with tumor progression in non-small cell lung cancer

It is indicated that GIRK1 may contribute to tumor progression and GirK1 gene expression can serve as a useful prognostic marker in the overall and stage I NSCLCs.

Protein expression of G-protein inwardly rectifying potassium channels (GIRK) in breast cancer cells

The data indicates that functional GIRK channels exist in breast cancer cells that are involved in cellular signaling.

Expression of inwardly rectifying potassium channels (GIRKs) and beta-adrenergic regulation of breast cancer cell lines

The data suggests β-adrenergic receptors and GIRK channels may play a role in breast cancer.

Genomic organization and promoter analysis of the human G-protein-coupled K+ channel Kir3.1 (KCNJ3/HGIRK1).

To the authors' knowledge, this is the first promoter that has been isolated and characterized for an inwardly rectifying potassium channel and additional data suggest the existence of another promoter that can drive transcription of Kir3.1 mRNA from a distinct initiation site.

Overexpression of the G-protein inwardly rectifying potassium channel 1 (GIRK1) in primary breast carcinomas correlates with axillary lymph node metastasis.

It is found that GIRK1 overexpression correlated with lymph node metastasis (P < 0.0029), and overeexpression was greatest in tumors with more than one positive lymph node, indicating that GirK1 may be useful as a biomarker for lymph nodes metastasis and possibly a pharmaceutical target.

Contribution of KCNQ1 to the regulatory volume decrease in the human mammary epithelial cell line MCF-7.

The investigated volume-activated changes in response to hyposmotic stress suggest that KCNQ1 may play important physiological roles in the mammary epithelium, regulating cell volume and potentially mediating transepithelial K(+) secretion.
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