Gonadotropin-releasing hormone binding sites in human breast carcinoma

Science ◽  
1985 ◽  
Vol 229 (4717) ◽  
pp. 989-991 ◽  
Author(s):  
K. Eidne ◽  
C. Flanagan ◽  
R. Millar
Keyword(s):  
Breast Carcinoma ◽  
Binding Sites ◽  
Gonadotropin Releasing Hormone ◽  
Human Breast Carcinoma ◽  
Hormone Binding ◽  
Human Breast ◽  
Releasing Hormone

21. Progesterone and estradiol binding sites in human breast carcinoma

1975 ◽  
Vol 6 (11-12) ◽  
pp. xiv
Author(s):  
J.P. Raynaud ◽  
M.M. Bouton ◽  
D. Philibert ◽  
J.C. Delarue ◽  
F. Guerinot ◽  
...  
Keyword(s):  
Breast Carcinoma ◽  
Binding Sites ◽  
Human Breast Carcinoma ◽  
Human Breast

Coexistence of novel amylin-binding sites with calcitonin receptors in human breast carcinoma MCF-7 cells

1997 ◽  
Vol 155 (3) ◽  
pp. 423-431 ◽  
Author(s):  
U Zimmermann ◽  
B Fluehmann ◽  
W Born ◽  
JA Fischer ◽  
R Muff
Keyword(s):  
Breast Carcinoma ◽  
Cyclic Amp ◽  
Binding Sites ◽  
Human Breast Carcinoma ◽  
Human Breast ◽  
T47d Cells ◽  
Amino Terminal ◽  
Cyclic Amp Accumulation ◽  
Human Amylin ◽  
Mcf 7

Amylin, calcitonin (CT) and calcitonin gene-related peptide (CGRP) share limited structural homology including amino-terminal ring structures linked by a disulfide bridge and amidated carboxy-termini. Here, we have compared [125I]Bolton-Hunter-[Lys1] rat amylin ([125I]amylin) binding and the stimulation of cyclic AMP accumulation by human (h) amylin, hCT and hCGRP-I in the human breast carcinoma cell lines MCF-7 and T47D, which predominantly express hCT1a and hCT1b receptor isoforms (hCTR1a, hCTR1b) at a similar total number of hCT-binding sites. In MCF-7 cells, half-maximal inhibition (IC50) of [125I]amylin binding by human amylin was observed at 3.6 +/- 0.8 nM (n = 6). hCT and hCGRP-I displaced [125I]amylin binding with 22 and 66 times higher IC50. [125I]hCT binding was inhibited by hCT with an IC50 of 8.1 +/- 1.9 nM (n = 5), and human amylin and hCGRP-I were over 100 times less potent. In T47D cells, on the other hand, specific binding of [125I]amylin was not observed, but hCT inhibited [125I]hCT binding with an IC50 of 3.2 +/- 0.4 nM (n = 3), and human amylin and hCGRP-I had over 200 times higher IC50. In MCF-7 cells, half-maximal stimulation (EC50) of cyclic AMP accumulation by human amylin, hCT and hCGRP-I occurred at 1.4 +/- 0.2, 1.7 +/- 0.4 and 6.3 +/- 1.3 nM respectively. In T47D cells, the EC50 of hCT was 0.32 +/- 0.02 nM (n = 3), and 30- and 1900-fold higher with human amylin and hCGRP-I. In conclusion, the expression of hCTR1a and hCTR1b and [125I]hCT binding were indistinguishable in MCF-7 and T47D cells. Yet, [125I]amylin binding was only recognized in MCF-7 cells, consistent with a distinct amylin receptor.

Pituitary Gonadotropin-Releasing Hormone Binding Sites in Persistent Estrous Rats

1988 ◽  
Vol 48 (5) ◽  
pp. 489-494 ◽  
Author(s):  
Katalin Köves ◽  
Bernard Kerdelhué ◽  
Judith Molnár ◽  
Valér Csernus ◽  
Béla Halász
Keyword(s):  
Binding Sites ◽  
Gonadotropin Releasing Hormone ◽  
Hormone Binding ◽  
Releasing Hormone ◽  
Pituitary Gonadotropin

Gonadotropin releasing hormone binding sites in human epithelial ovarian carcinomata

1989 ◽  
Vol 25 (2) ◽  
pp. 215-221 ◽  
Author(s):  
Günter Emons ◽  
Gurcharan S. Pahwa ◽  
Christoph Brack ◽  
Rita Sturm ◽  
Friedhelm Oberheuser ◽  
...  
Keyword(s):  
Binding Sites ◽  
Gonadotropin Releasing Hormone ◽  
Hormone Binding ◽  
Releasing Hormone
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