HECTD3 inhibits NLRP3 inflammasome assembly and activation by blocking NLRP3-NEK7 interaction

The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been r...

Full description

Saved in:
Bibliographic Details
Published inCell death & disease Vol. 15; no. 1; p. 86
Main Authors Cheng, Zhuo, Huang, Maobo, Li, Wei, Hou, Lei, Jin, Li, Fan, Qijin, Zhang, Linqiang, Li, Chengbin, Zeng, Li, Yang, Chuanyu, Liang, Bin, Li, Fubing, Chen, Ceshi
Format Journal Article
LanguageEnglish
Published England Springer Nature B.V 24.01.2024
Nature Publishing Group UK
Nature Publishing Group
Subjects
Online AccessGet full text

Cover

Loading…
Abstract The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been reported to participate in autoimmune and infectious diseases. However, the relationship between HECTD3 and the NLRP3 inflammasome has not been well studied. Herein, we show that HECTD3 blocks the interaction between NEK7 and NLRP3 to inhibit NLRP3 inflammasome assembly and activation. In BMDMs, Hectd3 deficiency promotes the assembly and activation of NLRP3 inflammasome and the secretion of IL-1β, while the overexpression of HECTD3 inhibits these processes. Unexpectedly, HECTD3 functions in an E3 activity independent manner. Mechanically, the DOC domain of HECTD3 interacts with NACHT/LRR domain of NLRP3, which blocks NLRP3-NEK7 interaction and NLRP3 oligomerization. Furthermore, HECTD3 inhibits monosodium urate crystals (MSU)-induced gouty arthritis, a NLRP3-related disease. Thus, we reveal a novel regulatory mechanism of NLRP3 by HECTD3 and suggest HECTD3 could be a potential therapeutic target for NLRP3-dependent pathologies.
AbstractList The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been reported to participate in autoimmune and infectious diseases. However, the relationship between HECTD3 and the NLRP3 inflammasome has not been well studied. Herein, we show that HECTD3 blocks the interaction between NEK7 and NLRP3 to inhibit NLRP3 inflammasome assembly and activation. In BMDMs, Hectd3 deficiency promotes the assembly and activation of NLRP3 inflammasome and the secretion of IL-1β, while the overexpression of HECTD3 inhibits these processes. Unexpectedly, HECTD3 functions in an E3 activity independent manner. Mechanically, the DOC domain of HECTD3 interacts with NACHT/LRR domain of NLRP3, which blocks NLRP3-NEK7 interaction and NLRP3 oligomerization. Furthermore, HECTD3 inhibits monosodium urate crystals (MSU)-induced gouty arthritis, a NLRP3-related disease. Thus, we reveal a novel regulatory mechanism of NLRP3 by HECTD3 and suggest HECTD3 could be a potential therapeutic target for NLRP3-dependent pathologies.
The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been reported to participate in autoimmune and infectious diseases. However, the relationship between HECTD3 and the NLRP3 inflammasome has not been well studied. Herein, we show that HECTD3 blocks the interaction between NEK7 and NLRP3 to inhibit NLRP3 inflammasome assembly and activation. In BMDMs, Hectd3 deficiency promotes the assembly and activation of NLRP3 inflammasome and the secretion of IL-1β, while the overexpression of HECTD3 inhibits these processes. Unexpectedly, HECTD3 functions in an E3 activity independent manner. Mechanically, the DOC domain of HECTD3 interacts with NACHT/LRR domain of NLRP3, which blocks NLRP3-NEK7 interaction and NLRP3 oligomerization. Furthermore, HECTD3 inhibits monosodium urate crystals (MSU)-induced gouty arthritis, a NLRP3-related disease. Thus, we reveal a novel regulatory mechanism of NLRP3 by HECTD3 and suggest HECTD3 could be a potential therapeutic target for NLRP3-dependent pathologies.
Abstract The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been reported to participate in autoimmune and infectious diseases. However, the relationship between HECTD3 and the NLRP3 inflammasome has not been well studied. Herein, we show that HECTD3 blocks the interaction between NEK7 and NLRP3 to inhibit NLRP3 inflammasome assembly and activation. In BMDMs, Hectd3 deficiency promotes the assembly and activation of NLRP3 inflammasome and the secretion of IL-1β, while the overexpression of HECTD3 inhibits these processes. Unexpectedly, HECTD3 functions in an E3 activity independent manner. Mechanically, the DOC domain of HECTD3 interacts with NACHT/LRR domain of NLRP3, which blocks NLRP3-NEK7 interaction and NLRP3 oligomerization. Furthermore, HECTD3 inhibits monosodium urate crystals (MSU)-induced gouty arthritis, a NLRP3-related disease. Thus, we reveal a novel regulatory mechanism of NLRP3 by HECTD3 and suggest HECTD3 could be a potential therapeutic target for NLRP3-dependent pathologies.
