PMID- 28803490
OWN - NLM
STAT- MEDLINE
DCOM- 20180723
LR  - 20211204
IS  - 1563-5279 (Electronic)
IS  - 0020-7454 (Linking)
VI  - 128
IP  - 2
DP  - 2018 Feb
TI  - Parkin, PINK1 and DJ1 as possible modulators of mTOR pathway in ganglioglioma.
PG  - 167-174
LID - 10.1080/00207454.2017.1366906 [doi]
AB  - PURPOSE: Ganglioglioma (GG) is a non-malignant tumor classified as G1 by the WHO. 
      Although we currently know that the neoplasm may result from the hyperactivity of 
      protein kinase B (PKB or Akt) or extracellular-regulated kinase (Erk), which 
      upregulates mammalian target of rapamycin kinase (mTOR) and leads to translation 
      of proteins responsible for cell cycle regulation, there are still many questions 
      to be answered. In the current paper we try to analyze the link between GG 
      formation and activity of three proteins known to play a role in neuroprotection 
      (parkin, PINK1 and DJ1). MATERIALS AND METHODS: In our paper, we review the 
      current information on the involvement of these proteins in the transmission of 
      information in the cell and triggering various cell signals, like survival or 
      apoptosis. We also review current literature data on involvement of parkin, DJ1 
      and PINK1 in the regulation of mTOR, the pathway probably contributing to the 
      development of GG. RESULTS: Parkin is an E3 ubiquitin ligase, shown to trigger 
      proteasome-dependent degradation and autophagy, necessary for the maintenance of 
      homeostasis in neurons. PINK1, a mitochondrial protein kinase, is required for 
      mitochondrial maintenance and neuronal survival. DJ1 is a sensor of reactive 
      oxygen species, and protects the cells against oxidative stress. Mutations in the 
      genes encoding these three proteins are known to underlie autosomal recessive 
      forms of Parkinson's disease, as well as other neurodegenerative and 
      neuroinflammatory disorders. CONCLUSION: It appears that mutations of parkin, 
      PINK1 and DJ1 may result in the development of both neurodegeneration and tumors. 
      Also, these proteins might be used as markers of disease, thus allowing better 
      diagnosis and therapy.
FAU - Drapalo, Katarzyna
AU  - Drapalo K
AD  - a Center for Biostructure Research, Department of Histology and Embryology , 
      Medical University of Warsaw , Warsaw , Poland.
FAU - Jozwiak, Jaroslaw
AU  - Jozwiak J
AD  - a Center for Biostructure Research, Department of Histology and Embryology , 
      Medical University of Warsaw , Warsaw , Poland.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170828
PL  - England
TA  - Int J Neurosci
JT  - The International journal of neuroscience
JID - 0270707
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.3.2.27 (parkin protein)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (PTEN-induced putative kinase)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 3.1.2.- (PARK7 protein, human)
RN  - EC 3.1.2.- (Protein Deglycase DJ-1)
SB  - IM
MH  - Brain Neoplasms/*metabolism/pathology
MH  - Ganglioglioma/*metabolism/pathology
MH  - Humans
MH  - Protein Deglycase DJ-1/*metabolism
MH  - Protein Kinases/*metabolism
MH  - Signal Transduction/*physiology
MH  - TOR Serine-Threonine Kinases/*metabolism
MH  - Ubiquitin-Protein Ligases/*metabolism
OTO - NOTNLM
OT  - DJ1
OT  - PINK1
OT  - ganglioglioma
OT  - mTOR
OT  - parkin
EDAT- 2017/08/15 06:00
MHDA- 2018/07/24 06:00
CRDT- 2017/08/15 06:00
PHST- 2017/08/15 06:00 [pubmed]
PHST- 2018/07/24 06:00 [medline]
PHST- 2017/08/15 06:00 [entrez]
AID - 10.1080/00207454.2017.1366906 [doi]
PST - ppublish
SO  - Int J Neurosci. 2018 Feb;128(2):167-174. doi: 10.1080/00207454.2017.1366906. Epub 
      2017 Aug 28.