PMID- 28157553
OWN - NLM
STAT- MEDLINE
DCOM- 20170911
LR  - 20180221
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 83
DP  - 2017 Mar
TI  - Immunoproteasome subunit deficiency has no influence on the canonical pathway of 
      NF-kappaB activation.
PG  - 147-153
LID - S0161-5890(17)30025-1 [pii]
LID - 10.1016/j.molimm.2017.01.019 [doi]
AB  - Activation of the pro-inflammatory transcription factor NF-kappaB requires 
      signal-induced proteasomal degradation of the inhibitor of NF-kappaB (IkappaB) in order 
      to allow nuclear translocation. Most cell types are capable of expressing two 
      types of 20S proteasome core particles, the constitutive proteasome and 
      immunoproteasome. Inducible under inflammatory conditions, the immunoproteasome 
      is mainly characterized through an altered cleavage specificity compared to the 
      constitutive proteasome. However, the question whether immunoproteasome subunits 
      affect NF-kappaB signal transduction differently from constitutive subunits is still 
      up for debate. To study the effect of immunoproteasomes on LPS- or TNF-alpha-induced 
      NF-kappaB activation, we used IFN-gamma stimulated peritoneal macrophages and mouse 
      embryonic fibroblasts derived from mice deficient for the immunoproteasome 
      subunits low molecular mass polypeptide (LMP) 2, or LMP7 and multicatalytic 
      endopeptidase complex-like 1 (MECL-1). Along the canonical signaling pathway of 
      NF-kappaB activation no differences in the extent and kinetic of IkappaB degradation were 
      observed. Neither the nuclear translocation and DNA binding of NF-kappaB nor the 
      production of the NF-kappaB dependent cytokines TNF-alpha, IL-6, and IL-10 differed 
      between immunoproteasome deficient and proficient cells. Hence, we conclude that 
      immunoproteasome subunits have no specialized function for canonical NF-kappaB 
      activation.
CI  - Copyright (c) 2017. Published by Elsevier Ltd.
FAU - Bitzer, Annegret
AU  - Bitzer A
AD  - Division of Immunology, Department of Biology, University of Konstanz, D-78457 
      Konstanz, Germany.
FAU - Basler, Michael
AU  - Basler M
AD  - Division of Immunology, Department of Biology, University of Konstanz, D-78457 
      Konstanz, Germany; Biotechnology Institute Thurgau (BITg) at the University of 
      Konstanz, CH-8280 Kreuzlingen, Switzerland.
FAU - Krappmann, Daniel
AU  - Krappmann D
AD  - Research Unit Cellular Signal Integration, Institute of Molecular Toxicology and 
      Pharmacology, Helmholtz Zentrum Munchen - German Research Center for 
      Environmental Health, Ingolstadter Landstr. 1, D-85764 Neuherberg, Germany.
FAU - Groettrup, Marcus
AU  - Groettrup M
AD  - Division of Immunology, Department of Biology, University of Konstanz, D-78457 
      Konstanz, Germany; Biotechnology Institute Thurgau (BITg) at the University of 
      Konstanz, CH-8280 Kreuzlingen, Switzerland. Electronic address: 
      Marcus.Groettrup@uni-konstanz.de.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170131
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (NF-kappa B)
RN  - 144416-78-4 (LMP-2 protein)
RN  - EC 3.4.22.- (Cysteine Endopeptidases)
RN  - EC 3.4.25.1 (LMP7 protein)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
RN  - EC 3.4.25.1 (Psmb10 protein, mouse)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cysteine Endopeptidases/deficiency/immunology
MH  - Electrophoretic Mobility Shift Assay
MH  - Enzyme Activation/immunology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fibroblasts/*immunology
MH  - Macrophages, Peritoneal/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - NF-kappa B/*immunology/metabolism
MH  - Proteasome Endopeptidase Complex/deficiency/*immunology
MH  - *Signal Transduction/immunology
OTO - NOTNLM
OT  - Immunoproteasome
OT  - Inflammation
OT  - LMP2
OT  - LMP7
OT  - NF-kappaB
EDAT- 2017/02/06 06:00
MHDA- 2017/09/12 06:00
CRDT- 2017/02/04 06:00
PHST- 2016/10/19 00:00 [received]
PHST- 2017/01/13 00:00 [revised]
PHST- 2017/01/20 00:00 [accepted]
PHST- 2017/02/06 06:00 [pubmed]
PHST- 2017/09/12 06:00 [medline]
PHST- 2017/02/04 06:00 [entrez]
AID - S0161-5890(17)30025-1 [pii]
AID - 10.1016/j.molimm.2017.01.019 [doi]
PST - ppublish
SO  - Mol Immunol. 2017 Mar;83:147-153. doi: 10.1016/j.molimm.2017.01.019. Epub 2017 
      Jan 31.