Abstract The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely understood. Dysregulation of NLRP3 can cause diverse inflammatory diseases. HECTD3 is a E3 ubiquitin ligase of the HECT family that has been reported to participate in autoimmune and infectious diseases. However, the relationship between HECTD3 and the NLRP3 inflammasome has not been well studied. Herein, we show that HECTD3 blocks the interaction between NEK7 and NLRP3 to inhibit NLRP3 inflammasome assembly and activation. In BMDMs, Hectd3 deficiency promotes the assembly and activation of NLRP3 inflammasome and the secretion of IL-1β, while the overexpression of HECTD3 inhibits these processes. Unexpectedly, HECTD3 functions in an E3 activity independent manner. Mechanically, the DOC domain of HECTD3 interacts with NACHT/LRR domain of NLRP3, which blocks NLRP3-NEK7 interaction and NLRP3 oligomerization. Furthermore, HECTD3 inhibits monosodium urate crystals (MSU)-induced gouty arthritis, a NLRP3-related disease. Thus, we reveal a novel regulatory mechanism of NLRP3 by HECTD3 and suggest HECTD3 could be a potential therapeutic target for NLRP3-dependent pathologies.
ArticleNumber 86
Author Zeng, Li
Cheng, Zhuo
Hou, Lei
Li, Wei
Fan, Qijin
Yang, Chuanyu
Liang, Bin
Li, Fubing
Chen, Ceshi
Huang, Maobo
Li, Chengbin
Jin, Li
Zhang, Linqiang
Author_xml – sequence: 1
  givenname: Zhuo
  surname: Cheng
  fullname: Cheng, Zhuo
  organization: Kunming College of Life Sciences, University of Chinese Academy Sciences, Kunming, 650204, China
– sequence: 2
  givenname: Maobo
  surname: Huang
  fullname: Huang, Maobo
  organization: The First People's Hospital of Kunming City & Calmette Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan, China
– sequence: 3
  givenname: Wei
  surname: Li
  fullname: Li, Wei
  organization: Kunming College of Life Sciences, University of Chinese Academy Sciences, Kunming, 650204, China
– sequence: 4
  givenname: Lei
  surname: Hou
  fullname: Hou, Lei
  organization: Department of Breast Disease, Henan Breast Cancer Center, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, 450008, China
– sequence: 5
  givenname: Li
  surname: Jin
  fullname: Jin, Li
  organization: The First Affiliated Hospital, Kunming Medical University, Kunming, 650032, China
– sequence: 6
  givenname: Qijin
  surname: Fan
  fullname: Fan, Qijin
  organization: College of Life Sciences, Yunnan University, Kunming, 650500, China
– sequence: 7
  givenname: Linqiang
  surname: Zhang
  fullname: Zhang, Linqiang
  organization: College of Life Sciences, Yunnan University, Kunming, 650500, China
– sequence: 8
  givenname: Chengbin
  surname: Li
  fullname: Li, Chengbin
  organization: College of Life Sciences, Yunnan University, Kunming, 650500, China
– sequence: 9
  givenname: Li
  surname: Zeng
  fullname: Zeng, Li
  organization: Kunming College of Life Sciences, University of Chinese Academy Sciences, Kunming, 650204, China
– sequence: 10
  givenname: Chuanyu
  surname: Yang
  fullname: Yang, Chuanyu
  organization: Kunming College of Life Sciences, University of Chinese Academy Sciences, Kunming, 650204, China
– sequence: 11
  givenname: Bin
  surname: Liang
  fullname: Liang, Bin
  organization: College of Life Sciences, Yunnan University, Kunming, 650500, China
– sequence: 12
  givenname: Fubing
  surname: Li
  fullname: Li, Fubing
  email: mtlfb0408@163.com
  organization: Academy of Biomedical Engineering, Kunming Medical University, Kunming, 650500, China. mtlfb0408@163.com
– sequence: 13
  givenname: Ceshi
  orcidid: 0000-0001-6398-3516
  surname: Chen
  fullname: Chen, Ceshi
  email: chenc@kmmu.edu.cn, chenc@kmmu.edu.cn, chenc@kmmu.edu.cn
  organization: The Third Affiliated Hospital, Kunming Medical University, Kunming, 650118, China. chenc@kmmu.edu.cn
BackLink https://www.ncbi.nlm.nih.gov/pubmed/38267403$$D View this record in MEDLINE/PubMed
BookMark eNpdkl9vFCEUxYmpsbX2C_hgJvHFl1EuMAw8GbOutnFTjamPhgDDbFlnoIXZJvvtZXdq08oL_875Be49L9FRiMEh9Brwe8BUfMgMGMgaE1Zjzlpas2fohGAGNRNCHj1aH6OznDe4DEoxafgLdEwF4S3D9AT9Pl8urj7Tyodrb_yUq8vVzx_7bT_ocdQ5jq7SObvRDLtKh67SdvJ3evIxVGZXmSHaPz6sZ1t9ufzWFu_k0l4Wwyv0vNdDdmf38yn69WV5tTivV9-_Xiw-rWrLmJhqarteUwm9kIyD7ZjDDQXJnZMNYGsaynUjNAFpLTEWCAWnqTCmBS41FvQUXczcLuqNukl-1GmnovbqcBDTWuk0eTs4JUxrDSbWcMcZEbqALZHOdrIUhzNbWB9n1s3WjK6zLkxJD0-gT2-Cv1breKcACyxAtIXw7p6Q4u3W5UmNPls3DDq4uM2KSBANQAOySN_-J93EbQqlVgdVaTFvmqIis8qmmHNy_cNrAKt9GtScBlXSoA5pUKyY3jz-x4PlX-_pX_oxr9A
