publication . Article . Other literature type . 2019

DPP8/9 inhibitors are universal activators of functional NLRP1 alleles.

Marian C. Okondo; Ashley J. Chui; Daniel A. Bachovchin; Daniel A. Bachovchin; Daniel P. Ball; Darren C. Johnson; Kuo Gai; Sahana D. Rao;
Open Access
  • Published: 01 Aug 2019 Journal: Cell Death & Disease, volume 10 (eissn: 2041-4889, Copyright policy)
  • Publisher: Springer Science and Business Media LLC
Abstract
Abstract Intracellular pathogenic structures or activities stimulate the formation of inflammasomes, which recruit and activate caspase-1 and trigger an inflammatory form of cell death called pyroptosis. The well-characterized mammalian inflammasome sensor proteins all detect one specific type of signal, for example double-stranded DNA or bacterial flagellin. Remarkably, NLRP1 was the first protein discovered to form an inflammasome, but the pathogenic signal that NLRP1 detects has not yet been identified. NLRP1 is highly polymorphic, even among inbred rodent strains, and it has been suggested that these diverse NLRP1 alleles may have evolved to detect entirely ...
Subjects
free text keywords: Immunology, Cell Biology, Cancer Research, Cellular and Molecular Neuroscience, Cytology, QH573-671, Article, Cell death, Cell death and immune response, Immune cell death, Monocytes and macrophages, DNA, chemistry.chemical_compound, chemistry, Biology, Programmed cell death, Proteases, Serine, Intracellular, Pyroptosis, Inflammasome, medicine.drug, medicine, NLRP1
Related Organizations
Funded by
NIH| MOUSE GENETICS
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 2P30CA008748-43
  • Funding stream: NATIONAL CANCER INSTITUTE
,
NIH| Tri-Institutional PhD Program in Chemical Biology
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1T32GM115327-01
  • Funding stream: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES
,
NIH| Characterizing the Mechanism of DPP8/9 Inhibitor-Induced Pyroptosis
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01AI137168-01
  • Funding stream: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
43 references, page 1 of 3

Broz, P, Dixit, VM. Inflammasomes: mechanism of assembly, regulation and signalling. Nat. Rev. Immunol.. 2016; 16: 407-420 [OpenAIRE] [PubMed] [DOI]

Lamkanfi, M, Dixit, VM. Mechanisms and functions of inflammasomes. Cell. 2014; 157: 1013-1022 [OpenAIRE] [PubMed] [DOI]

Shi, J. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature. 2015; 526: 660-665 [OpenAIRE] [PubMed] [DOI]

Kayagaki, N. Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling. Nature. 2015; 526: 666-671 [OpenAIRE] [PubMed] [DOI]

Miao, EA. Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria. Nat. Immunol.. 2010; 11: 1136-1142 [OpenAIRE] [PubMed] [DOI]

Aachoui, Y. Caspase-11 protects against bacteria that escape the vacuole. Science. 2013; 339: 975-978 [OpenAIRE] [PubMed] [DOI]

Jorgensen, I, Lopez, JP, Laufer, SA, Miao, EA. IL-1beta, IL-18, and eicosanoids promote neutrophil recruitment to pore-induced intracellular traps following pyroptosis. Eur. J. Immunol.. 2016; 46: 2761-2766 [OpenAIRE] [PubMed] [DOI]

Boyden, ED, Dietrich, WF. Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin. Nat. Genet.. 2006; 38: 240-244 [OpenAIRE] [PubMed] [DOI]

D’Osualdo, A. CARD8 and NLRP1 undergo autoproteolytic processing through a ZU5-like domain. PLoS ONE. 2011; 6: e27396 [OpenAIRE] [PubMed] [DOI]

Finger, JN. Autolytic proteolysis within the function to find domain (FIIND) is required for NLRP1 inflammasome activity. J. Biol. Chem.. 2012; 287: 25030-25037 [OpenAIRE] [PubMed] [DOI]

Frew, BC, Joag, VR, Mogridge, J. Proteolytic processing of Nlrp1b is required for inflammasome activity. PLoS Pathog.. 2012; 8: e1002659 [OpenAIRE] [PubMed] [DOI]

Zhong, FL. Germline NLRP1 mutations cause skin inflammatory and cancer susceptibility syndromes via inflammasome activation. Cell. 2016; 167: 187-202 e117 [OpenAIRE] [PubMed] [DOI]

Sastalla, I. Transcriptional analysis of the three Nlrp1 paralogs in mice. BMC Genom.. 2013; 14: 188 [OpenAIRE] [DOI]

Liao, KC, Mogridge, J. Expression of Nlrp1b inflammasome components in human fibroblasts confers susceptibility to anthrax lethal toxin. Infect. Immun.. 2009; 77: 4455-4462 [OpenAIRE] [PubMed] [DOI]

