The CLINT1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human B lymphocytes, derived from the Raji cell line, with disruption of the CLINT1 gene. This pooled loss-of-function model captures heterogeneous editing outcomes, providing a versatile system for studying clathrin adaptor functions in a Burkitt lymphoma context without clonal selection.
Raji cells are an EBV-positive lymphoblastoid B-cell line established from a Burkitt lymphoma patient. They grow in suspension and serve as a well-characterized model for B-cell lymphoma biology and immune cell signaling, featuring active endocytic trafficking and sensitive mitotic machinery. Their non-adherent growth facilitates scalable assays, including flow cytometry and live-cell imaging, making them particularly suitable for trafficking and cell division studies.
CLINT1 (epsinR) is a clathrin adaptor at endosomes and the trans-Golgi network (TGN) that directs retrograde transport of sorting receptors such as TGN46 and the mannose-6-phosphate receptor. It is recruited by ARF1 GTPase and PtdIns4P and interacts with the AP-1 complex and clathrin heavy chain. In mitosis, CLINT1 partners with PLK1 and BUBR1 to assemble the mitotic spindle and ensure chromosome alignment. Consequently, CLINT1 disruption impairs both endosomal retrograde trafficking and mitotic fidelity.
In Raji lymphoma cells, CLINT1 knockout leads to mislocalization of TGN-resident proteins and defects in receptor recycling, potentially altering signaling cascades that drive B-cell proliferation. Simultaneously, mitotic spindle abnormalities may cause chromosome missegregation, impacting cell division and genomic stability. The polyclonal nature of the knockout population mirrors variable loss-of-function effects, making it ideal for pooled screening and for evaluating phenotypic consequences relevant to lymphoma.
These polyclonal knockout cells support a broad range of applications: immunofluorescence to assess TGN46 redistribution, Western blotting of clathrin adaptor complexes, flow cytometry to monitor surface receptor recycling, live-cell imaging of spindle dynamics, and MTS viability assays for anti-lymphoma drug screening. Co-immunoprecipitation can probe altered CLINT1 interactions. They are particularly valuable for functional genomics, endosomal trafficking analysis, and cancer drug target validation. For inquiries, contact Ascent Research.
