In Stock Cell Lines
The MLKL Knockout Marc-145 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the Marc-145 subclone of MA-104 African green monkey kidney epithelial cells (Chlorocebus aethiops). This model features disruption of the MLKL gene, which encodes the pseudokinase that executes necroptosis when phosphorylated by RIPK3. It is an ideal tool for elucidating necroptosis in PRRSV host-pathogen interactions and for screening small-molecule inhibitors of necroptosis. Researchers can assess cell death pathways via phospho-MLKL western blotting, LDH release assays, and flow cytometry, dissecting the interplay between viral infection and innate immune signaling.
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The MLKL Knockout Marc-145 Cell Line is a CRISPR/Cas9-edited knockout cell line in which the MLKL gene has been disrupted using CRISPR/Cas9-mediated genome editing, resulting in a loss-of-function model. Derived from the Marc-145 cell line, a subclone of the MA-104 African green monkey (Chlorocebus aethiops) kidney epithelial cells, this product provides a genetically defined system for studying programmed necrosis. The knockout has been generated to create a stable cell line lacking functional MLKL protein, enabling consistent and reproducible experimental outcomes.
The Marc-145 cell line is widely recognized as a standard host for porcine reproductive and respiratory syndrome virus (PRRSV) propagation. Originating from MA-104 African green monkey kidney epithelial cells, Marc-145 cells are highly permissive for PRRSV infection and replication, making them indispensable for virological research. Their epithelial nature also makes them a relevant model for studying cell death and innate immune responses triggered by viral pathogens.
MLKL (mixed lineage kinase domain-like pseudokinase) serves as the terminal executioner in the necroptosis pathway. Upon activation of death receptors (e.g., TNFR) or pattern recognition receptors (e.g., TLR3, TLR4, ZBP1), the upstream kinases RIPK1 and RIPK3 form the necrosome complex. RIPK3 directly phosphorylates MLKL, inducing a conformational change that promotes MLKL oligomerization and translocation to the plasma membrane. At the membrane, MLKL binds phosphatidylinositol phosphates and disrupts lipid bilayer integrity, leading to cell lysis, release of damage-associated molecular patterns (DAMPs), and potential crosstalk with pyroptotic signaling. Key interacting partners include RIPK3, FADD, HSP90, and caspase-8 within the intricate cell death regulatory network.
In the Marc-145 background, MLKL knockout offers a unique platform to dissect the role of necroptosis during PRRSV infection. PRRSV is known to modulate host cell death pathways to facilitate its lifecycle; ablating MLKL eliminates the necroptotic branch, allowing researchers to distinguish between apoptosis and necroptosis contributions to virus-induced cytopathology. Furthermore, this cell line can be employed to investigate how interferons and other innate immune signals upstream of MLKL intersect with PRRSV replication strategies. By uncoupling necroptosis from other cell death modalities, the model enables precise interrogation of viral pathogenesis and host defense mechanisms.
This knockout cell line is suited for a variety of experimental approaches. In necroptosis mechanism studies, users can monitor MLKL activation status via phospho-MLKL-specific western blotting and track MLKL translocation with immunofluorescence. Cell death can be quantified using LDH release assays or flow cytometry. For virology applications, virus titer assays and qPCR for viral RNA can assess the impact of MLKL loss on PRRSV replication. The cell line also serves as a valuable tool for high-throughput screening of small-molecule necroptosis inhibitors targeting the RIPK1/RIPK3/MLKL axis. For additional technical details or support, contact Ascent Research.