Cites_doi 10.1038/nature15514
10.1016/j.diabres.2014.04.006
10.1038/ni.1631
10.1084/jem.20171419
10.1038/nature04515
10.1016/j.molcel.2012.11.009
10.1016/j.mam.2020.100889
10.1074/jbc.M112.407130
10.1007/s10875-019-00638-z
10.1038/s41467-018-04947-6
10.1038/s41418-022-00947-8
10.1038/s41467-021-22987-3
10.1172/JCI120406
10.1038/s41423-021-00761-1
10.1002/jcp.25930
10.1038/nm.3806
10.1002/art.10326
10.1080/17460441.2023.2218641
10.1016/j.cell.2010.01.040
10.1111/j.1600-065X.2008.00734.x
10.1038/s41423-021-00740-6
10.1111/j.1600-065X.2008.00624.x
10.1038/ni.3333
10.1038/s41423-021-00683-y
10.1038/s41419-023-05923-9
10.4049/jimmunol.0901363
10.1038/s41586-019-1295-z
10.1038/ni.1636
10.1038/nature04516
10.1038/s41467-019-08605-3
10.3390/ijms23105365
10.1038/s41556-020-0510-3
10.1038/nature16959
10.1038/s41392-022-01057-0
ContentType Journal Article
Copyright 2024. The Author(s).
The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
The Author(s) 2024
Copyright_xml – notice: 2024. The Author(s).
– notice: The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: The Author(s) 2024
DBID CGR
CUY
CVF
ECM
EIF
NPM
AAYXX
CITATION
3V.
7X7
7XB
88A
88I
8FE
8FH
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BBNVY
BENPR
BHPHI
CCPQU
DWQXO
FYUFA
GHDGH
GNUQQ
HCIFZ
K9.
LK8
M0S
M2P
M7P
PIMPY
PQEST
PQQKQ
PQUKI
PRINS
Q9U
7X8
5PM
DOA
DOI 10.1038/s41419-024-06473-4
DatabaseName Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
CrossRef
ProQuest Central (Corporate)
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Biology Database (Alumni Edition)
Science Database (Alumni Edition)
ProQuest SciTech Collection
ProQuest Natural Science Collection
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central
ProQuest Central Essentials
Biological Science Collection
ProQuest Central
Natural Science Collection
ProQuest One Community College
ProQuest Central Korea
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Central Student
SciTech Premium Collection
ProQuest Health & Medical Complete (Alumni)
Biological Sciences
Health & Medical Collection (Alumni Edition)
Science Database
Biological Science Database
Publicly Available Content Database
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
ProQuest Central Basic
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ : Directory of Open Access Journals
DatabaseTitle MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
CrossRef
Publicly Available Content Database
ProQuest Central Student
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
SciTech Premium Collection
ProQuest One Community College
ProQuest Natural Science Collection
ProQuest Central China
ProQuest Biology Journals (Alumni Edition)
ProQuest Central
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
Natural Science Collection
ProQuest Central Korea
Biological Science Collection
ProQuest Science Journals (Alumni Edition)
ProQuest Biological Science Collection
ProQuest Central Basic
ProQuest Science Journals
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
Biological Science Database
ProQuest SciTech Collection
ProQuest Hospital Collection (Alumni)
ProQuest Health & Medical Complete
ProQuest One Academic UKI Edition
ProQuest One Academic
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList Publicly Available Content Database

MEDLINE
CrossRef

MEDLINE - Academic
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 4
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Biology
EISSN 2041-4889
EndPage 86
ExternalDocumentID oai_doaj_org_article_8b7cb02cb6e6428aa58c29ecd930264c
10_1038_s41419_024_06473_4
38267403
Genre Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: National Natural Science Foundation of China (National Science Foundation of China)
  grantid: U2102203
– fundername: National Natural Science Foundation of China (National Science Foundation of China)
  grantid: 81830087
– fundername: National Natural Science Foundation of China (National Science Foundation of China)
  grantid: 82000817
GroupedDBID ---
0R~
3V.
