Effects of antiprogestins RU486 and ZK98299 on the expression of cell cycle proteins of a medroxyprogesterone acetate (MPA)-induced murine mammary tumor

Author(s):  
Maria Peters ◽  
Silvia Vanzulli ◽  
Patricia Elizalde ◽  
Eduardo Charreau ◽  
Maria Goin
Author(s):  
Wm. J. Arnold ◽  
J. Russo ◽  
H. D. Soule ◽  
M. A. Rich

Our studies of mammary tumor virus have included the application of the unlabeled antibody enzyme method of Sternberger to mammary tumor derived mouse cells in culture and observation with an electron microscope. The method avoids the extravagance of covalent binding of indicator molecules (horseradish peroxidase) with precious antibody locator molecules by relying instead upon specific antibody-antigen linkages. Our reagents included: Primary Antibody, rabbit anti-murine mammary tumor virus (MuMTV) which was antiserum 113 AV-2; Secondary Antibody, goat anti-rabbit IgG gamma chain (Cappel Laboratories); andthe Indicator, rabbit anti-horseradish peroxidase - horseradish peroxidase complex (PAP) (Cappel Labs.). Dilutions and washes were made in 0.05 M Tris 0.15 M saline buffered to pH 7.4. Cell monolayers, after light fixation in glutaraldehyde, were incubated in place by a protocol adapted from Sternberger and Graham and Karnovsky, then embedded by our usual method for monolayers. Reagents were confined to specific areas by neoprene 0-rings (Parker Seal Co.) reducing the amount of reagent needed to 50 microliters, 1/6th of that required to wet a 35 mm petri dish.


2001 ◽  
Vol 11 (2) ◽  
pp. 113-118 ◽  
Author(s):  
K. J. Rolfe ◽  
L. J. Eva ◽  
A. B. Maclean ◽  
J. C. Crow ◽  
C. W. Perrett ◽  
...  

2000 ◽  
Vol 150 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Neil E. Hubbard ◽  
Debora Lim ◽  
Lauri Summers ◽  
Kent L. Erickson

1990 ◽  
Vol 17 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Edith Kordon ◽  
Claudia Lanari ◽  
Roberto Meiss ◽  
Patricia Elizalde ◽  
Eduardo Charreau ◽  
...  

2000 ◽  
Vol 278 (4) ◽  
pp. F515-F529 ◽  
Author(s):  
Stuart J. Shankland ◽  
Gunter Wolf

The response to glomerular and tubulointerstitial cell injury in most forms of renal disease includes changes in cell number (proliferation and apoptosis) and cell size (hyerptrophy). These events typically precede and may be reponsible for the accumulation of extracellular matrix proteins that leads to a decrease in renal function. There is increasing evidence showing that positive (cyclins and cyclin-dependent kinases) and negative (cyclin-dependent kinase inhibitors) cell cycle regulatory proteins have a critical role in regulating these fundamental cellular responses to immune and nonimmune forms of injury. Data now show that altering specific cell cycle proteins affects renal cell proliferation and improves renal function. Equally exciting is the expanding body of literature showing novel biological roles for cell cycle proteins in the regulation of cell hypertrophy and apoptosis. With increasing understanding of the role for cell cyle regulatory proteins in renal disease comes the hope for potential therapeutic inverventions.


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