mProX™ Human PROM1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 A notable decrease in colony-forming ability was observed as a result of PROM1 knockdown using either shRNA, without any such reduction occurring in doxycycline-treated control SEM cells, wherein the number of colonies was reduced to less than 50% of the uninduced control.
The percentage of colonies formed in the presence of 0.5 µg/ml doxycycline (+Dox) was measured in control and PROM1 shRNA 1 and 2 SEM cell lines, and compared with the uninduced control (Con = −Dox). The error bars depict the standard deviation of three (control) or four (shRNA) biological replicates, with **p < 0.01 indicating statistical significance, while ns denotes no significant difference.
Ref: Godfrey, Laura, et al. "H3K79me2/3 controls enhancer-promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells." Leukemia 35.1 (2021): 90-106.
Pubmed: 32242051
DOI: 10.1038/s41375-020-0808-y
Research Highlights
Wąsowska, Anna, et al. "Polygenic Risk Score and Rare Variant Burden Identified by Targeted Sequencing in a Group of Patients with Pigment Epithelial Detachment in Age-Related Macular Degeneration." Genes 14.9 (2023): 1707.
A group of researchers analyzed the results of ophthalmic imaging examinations from 334 patients to identify a specific subgroup of patients with pigment epithelial detachment (PED). Among the patients, a subgroup of 47 individuals with PED was identified. These patients were compared to two other groups - those with age-related macular degeneration without PED and healthy individuals. A polygenic risk score was established, explaining 16.3% of the disease variation. The most accurate predictive model included six non-coding variants: rs760306 (AMD), rs2230199 (CFH), rs1061170 (CFH), rs3753394 (C2), rs800292 (C3), and rs2230201 (C3).
Wąsowska, Anna, et al. "Polygenic Risk Score and Rare Variant Burden Identified by Targeted Sequencing in a Group of Patients with Pigment Epithelial Detachment in Age-Related Macular Degeneration." Genes 14.9 (2023): 1707.
Pubmed:
37761846
DOI:
10.3390/genes14091707
Schneider, Pauline. et al. "Modelling acquired resistance to DOT1L inhibition exhibits the adaptive potential of KMT2A-rearranged acute lymphoblastic leukemia." Experimental hematology & oncology, 2023.
In KMT2A-rearranged acute lymphoblastic leukemia (ALL), an aggressive malignancy, the oncogenic KMT2A-fusion proteins inappropriately recruit DOT1L to promote leukemogenesis, highlighting DOT1L as a potential therapeutic target. However, the first-in-class DOT1L inhibitor pinometostat eventually becomes ineffective in treating this type of leukemia. To gain insight into this phenomenon, a team established acquired resistance to pinometostat in pediatric KMT2A::AFF1-rearranged ALL cells.
Schneider, Pauline. et al. "Modelling acquired resistance to DOT1L inhibition exhibits the adaptive potential of KMT2A-rearranged acute lymphoblastic leukemia." Experimental hematology & oncology, 2023.
Pubmed:
37740239
DOI:
10.1186/s40164-023-00445-8