53G
5VS
70F
7X7
88A
88I
8FE
8FH
8FI
8FJ
AAJSJ
ABUWG
ACGFS
ACSMW
ADBBV
AENEX
AFKRA
AJTQC
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AOIJS
AZQEC
BAWUL
BBNVY
BCNDV
BENPR
BHPHI
BPHCQ
BVXVI
C6C
CCPQU
CGR
CUY
CVF
DIK
DWQXO
E3Z
EBLON
EBS
ECM
EIF
EMOBN
FRP
FYUFA
GNUQQ
GROUPED_DOAJ
HCIFZ
HMCUK
HYE
HZ~
KQ8
LK8
M0L
M2P
M48
M7P
M~E
NAO
NPM
O5R
O5S
O9-
OK1
PIMPY
PQQKQ
PROAC
RIG
RNT
RPM
SNYQT
TR2
UKHRP
W2D
AAYXX
CITATION
7XB
8FK
K9.
PQEST
PQUKI
PRINS
Q9U
7X8
AFGXO
5PM
AAADF
ID FETCH-LOGICAL-c448t-3cdfa391f89461cd4e053196ee9510cb536a58a219cc2bc1231ea38bb7169a083
IEDL.DBID RPM
ISSN 2041-4889
IngestDate Thu Jul 04 21:06:45 EDT 2024
Tue Sep 17 21:29:53 EDT 2024
Fri Aug 16 12:01:47 EDT 2024
Fri Sep 13 05:02:03 EDT 2024
Fri Aug 23 01:19:27 EDT 2024
Sat Sep 28 08:09:01 EDT 2024
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Language English
License 2024. The Author(s).
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c448t-3cdfa391f89461cd4e053196ee9510cb536a58a219cc2bc1231ea38bb7169a083
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0000-0001-6398-3516
OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10808187/
PMID 38267403
PQID 2918141655
PQPubID 2041963
PageCount 1
ParticipantIDs doaj_primary_oai_doaj_org_article_8b7cb02cb6e6428aa58c29ecd930264c
pubmedcentral_primary_oai_pubmedcentral_nih_gov_10808187
proquest_miscellaneous_2918511519
proquest_journals_2918141655
crossref_primary_10_1038_s41419_024_06473_4
pubmed_primary_38267403
PublicationCentury 2000
PublicationDate 2024-01-24
PublicationDateYYYYMMDD 2024-01-24
PublicationDate_xml – month: 01
  year: 2024
  text: 2024-01-24
  day: 24
PublicationDecade 2020
PublicationPlace England
PublicationPlace_xml – name: England
– name: London
PublicationTitle Cell death & disease
PublicationTitleAlternate Cell Death Dis
PublicationYear 2024
Publisher Springer Nature B.V
Nature Publishing Group UK
Nature Publishing Group
Publisher_xml – name: Springer Nature B.V
– name: Nature Publishing Group UK
– name: Nature Publishing Group
References F Li (6473_CR20) 2018; 128
T Xu (6473_CR32) 2022; 29
LM Booshehri (6473_CR14) 2019; 39
Z Hoseini (6473_CR16) 2018; 233
Y Huang (6473_CR25) 2020; 22
F Martinon (6473_CR9) 2006; 440
K Zhu (6473_CR31) 2021; 18
J Huang (6473_CR21) 2023; 14
RC Coll (6473_CR24) 2015; 21
FG Bauernfeind (6473_CR7) 2009; 183
Y Chen (6473_CR28) 2021; 18
S Mariathasan (6473_CR8) 2006; 440
WP Arend (6473_CR12) 2008; 223
K Schroder (6473_CR1) 2010; 140
BF Py (6473_CR23) 2013; 49
L Wang (6473_CR18) 2020; 76
H Jiang (6473_CR27) 2017; 214
JJ Cho (6473_CR22) 2019; 10
L Franchi (6473_CR3) 2009; 227
J Shi (6473_CR13) 2015; 526
H He (6473_CR29) 2018; 9
C Schiltz (6473_CR34) 2002; 46
H Sharif (6473_CR4) 2019; 570
Y He (6473_CR6) 2016; 530
Y Huang (6473_CR2) 2021; 18
D Trisciuzzi (6473_CR30) 2023; 18
H Shi (6473_CR5) 2016; 17
F Li (6473_CR19) 2022; 7
C Juliana (6473_CR26) 2012; 287
D Wang (6473_CR33) 2021; 12
A Halle (6473_CR10) 2008; 9
V Hornung (6473_CR11) 2008; 9
T Murakami (6473_CR15) 2022; 23
N Esser (6473_CR17) 2014; 105
References_xml – volume: 526
  start-page: 660
  year: 2015
