PMID- 29051813
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2045-3701 (Print)
IS  - 2045-3701 (Electronic)
IS  - 2045-3701 (Linking)
VI  - 7
DP  - 2017
TI  - Differential impact of various reactive oxygen species (ROS) on HIF-1alpha/p53 direct 
      interaction in SK-N-MC neuroblastoma cells.
PG  - 52
LID - 10.1186/s13578-017-0180-4 [doi]
LID - 52
AB  - BACKGROUND: A vital property of eukaryotic cells physiology is their rather quick 
      response to variation of oxygen tension, mainly by a transcription factor known 
      as hypoxia-inducible factor-1 (HIF-1). Aside from its transcriptional regulation, 
      other mechanisms, such as post translational modifications and protein-protein 
      interactions, the interaction between HIF-1alpha and p53 has attracted more attention 
      mainly due to simultaneous enhancement in the protein levels of these two anti- 
      and pro-apoptotic vital transcriptional factors within the ROS-stressed cells. 
      METHODS: In this study, we measured cell viability following exposure of the 
      cells to H(2)O(2), menadione and Cobalt Chloride by MTT, and ROS content was 
      measured under the same condition. The immunoblotting technique has been used to 
      establish the presence and amount of Caspase, HIF-1alpha and p53 proteins. Then, the 
      effect of different ROS on interaction between HIF-1alpha and p53 proteins was 
      examined by co-immunoprecipitation. RESULTS: The results showed that cells 
      viability and intracellular ROS content were modulated in response to menadione, 
      H(2)O(2) and Cobalt Chloride. These agents had different influence on HIF-1alpha 
      signaling pathways as well as its interactions with p53 protein. It appeared that 
      direct communication between HIF-1alpha and p53 proteins by ROS stresses, under both 
      normoxic and hypoxic conditions, was governed by HIF-1alpha at a certain induced 
      level. CONCLUSIONS: Our data indicated that stabilization, a prerequisite for 
      communication, of HIF-1alpha is dependent to the types of free radicals.
FAU - Parandavar, Elham
AU  - Parandavar E
AD  - Institute of Biochemistry and Biophysics, University of Tehran, P.O. Box 
      13145-1384 Tehran, Iran. ISNI: 0000 0004 0612 7950. GRID: grid.46072.37
FAU - Yazdanparast, Razieh
AU  - Yazdanparast R
AUID- ORCID: 0000-0003-4441-6975
AD  - Institute of Biochemistry and Biophysics, University of Tehran, P.O. Box 
      13145-1384 Tehran, Iran. ISNI: 0000 0004 0612 7950. GRID: grid.46072.37
LA  - eng
PT  - Journal Article
DEP - 20171010
PL  - England
TA  - Cell Biosci
JT  - Cell & bioscience
JID - 101561195
PMC - PMC5633900
OTO - NOTNLM
OT  - Apoptosis
OT  - HIF-1alpha
OT  - Hypoxia
OT  - Interaction
OT  - p53
EDAT- 2017/10/21 06:00
MHDA- 2017/10/21 06:01
PMCR- 2017/10/10
CRDT- 2017/10/21 06:00
PHST- 2017/07/23 00:00 [received]
PHST- 2017/09/30 00:00 [accepted]
PHST- 2017/10/21 06:00 [entrez]
PHST- 2017/10/21 06:00 [pubmed]
PHST- 2017/10/21 06:01 [medline]
PHST- 2017/10/10 00:00 [pmc-release]
AID - 180 [pii]
AID - 10.1186/s13578-017-0180-4 [doi]
PST - epublish
SO  - Cell Biosci. 2017 Oct 10;7:52. doi: 10.1186/s13578-017-0180-4. eCollection 2017.