ATP11B Knockout HEK293T Cell Line

The choice depends on whether you are studying ATP11B's role as a P4-type ATPase phospholipid flippase or modeling its emerging functions in cisplatin resistance and lipid asymmetry. The Knockout line is the standard tool for asking whether ATP11B is required for these processes — ATP11B is a P4-type ATPase phospholipid flippase that, together with the β-subunit CDC50A/TMEM30A, translocates phosphatidylserine (and to lesser extent PE) from the outer to inner leaflet of the plasma membrane to maintain phospholipid asymmetry; ATP11B has emerged as a mediator of cisplatin resistance and is implicated in white matter brain injury. Overexpression is useful for studying ATP11B gain-of-function effects. For lipid biology and cancer drug resistance research, the EDITGENE ATP11B Knockout in HEK293T is highly informative — HEK293T's very high transfection efficiency supports systematic structure-function studies. Rescue with wild-type or catalytically-dead ATP11B enables structure-function studies. The knockout is valuable for studying phospholipid flippase biology, cisplatin resistance mechanisms, and emerging ATP11B functions in neurological and cancer applications.

Primary applications: • Phosphatidylserine flipping: PS asymmetry analysis (annexin V exposure, lactadherin staining) in ATP11B-null cells. • Cisplatin resistance: in cisplatin-treated cells, ATP11B-mediated resistance mechanism studies. • White matter biology: in heterologous neural-relevant contexts, ATP11B's reported role in oligodendrocyte biology. • CDC50A partnership: TMEM30A/CDC50A β-subunit interaction analysis. EDITGENE recommends this HEK293T-based model for researchers investigating phospholipid flippase biology and emerging ATP11B-related cancer drug resistance.

Yes. ATP11B rescue experiments require attention to P4-ATPase architecture: • Construct design: use a codon-modified ATP11B sequence with a small intracellular tag (FLAG, HA). ATP11B is a P4-type ATPase with 10 transmembrane spans, cytoplasmic A, N, P domains — preserve membrane topology. • CDC50A partnership: rescue interpretation considers CDC50A/TMEM30A β-subunit expression for proper flippase function. • Catalytically-dead rescue: P-domain phospho-aspartate mutations abolish ATPase/flippase activity. • Functional readout: rescue should restore phosphatidylserine flipping activity. HEK293T transduces with very high efficiency and supports stable rescue line generation.