  ident: 6473_CR13
  publication-title: Nature
  doi: 10.1038/nature15514
  contributor:
    fullname: J Shi
– volume: 105
  start-page: 141
  year: 2014
  ident: 6473_CR17
  publication-title: Diabetes Res Clin Pract
  doi: 10.1016/j.diabres.2014.04.006
  contributor:
    fullname: N Esser
– volume: 9
  start-page: 847
  year: 2008
  ident: 6473_CR11
  publication-title: Nat Immunol
  doi: 10.1038/ni.1631
  contributor:
    fullname: V Hornung
– volume: 214
  start-page: 3219
  year: 2017
  ident: 6473_CR27
  publication-title: J Exp Med
  doi: 10.1084/jem.20171419
  contributor:
    fullname: H Jiang
– volume: 440
  start-page: 228
  year: 2006
  ident: 6473_CR8
  publication-title: Nature
  doi: 10.1038/nature04515
  contributor:
    fullname: S Mariathasan
– volume: 49
  start-page: 331
  year: 2013
  ident: 6473_CR23
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2012.11.009
  contributor:
    fullname: BF Py
– volume: 76
  start-page: 100889
  year: 2020
  ident: 6473_CR18
  publication-title: Mol Asp Med
  doi: 10.1016/j.mam.2020.100889
  contributor:
    fullname: L Wang
– volume: 287
  start-page: 36617
  year: 2012
  ident: 6473_CR26
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M112.407130
  contributor:
    fullname: C Juliana
– volume: 39
  start-page: 277
  year: 2019
  ident: 6473_CR14
  publication-title: J Clin Immunol
  doi: 10.1007/s10875-019-00638-z
  contributor:
    fullname: LM Booshehri
– volume: 9
  year: 2018
  ident: 6473_CR29
  publication-title: Nat Commun
  doi: 10.1038/s41467-018-04947-6
  contributor:
    fullname: H He
– volume: 29
  start-page: 1582
  year: 2022
  ident: 6473_CR32
  publication-title: Cell Death Differ
  doi: 10.1038/s41418-022-00947-8
  contributor:
    fullname: T Xu
– volume: 12
  year: 2021
  ident: 6473_CR33
  publication-title: Nat Commun
  doi: 10.1038/s41467-021-22987-3
  contributor:
    fullname: D Wang
– volume: 128
  start-page: 4148
  year: 2018
  ident: 6473_CR20
  publication-title: J Clin Investig
  doi: 10.1172/JCI120406
  contributor:
    fullname: F Li
– volume: 18
  start-page: 2372
  year: 2021
  ident: 6473_CR31
  publication-title: Cell Mol Immunol
  doi: 10.1038/s41423-021-00761-1
  contributor:
    fullname: K Zhu
– volume: 233
  start-page: 2116
  year: 2018
  ident: 6473_CR16
  publication-title: J Cell Physiol
  doi: 10.1002/jcp.25930
  contributor:
    fullname: Z Hoseini
– volume: 21
  start-page: 248
  year: 2015
  ident: 6473_CR24
  publication-title: Nat Med
  doi: 10.1038/nm.3806
  contributor:
    fullname: RC Coll
– volume: 46
  start-page: 1643
  year: 2002
  ident: 6473_CR34
  publication-title: Arthritis Rheum
  doi: 10.1002/art.10326
  contributor:
    fullname: C Schiltz
– volume: 18
  start-page: 737
  year: 2023
  ident: 6473_CR30
  publication-title: Expert Opin drug Discov
  doi: 10.1080/17460441.2023.2218641
  contributor:
    fullname: D Trisciuzzi
– volume: 140
  start-page: 821
  year: 2010
  ident: 6473_CR1
  publication-title: Cell
  doi: 10.1016/j.cell.2010.01.040
  contributor:
    fullname: K Schroder
– volume: 227
