PMID- 17689501
OWN - NLM
STAT- MEDLINE
DCOM- 20071214
LR  - 20211203
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1167
DP  - 2007 Sep 5
TI  - Increased autophagy in transgenic mice with a G93A mutant SOD1 gene.
PG  - 112-7
AB  - Autophagy, like the ubiquitin-proteasome system, is considered to play an 
      important role in preventing the accumulation of abnormal proteins. Rat 
      microtubule-associated protein 1 light chain 3 (LC3) is important for autophagy, 
      and the conversion from LC3-I into LC3-II is accepted as a simple method for 
      monitoring autophagy. We examined a SOD1G93A transgenic mouse model for 
      amyotrophic lateral sclerosis (ALS) to consider a possible relationship between 
      autophagy and ALS. In our study we analyzed LC3 and mammalian target of rapamycin 
      (mTOR), a suppressor of autophagy, by immunoassays. The level of LC3-II, which is 
      known to be correlated with the extent of autophagosome formation, was increased 
      in SOD1G93A transgenic mice at symptomatic stage compared with non-transgenic or 
      human wild-type SOD1 transgenic animals. Moreover, the ratio of phosphorylated 
      mTOR/Ser2448 immunopositive motor neurons to total motor neurons was decreased in 
      SOD1G93A-Tg mice. The present data show the possibility of increased autophagy in 
      an animal model for ALS. And autophagy may be partially regulated by an mTOR 
      signaling pathway in these animals.
FAU - Morimoto, Nobutoshi
AU  - Morimoto N
AD  - Department of Neurology, Graduate School of Medicine, Dentistry and 
      Pharmaceutical Sciences, Okayama University, 2-5-1 Shikata-cho, Okayama 700-8558, 
      Japan.
FAU - Nagai, Makiko
AU  - Nagai M
FAU - Ohta, Yasuyuki
AU  - Ohta Y
FAU - Miyazaki, Kazunori
AU  - Miyazaki K
FAU - Kurata, Tomoko
AU  - Kurata T
FAU - Morimoto, Mizuki
AU  - Morimoto M
FAU - Murakami, Tetsuro
AU  - Murakami T
FAU - Takehisa, Yasushi
AU  - Takehisa Y
FAU - Ikeda, Yoshio
AU  - Ikeda Y
FAU - Kamiya, Tatsushi
AU  - Kamiya T
FAU - Abe, Koji
AU  - Abe K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070707
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Map1lc3b protein, mouse)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (SOD1 protein, human)
RN  - 452VLY9402 (Serine)
RN  - EC 1.15.1.1 (Sod1 protein, mouse)
RN  - EC 1.15.1.1 (Sod1 protein, rat)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - EC 1.15.1.1 (Superoxide Dismutase-1)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.1.1 (mTOR protein, rat)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Amyotrophic Lateral Sclerosis/genetics/*metabolism/physiopathology
MH  - Animals
MH  - Autophagy/*genetics
MH  - Central Nervous System/metabolism/physiopathology
MH  - Disease Models, Animal
MH  - Female
MH  - Genetic Predisposition to Disease/genetics
MH  - Humans
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Microtubule-Associated Proteins/metabolism
MH  - Motor Neurons/metabolism
MH  - Mutation/genetics
MH  - Nerve Degeneration/genetics/*metabolism/physiopathology
MH  - Nerve Tissue Proteins/metabolism
MH  - Phosphorylation
MH  - Protein Kinases/analysis/*metabolism
MH  - Serine/metabolism
MH  - Spinal Cord/metabolism/physiopathology
MH  - Superoxide Dismutase/*genetics
MH  - Superoxide Dismutase-1
MH  - TOR Serine-Threonine Kinases
MH  - Up-Regulation/physiology
EDAT- 2007/08/11 09:00
MHDA- 2007/12/15 09:00
CRDT- 2007/08/11 09:00
PHST- 2007/04/26 00:00 [received]
PHST- 2007/05/31 00:00 [revised]
PHST- 2007/06/03 00:00 [accepted]
PHST- 2007/08/11 09:00 [pubmed]
PHST- 2007/12/15 09:00 [medline]
PHST- 2007/08/11 09:00 [entrez]
AID - S0006-8993(07)01356-X [pii]
AID - 10.1016/j.brainres.2007.06.045 [doi]
PST - ppublish
SO  - Brain Res. 2007 Sep 5;1167:112-7. doi: 10.1016/j.brainres.2007.06.045. Epub 2007 
      Jul 7.