Render Target: SSR
Render Timestamp: 2024-11-20T14:38:39.871Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-20 06:19:27.411
Product last modified at: 2024-05-30T07:02:36.045Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Gasdermin D (L60) Antibody #93709

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Inquiry Info. # 93709

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    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 29, 53
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Gasdermin D (L60) Antibody recognizes endogenous levels of total Gasdermin D protein. This antibody detects the N-terminal fragment of Gasdermin D upon proteolytic cleavage.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu60 of mouse Gasdermin D protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Gasdermin D (GSDMD), a member of the gasdermin family that includes GSDMA, GSDMB, and GSDMC, has been reported to have a critical role as a downstream effector of pyroptosis (1,2). Pyroptosis is a lytic type of cell death triggered by inflammasomes, multiprotein complexes assembled in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) that result in the activation of caspase-1 and subsequent cleavage of pro-inflammatory cytokines IL-1β and IL-18 (3). Gasdermin D was identified by two independent groups as a substrate of inflammatory caspases, caspase-1 and caspase-11/4/5, producing two fragments: GSDMD-N and GSDMD-C. Cleavage results in release of an intramolecular inhibitory interaction between the N- and C-terminal domains, allowing the N-terminal fragment GSDMD-N to initiate pyroptosis through the formation of pores on the plasma membrane (4-7).
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