CMTM6 Knockout Cell Line (HEK293)

The choice depends on whether you are studying CMTM6 (CKLF-like MARVEL transmembrane domain containing 6)'s role as a PD-L1 chaperone or modeling emerging PD-L1 regulatory mechanisms in cancer immunology. The Knockout line is the standard tool for asking whether CMTM6 is required for these processes — CMTM6 was identified through unbiased genome-wide haploid genetic screens (Burr et al. Nature 2017; Mezzadra et al. Nature 2017) as the critical regulator of PD-L1 surface expression and stability; CMTM6 colocalizes with PD-L1 at the plasma membrane and in recycling endosomes, protecting PD-L1 from lysosomal degradation by interfering with STUB1-mediated ubiquitination. Overexpression is useful for studying CMTM6 gain-of-function effects on PD-L1. For cancer immunotherapy research, the EDITGENE CMTM6 Knockout in HEK293 is highly informative — CMTM6 loss reduces PD-L1 surface levels by 50-90% in multiple cancer cell lines and enhances anti-tumor T cell activity, identifying CMTM6 as an emerging cancer immunotherapy target distinct from canonical anti-PD-L1 antibodies. CMTM4 paralog expression analysis aids interpretation given partial functional overlap. Rescue with wild-type CMTM6 enables structure-function studies. The knockout is valuable for studying PD-L1 trafficking and stability biology, and as a critical specificity tool for emerging CMTM6-targeted immunotherapy approaches (complementary to direct anti-PD-L1 therapy such as atezolizumab, durvalumab, avelumab).

Primary applications: • PD-L1 surface expression: flow cytometry analysis of PD-L1 (CD274) surface levels — CMTM6 KO reduces PD-L1 surface expression by 50-90%. • PD-L1 stability: PD-L1 protein half-life analysis (cycloheximide chase) and lysosomal degradation studies given CMTM6's role in protecting PD-L1 from degradation. • T cell suppression: in heterologous tumor-T cell co-culture systems, PD-L1-dependent T cell suppression should be reduced in CMTM6-null cells. • CMTM6-targeted therapy development: critical specificity control for emerging CMTM6-targeting compounds as a complementary strategy to anti-PD-L1 antibodies (atezolizumab, durvalumab, avelumab). EDITGENE recommends this model for researchers investigating PD-L1 regulatory biology and emerging CMTM6-targeted immunotherapy approaches — CMTM6 represents a novel therapeutic angle on the PD-1/PD-L1 axis.

Yes. CMTM6 rescue experiments are well-established for PD-L1 regulatory research: • Construct design: use a codon-modified CMTM6 sequence with a small intracellular C-terminal tag (FLAG, HA). CMTM6 has four-transmembrane MARVEL domain architecture — preserve membrane topology. • Surface/membrane localization validation: confirm appropriate subcellular localization before PD-L1 surface expression assays. • CMTM4 paralog studies: CMTM4 expression analysis given partial functional overlap. • Functional readout: rescue should restore PD-L1 surface expression measured by flow cytometry (PD-L1/CD274 staining) and protein stability (cycloheximide chase). HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.