Newman, ZL. Susceptibility to anthrax lethal toxin-induced rat death is controlled by a single chromosome 10 locus that includes rNlrp1. PLoS Pathog.. 2010; 6: e1000906 [OpenAIRE] [PubMed] [DOI]

43 references, page 1 of 3
Abstract
Abstract Intracellular pathogenic structures or activities stimulate the formation of inflammasomes, which recruit and activate caspase-1 and trigger an inflammatory form of cell death called pyroptosis. The well-characterized mammalian inflammasome sensor proteins all detect one specific type of signal, for example double-stranded DNA or bacterial flagellin. Remarkably, NLRP1 was the first protein discovered to form an inflammasome, but the pathogenic signal that NLRP1 detects has not yet been identified. NLRP1 is highly polymorphic, even among inbred rodent strains, and it has been suggested that these diverse NLRP1 alleles may have evolved to detect entirely ...
Subjects
free text keywords: Immunology, Cell Biology, Cancer Research, Cellular and Molecular Neuroscience, Cytology, QH573-671, Article, Cell death, Cell death and immune response, Immune cell death, Monocytes and macrophages, DNA, chemistry.chemical_compound, chemistry, Biology, Programmed cell death, Proteases, Serine, Intracellular, Pyroptosis, Inflammasome, medicine.drug, medicine, NLRP1
Related Organizations
Funded by
NIH| MOUSE GENETICS
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 2P30CA008748-43
  • Funding stream: NATIONAL CANCER INSTITUTE
,
NIH| Tri-Institutional PhD Program in Chemical Biology
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1T32GM115327-01
  • Funding stream: NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES
,
NIH| Characterizing the Mechanism of DPP8/9 Inhibitor-Induced Pyroptosis
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1R01AI137168-01
  • Funding stream: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
43 references, page 1 of 3

Broz, P, Dixit, VM. Inflammasomes: mechanism of assembly, regulation and signalling. Nat. Rev. Immunol.. 2016; 16: 407-420 [OpenAIRE] [PubMed] [DOI]

Lamkanfi, M, Dixit, VM. Mechanisms and functions of inflammasomes. Cell. 2014; 157: 1013-1022 [OpenAIRE] [PubMed] [DOI]

Shi, J. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature. 2015; 526: 660-665 [OpenAIRE] [PubMed] [DOI]

Kayagaki, N. Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling. Nature. 2015; 526: 666-671 [OpenAIRE] [PubMed] [DOI]

Miao, EA. Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria. Nat. Immunol.. 2010; 11: 1136-1142 [OpenAIRE] [PubMed] [DOI]

Aachoui, Y. Caspase-11 protects against bacteria that escape the vacuole. Science. 2013; 339: 975-978 [OpenAIRE] [PubMed] [DOI]

Jorgensen, I, Lopez, JP, Laufer, SA, Miao, EA. IL-1beta, IL-18, and eicosanoids promote neutrophil recruitment to pore-induced intracellular traps following pyroptosis. Eur. J. Immunol.. 2016; 46: 2761-2766 [OpenAIRE] [PubMed] [DOI]

Boyden, ED, Dietrich, WF. Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin. Nat. Genet.. 2006; 38: 240-244 [OpenAIRE] [PubMed] [DOI]

D’Osualdo, A. CARD8 and NLRP1 undergo autoproteolytic processing through a ZU5-like domain. PLoS ONE. 2011; 6: e27396 [OpenAIRE] [PubMed] [DOI]

Finger, JN. Autolytic proteolysis within the function to find domain (FIIND) is required for NLRP1 inflammasome activity. J. Biol. Chem.. 2012; 287: 25030-25037 [OpenAIRE] [PubMed] [DOI]

Frew, BC, Joag, VR, Mogridge, J. Proteolytic processing of Nlrp1b is required for inflammasome activity. PLoS Pathog.. 2012; 8: e1002659 [OpenAIRE] [PubMed] [DOI]

Zhong, FL. Germline NLRP1 mutations cause skin inflammatory and cancer susceptibility syndromes via inflammasome activation. Cell. 2016; 167: 187-202 e117 [OpenAIRE] [PubMed] [DOI]

Sastalla, I. Transcriptional analysis of the three Nlrp1 paralogs in mice. BMC Genom.. 2013; 14: 188 [OpenAIRE] [DOI]

Liao, KC, Mogridge, J. Expression of Nlrp1b inflammasome components in human fibroblasts confers susceptibility to anthrax lethal toxin. Infect. Immun.. 2009; 77: 4455-4462 [OpenAIRE] [PubMed] [DOI]

Newman, ZL. Susceptibility to anthrax lethal toxin-induced rat death is controlled by a single chromosome 10 locus that includes rNlrp1. PLoS Pathog.. 2010; 6: e1000906 [OpenAIRE] [PubMed] [DOI]

43 references, page 1 of 3
Any information missing or wrong?Report an Issue