  start-page: 106
  year: 2009
  ident: 6473_CR3
  publication-title: Immunol Rev
  doi: 10.1111/j.1600-065X.2008.00734.x
  contributor:
    fullname: L Franchi
– volume: 18
  start-page: 2114
  year: 2021
  ident: 6473_CR2
  publication-title: Cell Mol Immunol
  doi: 10.1038/s41423-021-00740-6
  contributor:
    fullname: Y Huang
– volume: 223
  start-page: 20
  year: 2008
  ident: 6473_CR12
  publication-title: Immunol Rev
  doi: 10.1111/j.1600-065X.2008.00624.x
  contributor:
    fullname: WP Arend
– volume: 17
  start-page: 250
  year: 2016
  ident: 6473_CR5
  publication-title: Nat Immunol
  doi: 10.1038/ni.3333
  contributor:
    fullname: H Shi
– volume: 18
  start-page: 1425
  year: 2021
  ident: 6473_CR28
  publication-title: Cell Mol Immunol
  doi: 10.1038/s41423-021-00683-y
  contributor:
    fullname: Y Chen
– volume: 14
  start-page: 396
  year: 2023
  ident: 6473_CR21
  publication-title: Cell Death Dis
  doi: 10.1038/s41419-023-05923-9
  contributor:
    fullname: J Huang
– volume: 183
  start-page: 787
  year: 2009
  ident: 6473_CR7
  publication-title: J Immunol
  doi: 10.4049/jimmunol.0901363
  contributor:
    fullname: FG Bauernfeind
– volume: 570
  start-page: 338
  year: 2019
  ident: 6473_CR4
  publication-title: Nature
  doi: 10.1038/s41586-019-1295-z
  contributor:
    fullname: H Sharif
– volume: 9
  start-page: 857
  year: 2008
  ident: 6473_CR10
  publication-title: Nat Immunol
  doi: 10.1038/ni.1636
  contributor:
    fullname: A Halle
– volume: 440
  start-page: 237
  year: 2006
  ident: 6473_CR9
  publication-title: Nature
  doi: 10.1038/nature04516
  contributor:
    fullname: F Martinon
– volume: 10
  year: 2019
  ident: 6473_CR22
  publication-title: Nat Commun
  doi: 10.1038/s41467-019-08605-3
  contributor:
    fullname: JJ Cho
– volume: 23
  start-page: 5365
  year: 2022
  ident: 6473_CR15
  publication-title: Int J Mol Sci
  doi: 10.3390/ijms23105365
  contributor:
    fullname: T Murakami
– volume: 22
  start-page: 716
  year: 2020
  ident: 6473_CR25
  publication-title: Nat Cell Biol
  doi: 10.1038/s41556-020-0510-3
  contributor:
    fullname: Y Huang
– volume: 530
  start-page: 354
  year: 2016
  ident: 6473_CR6
  publication-title: Nature
  doi: 10.1038/nature16959
  contributor:
    fullname: Y He
– volume: 7
  start-page: 264
  year: 2022
  ident: 6473_CR19
  publication-title: Signal Transduct Target Ther
  doi: 10.1038/s41392-022-01057-0
  contributor:
    fullname: F Li
SSID ssj0000330256
Score 2.4071033
Snippet The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not completely...
Abstract The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not...
Abstract The NLRP3 inflammasome plays an important role in protecting the host from infection and aseptic inflammation, and its regulatory mechanism is not...
SourceID doaj
pubmedcentral
proquest
crossref
pubmed
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
StartPage 86
SubjectTerms Adenosine triphosphate
Arthritis
Arthritis, Gouty
Bacterial infections
Cancer
Crystals
Cytokines
Hospitals
Humans
Infections
Infectious diseases
