PMID- 12407445
OWN - NLM
STAT- MEDLINE
DCOM- 20030429
LR  - 20181113
IS  - 1522-8002 (Print)
IS  - 1476-5586 (Electronic)
IS  - 1476-5586 (Linking)
VI  - 4
IP  - 6
DP  - 2002 Nov-Dec
TI  - Met-HGF/SF signal transduction induces mimp, a novel mitochondrial carrier 
      homologue, which leads to mitochondrial depolarization.
PG  - 510-22
AB  - Met-hepatocyte growth factor/scatter factor (HGF/SF) signaling plays an important 
      role in epithelial tissue morphogenesis, lumen formation, and tumorigenicity. We 
      have recently demonstrated that HGF/SF also alters the metabolic activity of 
      cells by enhancing both the glycolytic and oxidative phosphorylation pathways of 
      energy production. Using differential display polymerase chain reaction, we 
      cloned a novel gene, designated mimp (Met-Induced Mitochondrial Protein), which 
      is upregulated in NIH-3T3 cells cotransfected with both HGF/SF and Met (HMH 
      cells). Northern and Western blot analyses showed that mimp is induced in several 
      Met-expressing cell lines following treatment with HGF/SF. Mimp encodes a 33-kDa 
      protein that shows sequence homology to the family of mitochondrial carrier 
      proteins (MCPs). Murine Mimp (mMimp) is expressed in a wide variety of tissues, 
      exhibiting an expression pattern similar to Met. Predominant expression is seen 
      in liver, kidney, heart, skeletal muscle, and testis. Using immunostaining for 
      HA-tagged mMimp and a GFP-mMimp chimeric protein as well as subcellular 
      fractionation, we determined that Mimp is primarily localized to the 
      mitochondria. Ectopic expression of mMimp in the Met-responsive adenocarcinoma 
      cell line, DA3, reduced the mitochondrial membrane potential (uncoupling 
      activity). The extent of the mitochondrial depolarization positively correlated 
      with the level of Mimp expression. Our results demonstrate that Mimp is a novel 
      mitochondrial carrier homologue upregulated by Met-HGF/SF signal transduction, 
      which leads to mitochondrial depolarization, and suggest novel links among 
      tyrosine kinase signaling, mitochondrial function, and cellular bioenergetics.
FAU - Yerushalmi, Gil M
AU  - Yerushalmi GM
AD  - Department of Human Microbiology, Sackler Faculty of Medicine, Tel-Aviv 
      University, Israel.
FAU - Leibowitz-Amit, Raya
AU  - Leibowitz-Amit R
FAU - Shaharabany, Miriam
AU  - Shaharabany M
FAU - Tsarfaty, Ilan
AU  - Tsarfaty I
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Neoplasia
JT  - Neoplasia (New York, N.Y.)
JID - 100886622
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA Primers)
RN  - 0 (DNA, Complementary)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (Mitochondrial Membrane Transport Proteins)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Mtch2 protein, mouse)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
SB  - IM
MH  - 3T3 Cells
MH  - Amino Acid Sequence
MH  - Animals
MH  - Blotting, Northern
MH  - Blotting, Western
MH  - Carrier Proteins/genetics/*metabolism
MH  - DNA Primers/chemistry
MH  - DNA, Complementary/metabolism
MH  - Electron Transport Complex IV/immunology/metabolism
MH  - Fluorescent Antibody Technique
MH  - *Gene Expression
MH  - Gene Expression Profiling
MH  - Gene Library
MH  - Hepatocyte Growth Factor/*physiology
MH  - Humans
MH  - Membrane Potentials
MH  - Membrane Transport Proteins/genetics/*metabolism
MH  - Mice
MH  - Mitochondria/physiology
MH  - Mitochondrial Membrane Transport Proteins
MH  - Mitochondrial Proteins/genetics/*metabolism
MH  - Molecular Sequence Data
MH  - Proto-Oncogene Proteins c-met/*physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sequence Homology, Amino Acid
MH  - *Signal Transduction
MH  - Transfection
PMC - PMC1503665
EDAT- 2002/10/31 04:00
MHDA- 2003/04/30 05:00
PMCR- 2002/11/01
CRDT- 2002/10/31 04:00
PHST- 2002/05/08 00:00 [received]
PHST- 2002/07/01 00:00 [accepted]
PHST- 2002/10/31 04:00 [pubmed]
PHST- 2003/04/30 05:00 [medline]
PHST- 2002/10/31 04:00 [entrez]
PHST- 2002/11/01 00:00 [pmc-release]
AID - 0272a [pii]
AID - 10.1038/sj.neo.7900272 [doi]
PST - ppublish
SO  - Neoplasia. 2002 Nov-Dec;4(6):510-22. doi: 10.1038/sj.neo.7900272.