Stimulation of insulin release by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate in the clonal cell line RINm5F despite a lowering of the free cytoplasmic Ca2+ concentration

1986 ◽  
Vol 887 (2) ◽  
pp. 236-241 ◽  
Author(s):  
Per Arkhammar ◽  
Thomas Nilsson ◽  
Per-Olof Berggren
Keyword(s):  
Cell Line ◽  
Insulin Release ◽  
Phorbol Ester ◽  
Clonal Cell Line ◽  
Clonal Cell ◽  
Stimulation Of

Binding of a tritiated thyrotropin-releasing factor to a prolactin secreting clonal cell line (GH3)

1973 ◽  
Vol 82 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Danielle Gourdji ◽  
A. Tixier-Vidal ◽  
Annie Morin ◽  
P. Pradelles ◽  
J.-L. Morgat ◽  
...  
Keyword(s):  
Cell Line ◽  
Clonal Cell Line ◽  
Clonal Cell

scholarly journals Characterization of phenotypic and genotypic diversity in subclones derived from a clonal cell line

2018 ◽  
Vol 34 (3) ◽  
pp. 613-623 ◽  
Author(s):  
Tharmala Tharmalingam ◽  
Hedieh Barkhordarian ◽  
Nicole Tejeda ◽  
Kristi Daris ◽  
Sam Yaghmour ◽  
...  
Keyword(s):  
Cell Line ◽  
Genotypic Diversity ◽  
Clonal Cell Line ◽  
Clonal Cell

MULTIPLE BENZOMORPHAN BINDING SITES IN A CLONAL CELL LINE

1981 ◽  
pp. 24-26
Author(s):  
R.E. West ◽  
R.W. McLawhon ◽  
G. Dawson ◽  
R.J. Miller
Keyword(s):  
Cell Line ◽  
Binding Sites ◽  
Clonal Cell Line ◽  
Clonal Cell

Establishment of an osteoinductive murine osteosarcoma clonal cell line showing osteoblastic phenotypic traits

Bone ◽  
1989 ◽  
Vol 10 (3) ◽  
pp. 195-200 ◽  
Author(s):  
T. Tsuda ◽  
K. Masuhara ◽  
H. Yoshikawa ◽  
N. Shimizu ◽  
K. Takaoka
Keyword(s):  
Cell Line ◽  
Phenotypic Traits ◽  
Clonal Cell Line ◽  
Clonal Cell ◽  
Murine Osteosarcoma

scholarly journals Phorbol esters rapidly stimulate amiloride-sensitive Na+/H+ exchange in a human leukemic cell line.

1984 ◽  
Vol 99 (1) ◽  
pp. 340-343 ◽  
Author(s):  
J M Besterman ◽  
P Cuatrecasas
Keyword(s):  
Cell Line ◽  
Phorbol Ester ◽  
Phorbol Esters ◽  
Leukemic Cell ◽  
Leukemic Cell Line ◽  
Human Leukemic Cell ◽  
Initial Event ◽  
Phorbol Ester Receptor ◽  
Human Leukemic Cell Line ◽  
Stimulation Of

The human, leukemic cell line, HL-60, undergoes differentiation in response to tumor-promoting phorbol esters. Recent studies have implicated stimulation of a Na+/H+ antiporter as an initial event in cellular differentiation and/or proliferation. The effects of phorbol esters on Na+-dependent H+ efflux from HL-60 cells were studied by pH-stat titration. Tumor-promoting phorbol diesters, but not the inactive parent alcohol, stimulated Na+-dependent H+ efflux in a rapid (within 1 min at 37 degrees C) and reversible manner. Stimulation was dependent on the concentration of extracellular sodium; lithium could substitute for sodium, but choline could not. Stimulation was dependent on the activity of extracellular protons and was inhibited completely by amiloride. The concentrations of phorbol diesters at which we observed half-maximal stimulation of Na+-dependent H+ efflux are very similar to the Kd reported in the literature for binding of these phorbol diesters to the phorbol ester receptor and the Km for phorbol diester activation of protein kinase C. Overall characterization of basal and phorbol ester-stimulated H+ efflux indicate that stimulation of a Na+/H+ antiporter constitutes a primary event in phorbol ester interaction with HL-60 cells.

scholarly journals Abnormal glucose metabolism accompanies failure of glucose to stimulate insulin release from a rat pancreatic cell line (RINm5F)

1983 ◽  
Vol 212 (2) ◽  
pp. 439-443 ◽  
Author(s):  
P A Halban ◽  
G A Praz ◽  
C B Wollheim
Keyword(s):  
Glucose Metabolism ◽  
Cell Line ◽  
Insulin Release ◽  
Glucose Utilization ◽  
Rinm5f Cells ◽  
Pancreatic Cell ◽  
Abnormal Glucose Metabolism ◽  
Isolated Rat Islets ◽  
Stimulate Insulin Release ◽  
Stimulation Of

Glucose metabolism and insulin release were studied in isolated rat islets and in an insulin-producing rat cell-line (RINm5F). Intact islets displayed two components of glucose utilization, with glucose stimulation of insulin release being associated with the high-Km component (reflecting glucokinase-like activity). Glucose failed to stimulate insulin release from RINm5F cells, which only displayed a single low-Km component of glucose utilization. Only low-Km (hexokinase-like) glucose-phosphorylating activity was found for disrupted RINm5F cells. These changes in glucose metabolism may contribute towards the failure of glucose to stimulate insulin release from RINm5F cells.

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