PMID- 15294014
OWN - NLM
STAT- MEDLINE
DCOM- 20050303
LR  - 20221207
IS  - 1470-8728 (Electronic)
IS  - 0264-6021 (Print)
IS  - 0264-6021 (Linking)
VI  - 383
IP  - Pt 1
DP  - 2004 Oct 1
TI  - The SARS coronavirus nucleocapsid protein induces actin reorganization and 
      apoptosis in COS-1 cells in the absence of growth factors.
PG  - 13-8
AB  - In March 2003, a novel coronavirus was isolated from patients exhibiting atypical 
      pneumonia, and was subsequently proven to be the causative agent of the disease 
      now referred to as SARS (severe acute respiratory syndrome). The complete genome 
      of the SARS-CoV (SARS coronavirus) has since been sequenced. The SARS-CoV 
      nucleocapsid (SARS-CoV N) protein shares little homology with other members of 
      the coronavirus family. In the present paper, we show that SARS-CoV N is capable 
      of inducing apoptosis of COS-1 monkey kidney cells in the absence of growth 
      factors by down-regulating ERK (extracellular-signal-regulated kinase), 
      up-regulating JNK (c-Jun N-terminal kinase) and p38 MAPK (mitogen-activated 
      protein kinase) pathways, and affecting their downstream effectors. SARS-CoV N 
      expression also down-regulated phospho-Akt and Bcl-2 levels, and activated 
      caspases 3 and 7. However, apoptosis was independent of the p53 and Fas 
      signalling pathways. Furthermore, activation of the p38 MAPK pathway was found to 
      induce actin reorganization in cells devoid of growth factors. At the 
      cytoskeletal level, SARS-CoV N down-regulated FAK (focal adhesion kinase) 
      activity and also down-regulated fibronectin expression. This is the first report 
      showing the ability of the N protein of SARS-CoV to induce apoptosis and actin 
      reorganization in mammalian cells under stressed conditions.
FAU - Surjit, Milan
AU  - Surjit M
AD  - Virology Group, International Centre for Genetic Engineering and Biotechnology, 
      Aruna Asaf Ali Road, New Delhi 110067, India.
FAU - Liu, Boping
AU  - Liu B
FAU - Jameel, Shahid
AU  - Jameel S
FAU - Chow, Vincent T K
AU  - Chow VT
FAU - Lal, Sunil K
AU  - Lal SK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Biochem J
JT  - The Biochemical journal
JID - 2984726R
RN  - 0 (Actins)
RN  - 0 (Culture Media, Serum-Free)
RN  - 0 (Fibronectins)
RN  - 0 (Growth Substances)
RN  - 0 (Integrins)
RN  - 0 (Nucleocapsid Proteins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Actins/*metabolism
MH  - Animals
MH  - Apoptosis/*physiology
MH  - COS Cells
MH  - Caspases/metabolism
MH  - Cell Line, Tumor
MH  - Chlorocebus aethiops
MH  - Culture Media, Serum-Free
MH  - Down-Regulation
MH  - Fibronectins/metabolism
MH  - Focal Adhesion Protein-Tyrosine Kinases
MH  - Growth Substances/physiology
MH  - Integrins/physiology
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Nucleocapsid Proteins/*physiology
MH  - Protein Serine-Threonine Kinases/metabolism
MH  - Protein-Tyrosine Kinases/metabolism
MH  - Proto-Oncogene Proteins/metabolism
MH  - Proto-Oncogene Proteins c-akt
MH  - Severe acute respiratory syndrome-related coronavirus/*physiology
MH  - Transfection
MH  - Up-Regulation
PMC - PMC1134038
EDAT- 2004/08/06 05:00
MHDA- 2005/03/04 09:00
PMCR- 2005/04/01
CRDT- 2004/08/06 05:00
PHST- 2004/08/05 00:00 [accepted]
PHST- 2004/08/02 00:00 [revised]
PHST- 2004/06/10 00:00 [received]
PHST- 2004/08/06 05:00 [pubmed]
PHST- 2005/03/04 09:00 [medline]
PHST- 2004/08/06 05:00 [entrez]
PHST- 2005/04/01 00:00 [pmc-release]
AID - BJ20040984 [pii]
AID - bj3830013 [pii]
AID - 10.1042/BJ20040984 [doi]
PST - ppublish
SO  - Biochem J. 2004 Oct 1;383(Pt 1):13-8. doi: 10.1042/BJ20040984.