EP 1044217 A2 20001018 - SAG: SENSITIVE TO APOPTOSIS GENE
Title (en)
SAG: SENSITIVE TO APOPTOSIS GENE
Title (de)
SAG: SENSITIVE-TO-APOPTOSIS GENE (APOPTOSIS INDUZIERBAR GEN)
Title (fr)
SAG: GENE SENSIBLE A L'APOPTOSE
Publication
Application
Priority
- US 9826705 W 19981215
- US 6817997 P 19971219
- US 9984098 P 19980911
Abstract (en)
[origin: WO9932514A2] The present invention provides novel genes and polypeptides derived therefrom encoding a redox-sensitive protein that promotes cell growth, protects cells from apoptosis, scavenges oxygen radicals and can be used for the reversion of a tumor phenotype. In an attempt to identify gene(s) responsible for 1,10-phenanthroline (OP)-induced apoptosis in tumor cells we have used the differential display technique and cloned an OP-inducible gene, SAG (Sensitive to Apoptosis Gene). SAG encodes a novel, redox-sensitive, heme-binding protein with a zinc RING finger domain. The SAG protein consists of 113 amino acids with a calculated molecular weight of 12.7 kDa. Sequence homology searches reveal that SAG is highly conserved among species, suggesting its functional importance. This suggestion is demonstrated by the finding that SAG disruption in yeast is lethal. Two SAG deletion mutants have been detected in human cancer cell lines originating from colon and testis, suggesting its possible role in human carcinogenesis. Overexpression of SAG protein in a human colon carcinoma line, DLD1, and a human neuroblastoma line, SY5Y, protects cells from apoptosis induced by OP, zinc and copper ions. Furthermore, antisense SAG transfection inhibits certain tumor cell phenotypes in DLD1 human cell line and microinjection of SAG RNA stimulates cell growth. We propose that SAG protein is a cellular protective molecule functioning as a redox sensor to buffer oxidative-stress induced damage as well as a growth factor to stimulate cell growth. SAG protein will be an ideal molecular target in the development of drugs against neurodegenerative disorders, cancers, muscle dystrophy, and promoting wound healing.
IPC 1-7
IPC 8 full level
A61K 31/711 (2006.01); A61K 38/00 (2006.01); A61K 48/00 (2006.01); A61P 17/02 (2006.01); A61P 35/00 (2006.01); A61P 39/06 (2006.01); A61P 43/00 (2006.01); C07K 14/47 (2006.01); C07K 16/18 (2006.01); C12N 1/15 (2006.01); C12N 1/19 (2006.01); C12N 1/21 (2006.01); C12N 5/10 (2006.01); C12N 15/09 (2006.01); C12Q 1/68 (2006.01); G01N 33/50 (2006.01); G01N 33/68 (2006.01)
CPC (source: EP KR)
A61P 17/02 (2017.12 - EP); A61P 35/00 (2017.12 - EP); A61P 39/06 (2017.12 - EP); A61P 43/00 (2017.12 - EP); C07K 14/47 (2013.01 - KR); C07K 14/4747 (2013.01 - EP); A61K 38/00 (2013.01 - EP); C12N 2799/022 (2013.01 - EP)
Citation (search report)
See references of WO 9932514A2
Designated contracting state (EPC)
AT BE CH CY DE DK ES FI FR GB GR IE IT LI LU MC NL PT SE
DOCDB simple family (publication)
WO 9932514 A2 19990701; WO 9932514 A3 19990910; AU 1918099 A 19990712; AU 765741 B2 20030925; BR 9813757 A 20001003; CA 2303483 A1 19990701; EP 1044217 A2 20001018; JP 2001526063 A 20011218; KR 20010033299 A 20010425; NZ 503417 A 20021220
DOCDB simple family (application)
US 9826705 W 19981215; AU 1918099 A 19981215; BR 9813757 A 19981215; CA 2303483 A 19981215; EP 98963962 A 19981215; JP 2000525451 A 19981215; KR 20007006741 A 20000617; NZ 50341798 A 19981215