mProX™ Human PLK2 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Patrick Liam (Creative Biolabs Scientific Support)
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Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 Glioma cell growth was influenced by the expression of PLK2.
Cell proliferation was assessed using a CCK8 assay, and a significant decrease in cell viability was observed in cells treated with shPLK2-1 and shPLK2-2 (P < 0.001).
Ref: Cao, Fang, et al. "Knocking down of Polo-like kinase 2 inhibits cell proliferation and induced cell apoptosis in human glioma cells." Life Sciences 270 (2021): 119084.
Pubmed: 33482186
DOI: 10.1016/j.lfs.2021.119084
Research Highlights
Song, Shuting. et al. "miR-3200 accelerates the growth of liver cancer cells by enhancing Rab7A." Non-coding RNA research, 2023.
Recent research suggests that miR-3200 may play a significant role in tumorigenesis, but its specific impact on human hepatocarcinogenesis remains unknown. The current study aims to shed light on this subject by providing evidence that miR-3200 promotes the growth of liver cancer cells. This finding highlights the potential of miR-3200 as a target for therapeutic interventions in liver cancer treatment.
Song, Shuting. et al. "miR-3200 accelerates the growth of liver cancer cells by enhancing Rab7A." Non-coding RNA research, 2023.
Pubmed:
37860266
DOI:
10.1016/j.ncrna.2023.10.005
Abdel-Ghani, Mai. et al. "Plk2 promotes synaptic destabilization through disruption of N-cadherin adhesion complexes during homeostatic adaptation to hyperexcitation." Journal of neurochemistry, 2023.
The process of synaptogenesis in the brain is largely regulated by specific synaptic cellular adhesion molecules (CAMs) like N-cadherin and amyloid precursor protein (APP). While N-cadherin is crucial for synapse development and plasticity, its role in synapse dismantling is not fully understood. Neurodegenerative diseases and excessive neuronal activity can lead to weakening and loss of synapses. Recent research has shown that Polo-like kinase 2 (Plk2) phosphorylates both N-cadherin and APP, resulting in their breakdown and impairment of synaptic structure. This disruption of N-cadherin's adhesive properties destabilizes excitatory synapses and contributes to their eventual elimination. This mechanism has potential implications for cognitive disorders associated with abnormal synapse loss.
Abdel-Ghani, Mai. et al. "Plk2 promotes synaptic destabilization through disruption of N-cadherin adhesion complexes during homeostatic adaptation to hyperexcitation." Journal of neurochemistry, 2023.
Pubmed:
37654026
DOI:
10.1111/jnc.15948
