Home Primary Antibodies MLKL Antibody [H6A20]

research use only

MLKL Antibody [H6A20]

Catalog No.: F4607

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:50
    Application
    WB, IP
    Reactivity
    Mouse
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    54 kDa
    Positive Control BaF3 cell; CTLL-2 cell; NIH/3T3 cell
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    MLKL Antibody [H6A20] detects endogenous levels of total MLKL protein.
    Clone
    H6A20
    Synonym(s)
    Mixed lineage kinase domain-like protein; Mlkl
    Background
    MLKL (Mixed Lineage Kinase Domain-Like protein) is a pseudokinase of the protein kinase superfamily that acts as the terminal effector of necroptosis, a form of regulated necrotic cell death triggered by TNF or TLR ligands when caspases are inhibited. MLKL consists of an N-terminal four-helix bundle (4HB) executioner domain (α1–α4 helices that form membrane-disrupting pores), a central two-helix “brace” region connecting domains, and a C-terminal pseudokinase domain (PsKD) that, despite lacking catalytic activity, binds nucleotides and regulates activation. Key residues for activation include Thr357/Ser358 in the activation loop and brace helix residues that maintain autoinhibitory interaction between the 4HB and PsKD. Upon necroptotic signaling, RIPK3 phosphorylates MLKL at Thr357/Ser358 within the necrosome complex (RIPK1/RIPK3/MLKL), relieving autoinhibition, promoting MLKL tetramerization or oligomerization, and enabling its translocation to the plasma membrane inner leaflet via PIP2 binding. There, MLKL forms pores that mediate ion influx, plasma membrane rupture, and lytic cell death. MLKL is integral to inflammatory signaling pathways (such as TNF/NF-κB) and distinguishes necroptosis from apoptosis. Dysregulation of MLKL-mediated necroptosis contributes to diseases including inflammatory bowel disease, sepsis, and neurodegeneration (e.g., ALS via neuronal cell death).
    References
    • https://pubmed.ncbi.nlm.nih.gov/30294675/
    • https://pubmed.ncbi.nlm.nih.gov/28498367/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
    If you have any other enquiries, please leave a message.

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