Purification of bone sialoprotein from the medium of the rat osteoblast-like cell line UMR 106-01 BSP

1994 ◽  
Vol 16 (3-4) ◽  
pp. 205-209 ◽  
Author(s):  
K. P. Mintz ◽  
R. J. Midura ◽  
L. W. Fisher
1994 ◽  
Vol 269 (7) ◽  
pp. 4845-4852
Author(s):  
K.P. Mintz ◽  
L.W. Fisher ◽  
W.J. Grzesik ◽  
V.C. Hascall ◽  
R.J. Midura

1990 ◽  
Vol 265 (9) ◽  
pp. 5285-5291
Author(s):  
R J Midura ◽  
D J McQuillan ◽  
K J Benham ◽  
L W Fisher ◽  
V C Hascall

1988 ◽  
Vol 255 (5) ◽  
pp. E660-E667 ◽  
Author(s):  
R. Civitelli ◽  
I. R. Reid ◽  
S. Westbrook ◽  
L. V. Avioli ◽  
K. A. Hruska

Parathyroid hormone (PTH)-stimulated signal transduction through mechanisms alternate to adenosine 3',5'-cyclic monophosphate (cAMP) production were studied in UMR 106-01 cells, a cell line with an osteoblastic phenotype. PTH produced transient, dose-related increases in cytosolic calcium [( Ca2+]i), inositol trisphosphates, and diacylglycerol (DAG). Both inositol 1,4,5-trisphosphate (Ins-1,4,5P3) and inositol 1,3,4-trisphosphate (Ins-1,3,4P3) production were rapidly stimulated by PTH. Consistent with the production of Ins-1,3,4P3, rapid stimulation of late eluting inositol tetrakisphosphate was observed. The effects on the inositol phosphates were induced rapidly, consistent with roles as signals for changes in [Ca2+]i. In saponin-permeabilized UMR 106-01 cells, Ins-1,4,5P3 stimulated 45Ca release from a nonmitochondrial intracellular pool. Thus the hypothesis that PTH-stimulated Ins-1,4,5P3 production initiates Ca2+ release and contributes to transient elevations of [Ca2+]i is supported. Pretreatment of UMR 106-01 cells with pertussis toxin had no effect on PTH stimulation of inositol phosphates. Pertussis toxin reduced PTH-stimulated elevations of [Ca2+]i, but cAMP analogues had an even greater effect than pertussis toxin. These data suggest that stimulation of cAMP production during PTH stimulation may negatively affect production of rises in [Ca2+]i during PTH stimulation. The inactivation of the inhibitory G protein of adenylate cyclase by pertussis toxin could explain its action similar to cAMP analogues. Cyclic nucleotides diminish the effects of PTH on [Ca2+]i, probably interacting on a biochemical step subsequent to or independent of Ins-1,4,5P3 release.


1995 ◽  
Vol 14 (2) ◽  
pp. 263-275 ◽  
Author(s):  
D M Thomas ◽  
S D Rogers ◽  
M W Sleeman ◽  
G M Pasquini ◽  
F R Bringhurst ◽  
...  

ABSTRACT This study characterizes the actions of insulin and parathyroid hormone (PTH) on the glucose transport system in the rat osteogenic sarcoma cell line UMR 106–01, which expresses a number of features of the osteoblast phenotype. Using [1,2-3H]2-deoxyglucose (2-DOG) as a label, UMR 106–01 cells were shown to possess a glucose transport system which was enhanced by insulin. In contrast, PTH influenced glucose transport in a biphasic manner with a stimulatory effect at 1 h and a more potent inhibitory effect at 16 h on basal and insulin-stimulated 2-DOG transport. To explore the mechanism of PTH action, a direct agonist of cAMP-dependent protein kinase (PKA) was tested. 8-Bromo-cAMP had no acute stimulatory effect but inhibited basal and insulin-stimulated 2-DOG transport at 16 h. This result suggested that the prolonged, but not the acute, effect of PTH was mediated by the generation of cAMP. Further studies with the cell line UMR 4–7, a UMR 106–01 clone stably transfected with an inducible mutant inactive regulatory subunit of PKA, confirmed that the inhibitory but not the stimulatory effect of PTH was mediated by the PKA pathway. Northern blot data indicated that the prolonged inhibitory effects of PTH and 8-bromo-cAMP on glucose transport were likely to be mediated in part by reduction in the levels of GLUT1 (HepG2/brain glucose transporter) mRNA.


2009 ◽  
Vol 11 (11) ◽  
pp. 1666-1675 ◽  
Author(s):  
Kenneth E. White ◽  
Frank A. Gesek ◽  
Peter A. Friedman
Keyword(s):  

2000 ◽  
Vol 19 (2) ◽  
pp. 237-253 ◽  
Author(s):  
Y. Long ◽  
G. P. Cai ◽  
Z. C. Guan ◽  
H. Liu ◽  
X. D. Liang

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