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    <!-- http://purl.obolibrary.org/obo/GO_0008219 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/GO_0008219">
        <rdfs:label rdf:datatype="http://www.w3.org/2001/XMLSchema#string">cell death</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/TXPO_0002149 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/TXPO_0002149">
        <rdfs:label rdf:datatype="http://www.w3.org/2001/XMLSchema#string">netosis</rdfs:label>
        <rdfs:subClassOf rdf:resource="http://purl.obolibrary.org/obo/GO_0008219"/>
        <ns3:IAO_0000115 rdf:datatype="http://www.w3.org/2001/XMLSchema#string">In response to several stimuli, neutrophils and eosinophils can release the so-called neutrophil extracellular traps (NETs), that is, microbicidal structures composed of nuclear chromatin, histones and granular antimicrobial proteins.
Netotic cells exhibit massive vacuolization of the cytoplasm, rapid chromatin decondensation and breakdown of both the nuclear and granular membranes, which is required for proper NET formation.  Netosis is insensitive to caspase inhibitors and necrostatin-1, further demonstrating that it constitutes a cell death subroutine distinct from apoptosis and regulated necrosis.

Netosis might be defined as a cell death subroutine that is: (i) restricted to granulocytic cells; (ii) insensitive to (and perhaps dependent on)163 caspase inhibition; (iii) insensitive to necrostatin; (iv) dependent on NAPDH oxidase-mediated superoxide generation; and (v) dependent on (components of) the autophagic machinery

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252826/</ns3:IAO_0000115>
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