PMID- 10644768
OWN - NLM
STAT- MEDLINE
DCOM- 20000229
LR  - 20220311
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 275
IP  - 4
DP  - 2000 Jan 28
TI  - Identification of a novel tumor necrosis factor-alpha-inducible gene, SCC-S2,
      containing the consensus sequence of a death effector domain of fas-associated
      death domain-like interleukin- 1beta-converting enzyme-inhibitory protein.
PG  - 2973-8
AB  - We report here the isolation and characterization of a novel tumor necrosis
      factor-alpha (TNF-alpha)-inducible gene, SCC-S2. Based on the nucleotide
      sequence, the SCC-S2 open reading frame contains a sequence in the amino terminus
      that shows a significant homology to death effector domain II of cell death
      regulatory protein, Fas-associated death domain-like interleukin-1beta-converting
      enzyme-inhibitory protein (FLIP). Unlike FLIP, the SCC-S2 open reading frame
      contains only one death effector domain and lacks the carboxyl-terminal
      caspase-like homology domain, raising the possibility that SCC-S2 may be a novel 
      member of the FLIP family. SCC-S2 mRNA expression is found in most normal tissues
      and malignant cells. The steady state level of SCC-S2 mRNA is significantly
      induced by TNF-alpha in different tumor cells (TNF-alpha at 20 ng/ml for 3 h:
      A549, approximately 2-9-fold; SKOV-3, approximately 3-fold; PCI-04A,
      approximately 3-6-fold). TNF-alpha treatment (100 ng/ml, 4 h) of HeLa cells
      transiently transfected with FLAG epitope-tagged SCC-S2 cDNA or expression vector
      alone led to an increase in the number of apoptotic cells as compared with the
      untreated counterpart. Interestingly, however, SCC-S2 transfectants revealed a
      significant decrease in the number of apoptotic cells as compared with the vector
      transfectants (p < 0.001). These data implicate a role of SCC-S2 as a negative
      mediator of apoptosis in certain cell types.
FAU - Kumar, D
AU  - Kumar D
AD  - Department of Radiation Medicine, Lombardi Cancer Center, Georgetown University
      Medical Center, Washington, D.C. 20007, USA.
FAU - Whiteside, T L
AU  - Whiteside TL
FAU - Kasid, U
AU  - Kasid U
LA  - eng
SI  - GENBANK/AF098933
SI  - GENBANK/AF098934
GR  - CA68322/CA/NCI NIH HHS/United States
GR  - CA74175/CA/NCI NIH HHS/United States
GR  - P30-CA51008/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Antigens, CD)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA, Complementary)
RN  - 0 (FADD protein, human)
RN  - 0 (Fas-Associated Death Domain Protein)
RN  - 0 (Proteins)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Serpins)
RN  - 0 (TNFAIP8 protein, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Viral Proteins)
RN  - 96282-35-8 (interleukin-1beta-converting enzyme inhibitor)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - Amino Acid Sequence
MH  - Antigens, CD/metabolism
MH  - Apoptosis
MH  - Apoptosis Regulatory Proteins
MH  - Base Sequence
MH  - Carrier Proteins/chemistry/*metabolism
MH  - DNA, Complementary
MH  - Fas-Associated Death Domain Protein
MH  - Gene Expression Regulation/*physiology
MH  - HeLa Cells
MH  - Humans
MH  - Molecular Sequence Data
MH  - Open Reading Frames
MH  - Proteins/*genetics
MH  - Receptors, Tumor Necrosis Factor/metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Sequence Homology, Amino Acid
MH  - Serpins/chemistry/*metabolism
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*physiology
MH  - *Viral Proteins
EDAT- 2000/01/25 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/01/25 09:00
PHST- 2000/01/25 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/01/25 09:00 [entrez]
AID - 10.1074/jbc.275.4.2973 [doi]
AID - S0021-9258(18)31063-9 [pii]
PST - ppublish
SO  - J Biol Chem. 2000 Jan 28;275(4):2973-8. doi: 10.1074/jbc.275.4.2973.