Inflammasomes
Inflammation
Inflammatory diseases
Interleukin-1beta
Kinases
Life sciences
NIMA-Related Kinases - genetics
NLR Family, Pyrin Domain-Containing 3 Protein - genetics
Oligomerization
Proteins
Therapeutic targets
Ubiquitin-protein ligase
Uric acid
SummonAdditionalLinks – databaseName: DOAJ : Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBYlEOil9F03aVGhtyJi62FLxzbZsPSxlJJALkVIY4ksdL0huznsv-9IcpbdUuilR9sySN8nab6RNCNC3gPoGlTnmI84yGWEnhnJI9PCexN7Hj2kAOdvs3Z6KT9fqaudq77SmbCSHrgAd6J9B77m4NuQpLJzSgM3AXoj0H2QkGffRu04U3kORjcdjfkYJVMLfbKSjUzxOlyyFF8pmNyzRDlh_99U5p-HJXesz_lj8miUjfRjqe4T8iAMT8lhuUhy84z8nE5OL84EnQ_Xcz9fr-js64_v6TEi4Qu3Wi4CRZUcFv7XhrqhpymcoSzGUr-hHi1aWjIvv7HZ5EtHUx6J2xL18Jxcnk8uTqdsvDiBAXpbayagj06YJmoj2wZ6GcpQCyHpKfBKtAijw8kKgHtA49UEJ7T3KXWOQ1H2ghwMyyG8IhQBN84oCE2IsgNpNBIrOuFVHVtZi4p8uAfR3pT8GDbvawttC-QWIbcZcisr8inhvC2ZclvnF8i4HRm3_2K8Isf3LNlxwK0sNyhVUFwqVZF32884VNL-hxvC8q6UQX2JmrUiLwup25oIdLO63B69R_deVfe_DPPrnI47ndJE2dO9_h-NOyIPee6jDePymBysb-_CG5Q9a_829_Df_Vr-7Q
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: ProQuest Central
  dbid: BENPR
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3da9swEBddymAvY9_z1g0N9jZEbEu2pafRj5Swj1BKC30ZQjpLa2Cxu8R9yH-_k-VkzSh7tHWG833ofjrpToR8BJApFJVh1qOTCw81UyL3THJrla9zbyEUOH-fldNL8eWquNoj000tTDhWuZkT-4m6biHkyMe5wliE6KEoxsaGLAB04883v1m4Pyrssw6XaTwg-3kgG5H9o8ns7Hybb0lx4Y7hfaibSbkcrwQSKoZBioWKS87ETmzqW_jfhzv_PT55Jx6dPiGPByBJD6Pmn5I91zwjD-PVkuvn5Md0cnxxwum8uZ7bebeis2_nZ-HRowkszKpdOIq42S3srzU1TU1DgUNMz1K7phZjXEiix8_YbPK1oqGzxDLWQbwgl6eTi-MpG65SYIDrr45xqL3hKvNSiTKDWrjofM4FhAW24KUppMHpCyC3gOEsc4ZLa0MzHYMw7SUZNW3jXhMqjVFGFeAy50UFQklUNa-4LVJfipQn5NNGiPomdszQ_U43lzqKXKPIdS9yLRJyFOS8pQzdrvsX7fKnHpxHS1uBTXOwpQvLJYOsQq4c1Ap1WgpIyMFGS3pwwZX-azAJ-bAdRucJOyKmce1tpEHEiSg2Ia-iUreccFx4Vf3_yB1177C6O9LMr_sG3eHcJgKh6s3_-XpLHuW99WUsFwdk1C1v3TuEOJ19P1jvH0Bd-xc
  priority: 102
  providerName: ProQuest
– databaseName: Scholars Portal Open Access Journals
  dbid: M48
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwdV3db9MwED-NIdBeEJ8jMJCReEOGxnYS-wEhGJ0qYBVCq7QXZNmOzSqt6dZ2Ev3vOcdJRVF5jD8i6z58v7N9dwCvnZMDV1SG2oBKLoKrqRIsUMmtVaFmwboY4Hw6LkcT8eW8ON-DvtxRR8DlTtcu1pOaLC7f_r5ef0CFf59CxuW7pchFDMVhgsbQSU7FLbjNBBdR4k87uN_uzOi8o4nvYmd2Tz2AuxwhdyX6MlqdqWoz-u-Cof--pvzLPJ3ch3sdriQfkyA8gD3fPIQ7qdLk-hH8HA2Pzz5zMm0upna6WpLxtx_f42dAiZiZ5XzmCcJoP7OXa2KamsR4h3RaS-yaWDR58Uw9TaPj4deKxEQTixQW8RgmJ8Oz4xHtKitQh-7YinJXB8NVHqQSZe5q4ZMueh8Bl7MFL00hDe5mzjHr0Lrl3nBpbcytYxC1PYH9Zt74p0CkMcqowvncB1E5oSRynlfcFoNQIhEzeNMTUV-lBBq6vfjmUifqa6S-bqmvRQafIp03I2Py67ZhvvilO13S0lbODpizpY_ek8GlOqa8qxWytxQug6OeS7oXKM0UYhlEn0WRwatNN-pSvCAxjZ_fpDEIQBHUZnCYmLpZSS8UGcgtdm8tdbunmV60-brjM07ERdWz__70ORywVgZzysQR7K8WN_4Fgp2VfdlK8B9HVvj_
  priority: 102
  providerName: Scholars Portal
Title HECTD3 inhibits NLRP3 inflammasome assembly and activation by blocking NLRP3-NEK7 interaction
URI https://www.ncbi.nlm.nih.gov/pubmed/38267403
https://www.proquest.com/docview/2918141655/abstract/
https://search.proquest.com/docview/2918511519
https://pubmed.ncbi.nlm.nih.gov/PMC10808187
https://doaj.org/article/8b7cb02cb6e6428aa58c29ecd930264c
Volume 15
