Target intelligence / Profile preview

NOD-like receptor family pyrin domain containing 11 (NLRP11)

Target
NLRP11
Molecular classification
Pattern recognition receptor, NOD-like receptor (NLR), Inflammasome component, Scaffold/adaptor protein
01

Overview

NOD-like receptor family pyrin domain containing 11 (NLRP11) is a cytosolic pattern recognition receptor in humans that functions as an essential adaptor in the inflammasome pathway, facilitating the assembly and activation of the NLRP3 and caspase-4 inflammasomes in response to stress signals, intracellular bacterial lipopolysaccharide, and pathogenic infection[1][3][5]. NLRP11 contains N-terminal pyrin (PYD), central nucleotide-binding (NACHT), and C-terminal leucine-rich repeat (LRR) domains, permitting it to scaffold interactions between NLRP3 and ASC, promote caspase activation, and drive pyroptotic cell death and cytokine (IL-1β, IL-18) release in human macrophages[1][2][3][4]. Unique to primates, NLRP11 acts as a regulatory checkpoint; it can also attenuate Toll-like receptor (TLR) signaling by promoting TRAF6 degradation, thereby suppressing NF-κB activation and downstream inflammatory responses[4]. While not yet a direct drug target, NLRP11's essential role in both canonical and non-canonical inflammasome regulation highlights its significance in human immune defense and autoinflammatory pathogenesis.

Other names
NALP11PYPAF6NOD17PAN10CLR19.6PAAD-and NACHT domain-containing protein 10PYRIN-containing APAF1-like protein 6nucleotide-binding oligomerization domain protein 17
02

Mechanism of action

Drugs targeting NLRP11 would likely act by modulating inflammasome assembly or inhibiting caspase activation, but no direct agents known

03

Biological functions

Regulation and assembly of inflammasomesPattern recognition of cytosolic lipopolysaccharide (LPS)Caspase-1 and caspase-4 activationPyroptotic cell deathCytokine release (IL-1β, IL-18)Negative regulation of NF-κB signalingControl of TLR pathway via TRAF6 degradation
04

Disease associations

InflammationAutoinflammatory syndromes (contributing to NLRP3 mutant-mediated CAPS)Infectious disease (response to Gram-negative bacteria)Potentially cancer (B cell lymphoma expression noted)
05

Safety considerations

Therapeutic targeting might impair host defense against Gram-negative infectionsInhibition may dysregulate critical inflammatory cytokine responses

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