PMID- 23211594
OWN - NLM
STAT- MEDLINE
DCOM- 20130625
LR  - 20130115
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 430
IP  - 2
DP  - 2013 Jan 11
TI  - Proteomic profiling of brain cortex tissues in a Tau transgenic mouse model of 
      Alzheimer's disease.
PG  - 670-5
LID - S0006-291X(12)02283-8 [pii]
LID - 10.1016/j.bbrc.2012.11.093 [doi]
AB  - Alzheimer's disease (AD) involves regionalized neuronal death, synaptic loss, and 
      an accumulation of intracellular neurofibrillary tangles and extracellular senile 
      plaques. Although there have been numerous studies on tau proteins and AD in 
      various stages of neurodegenerative disease pathology, the relationship between 
      tau and AD is not yet fully understood. A transgenic mouse model expressing 
      neuron-specific enolase (NSE)-controlled human wild-type tau (NSE-htau23), which 
      displays some of the typical Alzheimer-associated pathological features, was used 
      to analyze the brain proteome associated with tau tangle deposition. 
      Two-dimensional electrophoresis was performed to compare the cortex proteins of 
      transgenic mice (6- and 12-month-old) with those of control mice. Differentially 
      expressed spots in different stages of AD were identified with ESI-Q-TOF 
      (electrospray ionization quadruple time-of-flight) mass spectrometry and liquid 
      chromatography/tandem mass spectrometry. Among the identified proteins, 
      glutathione S-transferase P 1 (GSTP1) and carbonic anhydrase II (CAII) were 
      down-regulated with the progression of AD, and secerin-1 (SCRN1) and V-type 
      proton ATPase subunit E 1 (ATP6VE1) were up-regulated only in the early stages, 
      and down-regulated in the later stages of AD. The proteins, which were further 
      confirmed by RT-PCR at the mRNA level and with western blotting at the protein 
      level, are expected to be good candidates as drug targets for AD. The study of 
      up- and down-regulation of proteins during the progression of AD helps to explain 
      the mechanisms associated with neuronal degeneration in AD.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Chang, Seong-Hun
AU  - Chang SH
AD  - School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, 
      Republic of Korea.
FAU - Jung, In-Soo
AU  - Jung IS
FAU - Han, Gi-Yeon
AU  - Han GY
FAU - Kim, Nam-Hee
AU  - Kim NH
FAU - Kim, Hyun-Jung
AU  - Kim HJ
FAU - Kim, Chan-Wha
AU  - Kim CW
LA  - eng
PT  - Journal Article
DEP - 20121202
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (MAPT protein, human)
RN  - 0 (Proteome)
RN  - 0 (tau Proteins)
SB  - IM
MH  - Alzheimer Disease/genetics/*metabolism
MH  - Animals
MH  - Cerebral Cortex/*metabolism
MH  - Chromatography, Liquid
MH  - Disease Models, Animal
MH  - Electrophoresis, Gel, Two-Dimensional
MH  - Humans
MH  - Mice
MH  - Mice, Transgenic
MH  - Protein Array Analysis
MH  - Proteome/analysis/*metabolism
MH  - Proteomics
MH  - Spectrometry, Mass, Electrospray Ionization
MH  - tau Proteins/*genetics
EDAT- 2012/12/06 06:00
MHDA- 2013/06/26 06:00
CRDT- 2012/12/06 06:00
PHST- 2012/10/30 00:00 [received]
PHST- 2012/11/20 00:00 [accepted]
PHST- 2012/12/06 06:00 [entrez]
PHST- 2012/12/06 06:00 [pubmed]
PHST- 2013/06/26 06:00 [medline]
AID - S0006-291X(12)02283-8 [pii]
AID - 10.1016/j.bbrc.2012.11.093 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2013 Jan 11;430(2):670-5. doi: 
      10.1016/j.bbrc.2012.11.093. Epub 2012 Dec 2.