PMID- 15169888
OWN - NLM
STAT- MEDLINE
DCOM- 20040630
LR  - 20181113
IS  - 0270-7306 (Print)
IS  - 1098-5549 (Electronic)
IS  - 0270-7306 (Linking)
VI  - 24
IP  - 12
DP  - 2004 Jun
TI  - ABIN-2 forms a ternary complex with TPL-2 and NF-kappa B1 p105 and is essential 
      for TPL-2 protein stability.
PG  - 5235-48
AB  - NF-kappa B1 p105 forms a high-affinity, stoichiometric interaction with TPL-2, a 
      MEK kinase essential for TLR4 activation of the ERK mitogen-activated protein 
      kinase cascade in lipopolysaccharide (LPS)-stimulated macrophages. Interaction 
      with p105 is required to maintain TPL-2 metabolic stability and also negatively 
      regulates TPL-2 MEK kinase activity. Here, affinity purification identified 
      A20-binding inhibitor of NF-kappa B 2 (ABIN-2) as a novel p105-associated 
      protein. Cotransfection experiments demonstrated that ABIN-2 could interact with 
      TPL-2 in addition to p105 but preferentially formed a ternary complex with both 
      proteins. Consistently, in unstimulated bone marrow-derived macrophages (BMDMs), 
      a substantial fraction of endogenous ABIN-2 was associated with both p105 and 
      TPL-2. Although the majority of TPL-2 in these cells was complexed with ABIN-2, 
      the pool of TPL-2 which could activate MEK after LPS stimulation was not, and LPS 
      activation of TPL-2 was found to correlate with its release from ABIN-2. 
      Depletion of ABIN-2 by RNA interference dramatically reduced steady-state levels 
      of TPL-2 protein without affecting levels of TPL-2 mRNA or p105 protein. In 
      addition, ABIN-2 increased the half-life of cotransfected TPL-2. Thus, optimal 
      TPL-2 stability in vivo requires interaction with ABIN-2 as well as p105. 
      Together, these data raise the possibility that ABIN-2 functions in the TLR4 
      signaling pathway which regulates TPL-2 activation.
FAU - Lang, V
AU  - Lang V
AD  - Division of Immune Cell Biology, National Institute for Medical Research, Mill 
      Hill, London NW7 1AA, United Kingdom.
FAU - Symons, A
AU  - Symons A
FAU - Watton, S J
AU  - Watton SJ
FAU - Janzen, J
AU  - Janzen J
FAU - Soneji, Y
AU  - Soneji Y
FAU - Beinke, S
AU  - Beinke S
FAU - Howell, S
AU  - Howell S
FAU - Ley, S C
AU  - Ley SC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Cell Biol
JT  - Molecular and cellular biology
JID - 8109087
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA, Complementary)
RN  - 0 (Macromolecular Substances)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (NF-kappa B p50 Subunit)
RN  - 0 (NFKB1 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Recombinant Proteins)
RN  - 0 (TLR4 protein, human)
RN  - 0 (TNIP2 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Toll-Like Receptors)
RN  - 0 (Transcription Factors)
RN  - 147257-52-1 (Nfkb1 protein, mouse)
RN  - EC 2.7.11.25 (MAP Kinase Kinase Kinases)
RN  - EC 2.7.11.25 (MAP3K8 protein, human)
RN  - EC 2.7.11.25 (Map3k8 protein, mouse)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Carrier Proteins/chemistry/genetics/*metabolism
MH  - Cell Line
MH  - DNA, Complementary/genetics
MH  - Enzyme Activation
MH  - HeLa Cells
MH  - Humans
MH  - In Vitro Techniques
MH  - MAP Kinase Kinase Kinases/chemistry/genetics/*metabolism
MH  - Macromolecular Substances
MH  - Macrophages/metabolism
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Molecular Sequence Data
MH  - NF-kappa B p50 Subunit
MH  - Proto-Oncogene Proteins/chemistry/genetics/*metabolism
MH  - RNA, Small Interfering/genetics
MH  - Receptors, Cell Surface/metabolism
MH  - Recombinant Proteins/chemistry/genetics/metabolism
MH  - Signal Transduction
MH  - Solubility
MH  - Toll-Like Receptor 4
MH  - Toll-Like Receptors
MH  - Transcription Factors/chemistry/deficiency/genetics/*metabolism
MH  - Transfection
PMC - PMC419892
EDAT- 2004/06/01 05:00
MHDA- 2004/07/01 05:00
PMCR- 2004/06/01
CRDT- 2004/06/01 05:00
PHST- 2004/06/01 05:00 [pubmed]
PHST- 2004/07/01 05:00 [medline]
PHST- 2004/06/01 05:00 [entrez]
PHST- 2004/06/01 00:00 [pmc-release]
AID - 24/12/5235 [pii]
AID - 1862-03 [pii]
AID - 10.1128/MCB.24.12.5235-5248.2004 [doi]
PST - ppublish
SO  - Mol Cell Biol. 2004 Jun;24(12):5235-48. doi: 10.1128/MCB.24.12.5235-5248.2004.