The CLIP1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal population derived from the human Raji B lymphoblastoid cell line. This product provides a loss-of-function model for the CLIP1 gene, encoding a microtubule plus-end tracking protein (+TIP) critical for cytoskeletal dynamics and intracellular trafficking. The polyclonal nature of the knockout pool offers a heterogeneous collection of edited alleles, enabling robust functional studies without clonal selection bias.
The Raji host cell line is an Epstein-Barr virus (EBV)-transformed B lymphoblastoid line originally isolated from a Burkitt’s lymphoma patient. These cells maintain key features of humoral immune cells, including antigen presentation and cytokine production, and serve as a well-established model for B cell malignancies. Their rapid proliferation and genetic tractability make them suitable for CRISPR-based gene disruption and subsequent functional analyses in a lymphoma-relevant context.
CLIP1 functions as a central regulator of microtubule plus-end dynamics, directly interacting with EB1 and CLASP1 to control microtubule stabilization and to link microtubule ends to cargo trafficking. It also associates with the dynactin complex component p150Glued and the motor protein Kinesin-1 to mediate vesicle motility along microtubules. Upstream, CLIP1 activity is modulated by EGFR/PI3K/Akt signaling and Rho family GTPases, particularly RhoA and Rac1, which coordinate focal adhesion turnover and cell migration. Through these interactions, CLIP1 promotes focal adhesion disassembly, endosomal redistribution, and microtubule-dependent transport processes.
In Raji B lymphoblastoid cells, disruption of CLIP1 is expected to perturb microtubule organization, impair endosomal trafficking, and hinder the dynamic remodeling of focal adhesions required for cell migration. Given the importance of cytoskeletal dynamics in lymphoma invasion and immune cell function, this knockout model provides a physiologically relevant platform to dissect CLIP1-dependent mechanisms in B cell lymphoma progression. The loss of CLIP1 may also affect antigen presentation and cytokine secretion, processes that rely on efficient vesicle transport.
This polyclonal knockout cell population is suitable for a range of research applications, including investigating microtubule-dependent trafficking in immune cells, screening for small molecules that modulate the CLIP1 interactome, and studying the role of focal adhesion turnover in lymphoma cell migration. Typical assays include immunofluorescence microscopy to visualize microtubule networks and EB1 comets, Western blotting to confirm CLIP1 depletion and assess partner protein levels, Transwell migration assays, co-immunoprecipitation of CLIP1 complexes, and flow cytometry for cell cycle analysis. For additional product information, please contact Ascent Research.
