scholarly journals Yin Yang-1 inhibits tumor cell growth and inhibits p21WAF1/Cip1 complex formation with cdk4 and cyclin D1

2012 ◽  
Author(s):  
Levon Khachigian
Keyword(s):  
Cell Growth ◽  
Complex Formation ◽  
Tumor Cell ◽  
Cyclin D1 ◽  
Tumor Cell Growth ◽  
Yin Yang 1 ◽  
Yin Yang

scholarly journals Analysis of wild-type and mutant p21WAF-1 gene activities.

1996 ◽  
Vol 16 (4) ◽  
pp. 1786-1793 ◽  
Author(s):  
J Lin ◽  
C Reichner ◽  
X Wu ◽  
A J Levine
Keyword(s):  
Amino Acid ◽  
Cell Growth ◽  
Tumor Cell ◽  
Cyclin D1 ◽  
Cyclin E ◽  
Growth Suppression ◽  
Nuclear Antigen ◽  
Tumor Cell Growth ◽  
Amino Acid Residues ◽  
Wild Type

The p21WAF-1 gene is positively regulated by the wild-type p53 protein. p21WAF-1 has been shown to interact with several cyclin-dependent kinase complexes and block the activity of G1 cyclin-dependent kinases (cdks). Mutational analysis with the p21WAF-1 gene localized a site, at amino acid residues 21 and 24 in the amino terminus of the protein, for p21WAF-1 binding to cyclins D and E. This region of the protein is conserved (residues 21 to 26) in other p21WAF-1 family members, p27kip-1 and p57kip-2. The same p21WAF-121,24 mutant also fails to bind to cyclin D1-cdk 4 or cyclin E-cdk 2 complexes in vitro, suggesting that amino acid residues 21 and 24 are important for p21WAF-1-cdk-cyclin trimeric complex interactions. The p21WAF-1 wild-type protein will suppress tumor cell growth in culture while p21WAF-1 mutant proteins with defects in residues 21 and 24 fail to suppress tumor cell growth. The overexpression of cyclin D or E in these cells will partially overcome the growth suppression of wild-type p21WAF-1 protein in cells. These results provide evidence that p21WAF-1 acts through cyclin D1-cdk4 and cyclin E-cdk2 complexes in vivo to induce the growth suppression. The p21WAF-1 binding sites for cyclins (residues 21 to 26), cdk2 (residues 49 to 71), and proliferating-cell nuclear antigen (residues 124 to 164) have all been mapped to discrete sites on the protein.

scholarly journals Structural and stereochemical studies of potent inhibitors of glucosylceramide synthase and tumor cell growth.

1995 ◽  
Vol 36 (3) ◽  
pp. 611-621
Author(s):  
A Abe ◽  
N S Radin ◽  
J A Shayman ◽  
L L Wotring ◽  
R E Zipkin ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth ◽  
Glucosylceramide Synthase

Bcl-2 targeting siRNA expressed by a T7 vector system inhibits human tumor cell growth in vitro

2004 ◽  
Author(s):  
Lori Holle ◽  
Labri Hicks ◽  
Wendy Song ◽  
Eric Holle ◽  
Thomas Wagner ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Human Tumor ◽  
Vector System ◽  
Tumor Cell Growth ◽  
Human Tumor Cell

scholarly journals Differential effect of subcellular localization of communication impairing gap junction protein connexin43 on tumor cell growth in vivo

Oncogene ◽  
2000 ◽  
Vol 19 (4) ◽  
pp. 505-513 ◽  
Author(s):  
V A Krutovskikh ◽  
S M Troyanovsky ◽  
C Piccoli ◽  
H Tsuda ◽  
M Asamoto ◽  
...  
Keyword(s):  
Cell Growth ◽  
Subcellular Localization ◽  
Tumor Cell ◽  
Gap Junction ◽  
Differential Effect ◽  
Tumor Cell Growth ◽  
Junction Protein ◽  
Gap Junction Protein
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