PMID- 28722750
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 142
IP  - 6
DP  - 2017 Sep
TI  - Protein kinase D exerts neuroprotective functions during oxidative stress via 
      nuclear factor kappa B-independent signaling pathways.
PG  - 948-961
LID - 10.1111/jnc.14131 [doi]
AB  - Members of the protein kinase D (PKD) family of serine/threonine kinases are 
      known to exert diverse roles in neuronal stress responses. Here, we show the 
      transient activation and nuclear translocation of endogenous PKD upon oxidative 
      stress induced by H(2) O(2) treatment in primary neuronal cultures. Using 
      pharmacological inhibition, we show that PKD activity protects neurons from 
      oxidative stress-induced cell death. Although members of the canonical nuclear 
      factor kappa-light-chain-enhancer of activated B cells (NF kappaB) pathway were 
      phosphorylated upon H(2) O(2) treatment, it was found that the neuronal response 
      to oxidative stress is not executed through the nuclear translocation and 
      activity of RelA. On the other hand, we demonstrate for the first time in 
      neuronal cells, the association of green fluorescent protein-tagged kinase 
      inactive PKD1 with mitochondrial membranes in vivo and the presence of PKD 
      activity in the close vicinity of mitochondria in vitro. Our findings thus 
      support the notion that the neuroprotective role of PKD is exerted independently 
      from NF kappaB signaling and suggest a potential mitochondrial function for PKD 
      in cultured neurons.
CI  - (c) 2017 International Society for Neurochemistry.
FAU - Liliom, Hanna
AU  - Liliom H
AD  - Department of Physiology and Neurobiology, Eotvos Lorand University, Budapest, 
      Hungary.
FAU - Tarnok, Krisztian
AU  - Tarnok K
AD  - Department of Physiology and Neurobiology, Eotvos Lorand University, Budapest, 
      Hungary.
FAU - Abraham, Zsofia
AU  - Abraham Z
AD  - Department of Physiology and Neurobiology, Eotvos Lorand University, Budapest, 
      Hungary.
FAU - Racz, Bence
AU  - Racz B
AD  - Department of Anatomy and Histology, University of Veterinary Medicine, Budapest, 
      Hungary.
FAU - Hausser, Angelika
AU  - Hausser A
AD  - Institute of Cell Biology and Immunology, University Stuttgart, Stuttgart, 
      Germany.
AD  - Stuttgart Research Center Systems Biology, University of Stuttgart, Stuttgart, 
      Germany.
FAU - Schlett, Katalin
AU  - Schlett K
AUID- ORCID: 0000-0001-9265-4236
AD  - Department of Physiology and Neurobiology, Eotvos Lorand University, Budapest, 
      Hungary.
AD  - MTA-ELTE-NAP B - Neuronal Cell Biology Research Group, Eotvos Lorand University, 
      Budapest, Hungary.
LA  - eng
SI  - GENBANK/AF025846
GR  - K81934/Hungarian Scientific Research Foundation/
GR  - 11475-4/2016/FEKUT/Hungarian Scientific Research Foundation/
GR  - KTIA_NAP_13-2014-0018/Hungarian Brain Research Program/
GR  - 73539/Hungarian Brain Research Program/
GR  - 4.2.4.A/1-11-1-2012-0001/Janos Bolyai Research Fellowship of the Hungarian 
      Academy of Sciences/
GR  - UNKP-16-3-ELTE 8495/72/Janos Bolyai Research Fellowship of the Hungarian Academy 
      of Sciences/
PT  - Journal Article
DEP - 20170831
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
OTO - NOTNLM
OT  - NF kappaB
OT  - neuron
OT  - neuroprotection
OT  - oxidative stress
OT  - protein kinase D
EDAT- 2017/07/20 06:00
MHDA- 2017/07/20 06:01
CRDT- 2017/07/20 06:00
PHST- 2017/01/27 00:00 [received]
PHST- 2017/06/28 00:00 [revised]
PHST- 2017/07/05 00:00 [accepted]
PHST- 2017/07/20 06:00 [pubmed]
PHST- 2017/07/20 06:01 [medline]
PHST- 2017/07/20 06:00 [entrez]
AID - 10.1111/jnc.14131 [doi]
PST - ppublish
SO  - J Neurochem. 2017 Sep;142(6):948-961. doi: 10.1111/jnc.14131. Epub 2017 Aug 31.