The IFT27 Knockout Jurkat Polyclonal Cells product provides a CRISPR/Cas9-mediated knockout cell population targeting the IFT27 gene in the Jurkat T-cell leukemia line. This polyclonal pool contains edited cells with IFT27 disruption, making it suitable for experiments where a heterogeneous knockout population is acceptable, such as screening or pooled assays. The knockout is generated by CRISPR/Cas9-directed gene editing without selection for clonal isolates, offering a representative mixture of loss-of-function alleles.
Jurkat cells are an immortalized human T lymphocyte line established from the peripheral blood of a 14-year-old boy with acute T-cell leukemia. Widely employed as a model system, Jurkat cells are particularly useful for studying T-cell receptor (TCR) signaling pathways, apoptosis mechanisms, and leukemia biology. Their robust growth in suspension culture facilitates high-throughput applications and genetic manipulation, making them a versatile platform for knockout studies.
IFT27 encodes a small GTPase that is a core component of the intraflagellar transport complex B (IFT-B), which together with IFT-A, kinesin-2, and dynein-2 mediates bidirectional trafficking of cargo along ciliary axonemes. Within the IFT-B complex, IFT27 directly interacts with IFT25 and IFT81, contributing to complex stability and ciliary protein transport. Although best characterized in ciliated cells, IFT27 also exhibits non-ciliary functions, particularly in cell cycle regulation. IFT27 acts downstream of cell cycle signals and IFT complex assembly factors, and its activity influences downstream targets such as cyclin B1, a key regulator of mitosis. In the broader context of Hedgehog signaling, ciliogenesis-related IFT components like IFT27 are essential for proper signal transduction, linking defects to ciliopathies and related disorders.
Because Jurkat cells are non-ciliated, IFT27 knockout in this background disconnects the gene from its canonical ciliary role, enabling dissection of cilia-independent functions. Loss of IFT27 in Jurkat cells may alter cell cycle progression, proliferation, and survival, providing a model to investigate how IFT proteins influence leukemia biology and T-cell function beyond the cilium. This polyclonal knockout population thus offers a unique tool for studying the interplay between cell cycle dysregulation and immune cell signaling in a disease-relevant hematopoietic context.
Researchers can employ this polyclonal knockout cell pool in a variety of assays, including Western blot to confirm IFT27 protein depletion, RT-qPCR for transcript analysis, and flow cytometry with propidium iodide staining to evaluate cell cycle distribution. Functional studies may involve proliferation and apoptosis assays to assess the impact of IFT27 loss on T-cell growth and viability. Furthermore, immunoprecipitation coupled with mass spectrometry can help identify IFT27 interaction partners in non-ciliated cells, while RNA-seq provides transcriptomic insights into pathways dysregulated upon knockout. For ciliopathy modeling, these cells can be compared with ciliated model systems to delineate specific non-ciliary contributions. For additional information or technical assistance, please contact Ascent Research.