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3da9swEBdtx2AvY9_z1gUN9jbUxJZsS49rlhK2JQulhbwMI53l1VA7JUkf8t_vJNmhGXvai8GWDMd96H4n3Z0I-QQgR5DmmpkKjVxUUDIlkopJboyqyqQy4AqcZ_Nsei2-LdPlEcn6WhiftA-mPmtvm7O2vvG5lXcNDPs8seFiNnZ5ceho8uExOc45fxCj-_UXQ3R05F2FzIjL4UbEwtXqJIK52krO3G08HIF1LvrLsjqH5Pv2_wts_p0z-cAJXTwjTzv0SL8EKp-TI9u-II_DfZK7l-TXdDK--spp3d7Upt5u6PzH5cK9Vij3Rm9WjaUIlm1jbndUtyV1VQ1hT5aaHTXo2NzOefiNzSffc-raSaxD8cMrcn0xuRpPWXd_AgMMuraMQ1lpruJKKpHFUAobLM5aB6vApDzTqdS4ZgEkBtCHxVZzaYzroKMRm70mJ-2qtW8JlVorrVKwsa1EDkJJlC_PuUlHVYZMjMjnnonFXWiTUfjjbS6LwP0CuV947hciIueOz_uZrsW1_7Ba_y46QRfS5GBGCZjMuhhJI6mQKAulQvFmAiJy2kup6OxuUyQKEQtizDSNyMf9MFqMOwbRrV3dhzkIMxG6RuRNEOqekl4pIiIPxH1A6uEIKqnvyt0r5bv___U9eZJ4JY1ZIk7JyXZ9bz8g5tmaASr6Mh-QR-eT-eJy4HcO8DkTcuC2FX8OvAn8AYo6BLM
link.rule.ids 230,315,733,786,790,870,891,2115,12083,21416,24346,27957,27958,31754,31755,33779,33780,43345,43840,53827,53829,74102,74659
linkProvider National Library of Medicine
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3db9MwELegE4IXxOcIDAgSb8haEjuJ_YTY6FRYF01TJ-0FWfbFZpVoMpruof895zgtFCEekzjR5c7n-93Zd0fIewCRQF5qahwqOXdQU8kzRwUzRro6cwZ8gvNZVUwu-der_GoIuHXDscrNmtgv1HULPkZ-mEm0RYge8vzjzU_qu0b53dWhhcZdsscZuiojsnc0rs4vtlGWBN11NOpDtkzCxGHH8SuSommiPs-SUb5jkfrC_f9Cm38fmvzDCp08Ig8H-Bh_CvJ-TO7Y5gm5FxpKrp-Sb5Px8ewzi-fN9dzMV11cTS_O_aVDwS901y5sjGjZLsyPdaybOvZpDSEoG5t1bNCy-dB5eI1W49My9vUkliH74Rm5PBnPjid0aKBAAb2uFWVQO81k6oTkRQo1t0HlrPW4CkzOCp0LjYsWQGYAjVhqNRPG-BI6GsHZczJq2sa-ILHQWmqZg02t4yVwKVDArGQmT1zBExaRDxsmqptQJ0P1-9tMqMByhSxXPcsVj8iR5_N2pK9x3d9ol9_VoDJKmBJMkoEprHeSNJIKmbRQS5RpwSEiBxspqUHxOvV7mkTk3fYxqozfB9GNbW_DGMSZiF0jsh-EuqWEobtV9v8jdsS9Q-ruk2Z-3Zfl9qc1Ef6UL_9P11tyfzI7m6rpl-r0FXmQ9TMxpRk_IKPV8ta-RpCzMm-GmfwLEsH6Sg
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3Nb9MwFLdgCMQF8U1ggJG4IatJ7CT2CcHWqrBRTWiTekGW_WKzSjQZTXfof89znBaKEMckTuS8D7_fs98HIW8BZApFZZj1qOTCQ82UyD2T3Frl69xbCAnOX2bl9EJ8nhfzIf6pG8Iqt2tiv1DXLYQ98lGu0BYheiiKkR_CIs6OJ--vfrLQQSqctA7tNG6SW2gl09DNoJpXu_2WFB13NO9D3kzK5agT-D3F0EixkHHJmdizTX0J_3_hzr_DJ_-wR5P75N4AJOmHyPkH5IZrHpLbsbXk5hH5Nh0fnR9zumguF3ax7ujs9OtZuPQoAkvTtUtHETe7pf2xoaapaUhwiNuz1G6oRRsXNtHja2w2PqloqCyxinkQj8nFZHx-NGVDKwUG6H-tGYfaG64yL5UoM6iFi8rnXEBYYAtemkIaXL4AcgtozjJnuLQ2FNMxCNOekIOmbdwzQqUxyqgCXOa8qEAoiazmFbdF6kuR8oS82xJRX8WKGbo_6eZSR5JrJLnuSa5FQj4GOu9GhmrX_Y129V0PyqOlrcCmOdjSBXfJ4FQhVw5qhTwtBSTkcMslPahgp38LTELe7B6j8oQTEdO49jqOQcSJKDYhTyNTdzPh6HhV_f_IPXbvTXX_SbO47At0h7hNBELV8__P6zW5gyKsTz_NTl6Qu3kviBnLxSE5WK-u3UtEO2v7qhfjX4Ox_RA
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=HECTD3+inhibits+NLRP3+inflammasome+assembly+and+activation+by+blocking+NLRP3-NEK7+interaction&rft.jtitle=Cell+death+%26+disease&rft.au=Cheng%2C+Zhuo&rft.au=Huang%2C+Maobo&rft.au=Li%2C+Wei&rft.au=Hou%2C+Lei&rft.date=2024-01-24&rft.eissn=2041-4889&rft.volume=15&rft.issue=1&rft.spage=86&rft_id=info:doi/10.1038%2Fs41419-024-06473-4&rft_id=info%3Apmid%2F38267403&rft.externalDocID=38267403
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2041-4889&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2041-4889&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2041-4889&client=summon