The METAP1D Knockout Raji Polyclonal Cells product consists of a heterogeneous population of Raji B lymphocytes modified via CRISPR/Cas9-mediated disruption of the METAP1D gene, yielding a loss-of-function model for pooled functional studies. This polyclonal knockout format captures diverse editing outcomes across the cell population, enabling robust investigation of methionine aminopeptidase 1D biology without clonal selection bias. The product is designed for advanced research into protein N-terminal processing, B-cell lymphoma mechanisms, and validation of cancer drug targets.
The host Raji cell line was originally established from a Burkitt lymphoma patient and carries the Epstein-Barr virus (EBV) genome alongside a t(8;14) chromosomal translocation that fuses the MYC oncogene to the immunoglobulin heavy chain locus. This genetic aberration drives constitutive MYC expression, sustaining proliferation and lending the cells their aggressive lymphoma phenotype. As a suspension-adapted B lymphocyte line, Raji retains humoral immune functions including antigen presentation and antibody production, making it a versatile model for B-cell biology and cancer research.
METAP1D encodes a methionine aminopeptidase that catalyzes the co-translational excision of N-terminal methionine from nascent polypeptides at the ribosome. It operates within a co-translational processing complex that includes METAP1 and METAP2, and its activity is potentially influenced by upstream MYC and mTOR signaling pathways. Downstream targets encompass newly synthesized proteins such as small GTPases, cell cycle regulators, and apoptosis factors, whose proper maturation depends on methionine removal. Disruption of METAP1D thus perturbs global N-termini composition, impacting protein stability and downstream signaling networks.
In the Raji cellular context, METAP1D knockout provides a direct means to test the reliance of MYC-driven lymphoma growth on co-translational protein processing. Loss of METAP1D function may compromise the maturation of factors essential for B-cell proliferation and survival, and it may also impair specialized processes such as antibody secretion and antigen presentation. This model is therefore highly relevant for dissecting the intersection between protein maturation and oncogenic signaling, with implications for understanding lymphomagenesis and the therapeutic targeting of methionine aminopeptidases in B-cell malignancies.
These polyclonal knockout cells are suitable for a broad range of experimental approaches. Researchers can employ western blotting and RT-qPCR for expression analysis, MTT and BrdU proliferation assays, Annexin V apoptosis assays, and flow cytometry to profile functional consequences. Mass spectrometry-based N-terminomics reveals proteome-wide processing alterations, while co-immunoprecipitation and RNA-seq help delineate interaction networks and transcriptome changes. Applications span functional genomics of methionine aminopeptidases, validation of METAP1D as a drug target, and mechanistic studies in B-cell lymphoma. For further information, please contact Ascent Research.
