mProX™ Human PBK Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 PBK is necessary for MDA-MB-231 cell proliferation.
In MDA-MB-231 cells, the establishment of the PBK shRNA or vector stable cell line was achieved through the utilization of the tetracycline-induced lentiviral expression system. The induction of shRNA expression was accomplished by subjecting the cells to doxycycline (1 μg/ml) for a duration of 3 days. Detection of PBK knockdown was conducted through immunoblotting, and the examination of the impact of PBK knockdown on cell proliferation was carried out via cell counting employing a hemacytometer. The data presented herein originate from no less than three independent experiments.
Ref: Dou, Xiaoyan, et al. "PBK/TOPK mediates geranylgeranylation signaling for breast cancer cell proliferation." Cancer cell international 15.1 (2015): 1-9.
Pubmed: 25745361
DOI: 10.1186/s12935-015-0178-0
Research Highlights
Liu, Dan. et al. "Identification of transcriptome characteristics of granulosa cells and the possible role of UBE2C in the pathogenesis of premature ovarian insufficiency." Journal of ovarian research, 2023.
Premature ovarian insufficiency (POI) is a common cause of infertility, marked by deterioration in ovarian function. The ovarian granulosa cells (GCs) surrounding oocytes are crucial for follicle development, and impaired GC function is a significant factor in POI. This study aimed to identify potential biomarkers for POI through RNA profiling and bioinformatics analysis of hub genes, as well as assess their correlation with immune infiltration. By examining these factors, we hope to gain a better understanding of the pathogenesis of POI and potentially improve diagnosis and treatment strategies.
Liu, Dan. et al. "Identification of transcriptome characteristics of granulosa cells and the possible role of UBE2C in the pathogenesis of premature ovarian insufficiency." Journal of ovarian research, 2023.
Pubmed:
37848988
DOI:
10.1186/s13048-023-01266-3
Zhang, Jinping. et al. "Impact of CRISPR/Cas9-Mediated CD73 Knockout in Pancreatic Cancer." Cancers, 2023.
Pancreatic cancer has one of the highest mortality rates among all cancers. Advanced stages of the disease often result in missed opportunities for surgical intervention, highlighting the pressing need for alternative treatment methods. Targeted therapy, particularly for specific cancer-related genes, has emerged as a promising approach to improve patient survival rates. Using flow cytometry and qRT-PCR, combined with bioinformatics techniques, researchers identified high levels of CD73 expression in pancreatic cancer. Utilizing CRISPR/Cas9 technology, CD73 was successfully knocked out in human and murine cell lines, leading to suppressed cell growth and migration, and inducing G1 cell cycle arrest. Further investigations also revealed inhibition of the ERK/STAT3 pathway and activation of the E-cadherin pathway in CD73-deficient cells. A CRISPR/Cas9 protein kinase library screening identified Pbk, Fastk, Cdk19, Adck5, Trim28, and Pfkp as potential regulators of CD73.
Zhang, Jinping. et al. "Impact of CRISPR/Cas9-Mediated CD73 Knockout in Pancreatic Cancer." Cancers, 2023.
Pubmed:
37835536
DOI:
10.3390/cancers15194842
