scholarly journals Mutated connexin43 proteins inhibit rat glioma cell growth suppression mediated by wild-type connexin43 in a dominant-negative manner

1998 ◽  
Vol 78 (4) ◽  
pp. 446-453 ◽  
Author(s):  
Yasufumi Omori ◽  
Hiroshi Yamasaki
Keyword(s):  
Cell Growth ◽  
Glioma Cell ◽  
Growth Suppression ◽  
Dominant Negative ◽  
Wild Type ◽  
Rat Glioma ◽  
Cell Growth Suppression

Tumor Cell Growth Suppression by Chalcone (1,3-Diphenyl-2-Propen-l-One)

1997 ◽  
Vol 12 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Hideo Kamei ◽  
Tatsurou Koide ◽  
Yoko Hashimoto ◽  
Takashi Kojima ◽  
Makoto Hasegawa
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Growth Suppression ◽  
Tumor Cell Growth ◽  
Cell Growth Suppression

scholarly journals Evidence for the multimeric structure of ferroportin

Blood ◽  
2006 ◽  
Vol 109 (5) ◽  
pp. 2205-2209 ◽  
Author(s):  
Ivana De Domenico ◽  
Diane McVey Ward ◽  
Giovanni Musci ◽  
Jerry Kaplan
Keyword(s):  
Iron Overload ◽  
Cultured Cells ◽  
Dominant Negative ◽  
Mouse Bone Marrow ◽  
C6 Cells ◽  
Wild Type ◽  
Negative Effects ◽  
Dominant Form ◽  
Rat Glioma ◽  
Glioma C6

Abstract Ferroportin (Fpn) (IREG1, SLC40A1, MTP1) is an iron transporter, and mutations in Fpn result in a genetically dominant form of iron overload disease. Previously, we demonstrated that Fpn is a multimer and that mutations in Fpn are dominant negative. Other studies have suggested that Fpn is not a multimer and that overexpression or epitope tags might affect the localization, topology, or multimerization of Fpn. We generated wild-type Fpn with 3 different epitopes, GFP, FLAG, and c-myc, and expressed these constructs in cultured cells. Co-expression of any 2 different epitope-tagged proteins in the same cell resulted in their quantitative coimmunoprecipitation. Treatment of Fpn-GFP/Fpn-FLAG–expressing cells with crosslinking reagents resulted in the crosslinking of Fpn-GFP and Fpn-FLAG. Western analysis of rat glioma C6 cells or mouse bone marrow macrophages exposed to crosslinking reagents showed that endogenous Fpn is a dimer. These results support the hypothesis that the dominant inheritance of Fpn–iron overload disease is due to the dominant-negative effects of mutant Fpn proteins.

Cell Growth Suppression of Astrocytoma C6 Cells by Glial Fibrillary Acidic Protein cDNA Transfection

2002 ◽  
Vol 63 (5) ◽  
pp. 1975-1978 ◽  
Author(s):  
Masahiro Toda ◽  
Masayuki Miura ◽  
Hiroaki Asou ◽  
Shigeo Toya ◽  
Keiichi Uyemura
Keyword(s):  
Cell Growth ◽  
Glial Fibrillary Acidic Protein ◽  
Growth Suppression ◽  
Acidic Protein ◽  
C6 Cells ◽  
Cell Growth Suppression

Studies on the mechanism of cell growth suppression by the retinoblastoma gene

1990 ◽  
Vol 14 ◽  
pp. 21
Author(s):  
J SETTLEMAN ◽  
P HINDS ◽  
D COBRINIK ◽  
T JACKS ◽  
S MITTNACHT ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Suppression ◽  
Retinoblastoma Gene ◽  
Cell Growth Suppression
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