PMID- 10233955
OWN - NLM
STAT- MEDLINE
DCOM- 19990607
LR  - 20240407
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 73
IP  - 6
DP  - 1999 Jun
TI  - Feline leukemia virus long terminal repeat activates collagenase IV gene 
      expression through AP-1.
PG  - 4931-40
AB  - Leukemia and lymphoma induced by feline leukemia viruses (FeLVs) are the 
      commonest forms of illness in domestic cats. These viruses do not contain 
      oncogenes, and the source of their pathogenic activity is not clearly understood. 
      Mechanisms involving proto-oncogene activation subsequent to proviral integration 
      and/or development of recombinant viruses with enhanced replication properties 
      are thought to play an important role in their disease pathogenesis. In addition, 
      the long terminal repeat (LTR) regions of these viruses have been shown to be 
      important determinants for pathogenicity and tissue specificity, by virtue of 
      their ability to interact with various transcription factors. Previously, we have 
      shown that, in the case of Moloney murine leukemia virus, the U3 region of the 
      LTR independently induces transcriptional activation of specific cellular genes 
      through an LTR-generated RNA transcript (S. Y. Choi and D. V. Faller, J. Biol. 
      Chem. 269:19691-19694, 1994; S.-Y. Choi and D. V. Faller, J. Virol. 69:7054-7060, 
      1995). In this report, we show that the U3 region of exogenous FeLV LTRs can 
      induce transcription from collagenase IV (matrix metalloproteinase 9) and 
      monocyte chemotactic protein 1 (MCP-1) promoters up to 12-fold. We also show that 
      AP-1 DNA-binding activity and transcriptional activity are strongly induced in 
      cells expressing FeLV LTRs and that LTR-specific RNA transcripts are generated in 
      those cells. Activation of mitogen-activated protein kinase kinases 1 and 2 (MEK1 
      and -2) by the LTR is an intermediate step in the FeLV LTR-mediated induction of 
      AP-1 activity. These findings thus suggest that the LTRs of FeLVs can 
      independently activate transcription of specific cellular genes. This 
      LTR-mediated cellular gene transactivation may play an important role in 
      tumorigenesis or preleukemic states and may be a generalizable activity of 
      leukemia-inducing retroviruses.
FAU - Ghosh, S K
AU  - Ghosh SK
AD  - Cancer Research Center, Boston University School of Medicine, Boston, 
      Massachusetts, USA.
FAU - Faller, D V
AU  - Faller DV
LA  - eng
GR  - CA50459/CA/NCI NIH HHS/United States
GR  - P60AR20613/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factor AP-1)
RN  - 9007-49-2 (DNA)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 1)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 2)
RN  - EC 2.7.12.2 (Map2k1 protein, mouse)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
RN  - EC 3.4.24.- (Collagenases)
SB  - IM
MH  - 3T3 Cells
MH  - Animals
MH  - Cats
MH  - Chemokine CCL2/genetics
MH  - Collagenases/*genetics
MH  - DNA/metabolism
MH  - *Gene Expression Regulation, Enzymologic
MH  - Genes, MHC Class I
MH  - Leukemia Virus, Feline/*genetics
MH  - MAP Kinase Kinase 1
MH  - MAP Kinase Kinase 2
MH  - Mice
MH  - *Mitogen-Activated Protein Kinase Kinases
MH  - Promoter Regions, Genetic
MH  - Protein Serine-Threonine Kinases/antagonists & inhibitors
MH  - Protein-Tyrosine Kinases/antagonists & inhibitors
MH  - RNA, Messenger/biosynthesis
MH  - *Terminal Repeat Sequences
MH  - Transcription Factor AP-1/*physiology
MH  - Transcriptional Activation
PMC - PMC112537
EDAT- 1999/05/11 00:00
MHDA- 1999/05/11 00:01
PMCR- 1999/06/01
CRDT- 1999/05/11 00:00
PHST- 1999/05/11 00:00 [pubmed]
PHST- 1999/05/11 00:01 [medline]
PHST- 1999/05/11 00:00 [entrez]
PHST- 1999/06/01 00:00 [pmc-release]
AID - 1863 [pii]
AID - 10.1128/JVI.73.6.4931-4940.1999 [doi]
PST - ppublish
SO  - J Virol. 1999 Jun;73(6):4931-40. doi: 10.1128/JVI.73.6.4931-4940.1999.