PMID- 23770847
OWN - NLM
STAT- MEDLINE
DCOM- 20140620
LR  - 20240323
IS  - 1476-5594 (Electronic)
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 33
IP  - 19
DP  - 2014 May 8
TI  - The API2-MALT1 fusion exploits TNFR pathway-associated RIP1 ubiquitination to 
      promote oncogenic NF-kappaB signaling.
PG  - 2520-30
LID - 10.1038/onc.2013.195 [doi]
AB  - The API2-MALT1 fusion oncoprotein is created by the recurrent t(11;18)(q21;q21) 
      chromosomal translocation in mucosa-associated lymphoid tissue (MALT) lymphoma. 
      We identified receptor interacting protein-1 (RIP1) as a novel 
      API2-MALT1-associated protein, and demonstrate that RIP1 is required for 
      API2-MALT1 to stimulate canonical nuclear factor kappa B (NF-kappaB). API2-MALT1 
      promotes ubiquitination of RIP1 at lysine (K) 377, which is necessary for full 
      NF-kappaB activation. Furthermore, we found that TNF receptor-associated factor 2 
      (TRAF2) recruitment is required for API2-MALT1 to induce RIP1 ubiquitination, 
      NF-kappaB activation and cellular transformation. Although both TRAF2 and RIP1 
      interact with the API2 moiety of API2-MALT1, this moiety alone is insufficient to 
      induce RIP1 ubiquitination or activate NF-kappaB, indicating that 
      API2-MALT1-dependent RIP1 ubiquitination represents a gain of function requiring 
      the concerted actions of both the API2 and MALT1 moieties of the fusion. 
      Intriguingly, constitutive RIP1 ubiquitination was recently demonstrated in 
      several solid tumors, and now our study implicates RIP1 ubiquitination as a 
      critical component of API2-MALT1-dependent lymphomagenesis.
FAU - Rosebeck, S
AU  - Rosebeck S
AD  - Department of Pediatrics and Communicable Diseases, University of Michigan 
      Medical School, Ann Arbor, MI, USA.
FAU - Rehman, A O
AU  - Rehman AO
AD  - Department of Pediatrics and Communicable Diseases, University of Michigan 
      Medical School, Ann Arbor, MI, USA.
FAU - Apel, I J
AU  - Apel IJ
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, 
      USA.
FAU - Kohrt, D
AU  - Kohrt D
AD  - Department of Pediatrics and Communicable Diseases, University of Michigan 
      Medical School, Ann Arbor, MI, USA.
FAU - Appert, A
AU  - Appert A
AD  - Division of Molecular Histopathology, Department of Pathology, University of 
      Cambridge, Laboratory Block, Addenbrooke's Hospital, Cambridge, UK.
FAU - O'Donnell, M A
AU  - O'Donnell MA
AD  - Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
FAU - Ting, A T
AU  - Ting AT
AD  - Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
FAU - Du, M-Q
AU  - Du MQ
AD  - Division of Molecular Histopathology, Department of Pathology, University of 
      Cambridge, Laboratory Block, Addenbrooke's Hospital, Cambridge, UK.
FAU - Baens, M
AU  - Baens M
AD  - 1] Human Genome Laboratory, Molecular Genetics, Center for Human Genetics, 
      Catholic University Leuven, Leuven, Belgium [2] Human Genome Laboratory, 
      Department of Molecular and Developmental Genetics, Flanders Institute for 
      Biotechnology (VIB), Leuven, Belgium.
FAU - Lucas, P C
AU  - Lucas PC
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, 
      USA.
FAU - McAllister-Lucas, L M
AU  - McAllister-Lucas LM
AD  - Department of Pediatrics and Communicable Diseases, University of Michigan 
      Medical School, Ann Arbor, MI, USA.
LA  - eng
GR  - T32 HL007622/HL/NHLBI NIH HHS/United States
GR  - T32-HL007622-21A2/HL/NHLBI NIH HHS/United States
GR  - R01 CA124540/CA/NCI NIH HHS/United States
GR  - R01 HL082914/HL/NHLBI NIH HHS/United States
GR  - R01CA124540/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20130617
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (AGFG1 protein, human)
RN  - 0 (API2-MALT1 fusion protein, human)
RN  - 0 (NF-kappa B)
RN  - 0 (Nuclear Pore Complex Proteins)
RN  - 0 (Oncogene Proteins, Fusion)
RN  - 0 (RNA-Binding Proteins)
RN  - 0 (TNF Receptor-Associated Factor 2)
SB  - IM
MH  - Blotting, Western
MH  - Cell Line, Tumor
MH  - HEK293 Cells
MH  - Humans
MH  - Immunoprecipitation
MH  - Lymphoma, B-Cell, Marginal Zone/*genetics/metabolism
MH  - NF-kappa B/*metabolism
MH  - Nuclear Pore Complex Proteins/genetics/*metabolism
MH  - Oncogene Proteins, Fusion/*genetics
MH  - Oncogenes
MH  - RNA-Binding Proteins/genetics/*metabolism
MH  - Signal Transduction/*physiology
MH  - TNF Receptor-Associated Factor 2/genetics/*metabolism
MH  - Transfection
MH  - Ubiquitination
PMC - PMC4237018
MID - NIHMS550123
COIS- CONFLICT OF INTEREST The authors declare no conflict of interest.
EDAT- 2013/06/19 06:00
MHDA- 2014/06/21 06:00
PMCR- 2014/11/19
CRDT- 2013/06/18 06:00
PHST- 2012/08/20 00:00 [received]
PHST- 2013/01/29 00:00 [revised]
PHST- 2013/04/03 00:00 [accepted]
PHST- 2013/06/18 06:00 [entrez]
PHST- 2013/06/19 06:00 [pubmed]
PHST- 2014/06/21 06:00 [medline]
PHST- 2014/11/19 00:00 [pmc-release]
AID - onc2013195 [pii]
AID - 10.1038/onc.2013.195 [doi]
PST - ppublish
SO  - Oncogene. 2014 May 8;33(19):2520-30. doi: 10.1038/onc.2013.195. Epub 2013 Jun 17.