|MLKL (D6W1K) Rabbit mAb 37705||20 µl||
|Phospho-MLKL (Ser345) (D6E3G) Rabbit mAb 37333||20 µl||
|Caspase-3 (D3R6Y) Rabbit mAb 14220||20 µl||
||H M R Mk||35, 19, 17||Rabbit IgG|
|Phospho-RIP3 (Thr231/Ser232) (E7S1R) Rabbit mAb 91702||20 µl||
|Gasdermin D (E9S1X) Rabbit mAb 39754||20 µl||
||H M R||53, 30||Rabbit IgG|
|Cleaved Gasdermin D (Asp276) (E3E3P) Rabbit mAb 10137||20 µl||
|IL-1β (D3H1Z) Rabbit mAb 12507||20 µl||
|Cleaved-IL-1β (Asp117) (E7V2A) Rabbit mAb 63124||20 µl||
|RIP3 (D4G2A) Rabbit mAb 95702||20 µl||
|Anti-rabbit IgG, HRP-linked Antibody 7074||100 µl||
Monoclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of mouse MLKL, or synthetic peptides corresponding to residues surrounding Leu60 of mouse Gasdermin D, Asp276 of mouse Gasdermin D, His124 of mouse IL-1β, Asp117 of mouse IL-1β, Val370 of mouse RIP3, or synthetic phosphopeptides corresponding to residues surrounding Ser345 of mouse MLKL and Thr231/Ser232 of mouse RIP3, or recombinant protein specific to the p20 subunit of human caspase-3 protein.
Programmed cell death (PCD) plays important roles in organismal development and immune responses. There are three major PCD pathways: apoptosis, pyroptosis, and necroptosis. Apoptosis is a non-inflammatory cell death and is characterized by a series of proteolytic cleavage, beginning with the initiator caspases (caspases-8/9), then the executioner caspases (caspases-3/6/7), followed by cleavage of substrate proteins to drive apoptotic cell death (1,2). During pyroptosis, caspase-1 is proteolytically activated through a protein complex called inflammasome, then the activated caspase-1 can cleave Gasdermin D (GSDMD), IL-1β, and IL-18. The freed GSDMD N-terminal domains from the cleavage form pores in the plasma membrane to drive pyroptotic cell lysis and release of the cleaved and matured IL-1β and IL-18, as well as damage-associated molecular patterns (DAMPs) (3,4). The key steps in necroptosis include the receptor-interacting protein kinase 3 (RIPK3)-dependent phosphorylation of mixed lineage kinase domain-like protein (MLKL), translocation of phosphorylated MLKL to plasma membrane, and disruption of plasma membrane integrity (5,6). In contrast to the non-inflammatory nature of apoptosis, both pyroptosis and necroptosis are proinflammatory (7). While early studies of these PCD pathways focused on their distinct individual features and underlying mechanisms, recent findings point to crosstalk and redundancies among these processes under certain conditions, where the three pathways are activated, not independently of each other, and compensatory responses occur when one pathway is blocked. This new form of PCD with key features of pyroptosis, apoptosis, and/or necroptosis has been termed PANoptosis (8,9). PANoptosis is a coordinated cell death pathway driven by a cytoplasmic protein complex named the PANoptosome, whose components provide scaffold and catalytic functions to engage pyroptosis, apoptosis, and/or necroptosis (10,11).
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