The cAMP-responsive element binding protein (CREB) is a nuclear transcription factor vital for cell growth and regulation, and its overexpression is associated with myeloid leukemia. Researchers have demonstrated that CREB contributes significantly to hematopoietic stem cell (HSC) proliferation and myeloid leukemia progression. They employed RNA interference to knock down CREB expression, leading to decreased proliferation in both HSCs and myeloid leukemia cells. The use of Ba/F3 cells expressing either Bcr-Abl wild-type or the imatinib-resistant T315I mutation highlighted CREB's critical role in leukemogenesis, revealing that CREB knockdown resulted in significantly reduced leukemic infiltration in vivo and extended survival in mouse models.
Figure 1. The researchers utilized Western blot and lentiviral transduction methods to analyze CREB expression in Ba/F3 cells, demonstrating its role in inhibiting leukemia progression and improving survival. (Cheng JC, et al., 2008)
Creative Biogene offers a Human BCR-ABL-T315I Stable Cell Line-Ba/F3, tailored for studies in leukemia research, particularly those targeting Bcr-Abl-mediated signaling pathways. Our stable cell line serves as an invaluable tool for exploring the role of various genetic alterations and therapeutic responses in hematological malignancies.
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The emergence of the Human BCR-ABL-T315I Stable Cell Line Ba/F3 product has provided strong support for the study of BCR-ABL fusion proteins, allowing me to better explore the complex mechanisms behind them during experiments.
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Through this product, we can quickly and accurately study the impact of T315I mutation on the function of BCR-ABL fusion protein, thereby better understanding the resistance mechanisms of CML and ALL.
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