Scatchard Plot Analysis of Ligand-Erythrocyte Interactions

1978 ◽  
Vol 67 (9) ◽  
pp. 1344-1345 ◽  
Author(s):  
D.L. Parsons ◽  
J.J. Vallner
Keyword(s):  
Scatchard Plot ◽  
Plot Analysis ◽  
Scatchard Plot Analysis

Evidence for p55–p75 heterodimers in the absence of IL-2 from Scatchard plot analysis

1992 ◽  
Vol 4 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Byron Goldstein ◽  
David Jones ◽  
Ioannis G. Kevrekidis ◽  
Alan S. Perelson
Keyword(s):  
Scatchard Plot ◽  
Plot Analysis ◽  
Scatchard Plot Analysis

Effect of receptor occupancy on [3H]dexamethasone binding to circulating leukocytes

1980 ◽  
Vol 94 (3) ◽  
pp. 376-380 ◽  
Author(s):  
Tohru Murakami ◽  
David D. Brandon ◽  
D. Lynn Loriaux ◽  
Mortimer B. Lipsett
Keyword(s):  
Glucocorticoid Receptor ◽  
Binding Capacity ◽  
Receptor Occupancy ◽  
Binding Study ◽  
Scatchard Plot ◽  
Total Binding ◽  
Plot Analysis ◽  
Scatchard Plot Analysis ◽  
Receptor Concentration

Abstract. To determine the effect of steroid occupancy of the glucocorticoid receptor on the measurement of total receptor concentration using Scatchard plot of [3H]dexamethasone (Dex) binding to circulating leukocytes, leukocytes were incubated with 10−7m cortisol or 10−9m Dex prior to [3H]Dex binding study. Total binding capacity calculated from Scatchard plot analysis of [3H]Dex binding was not significantly reduced after pre-incubation with cortisol. However, total binding capacity was significantly lower after pre-incubation with Dex. These data suggest that total glucocorticoid receptor concentration can be measured from a 3 h incubation of leukocytes obtained from untreated patients.

Binding of mitochondrial malate dehydrogenase to mitoplasts

1979 ◽  
Vol 57 (6) ◽  
pp. 662-665 ◽  
Author(s):  
Paula M. Strasberg ◽  
Keith A. Webster ◽  
Hasmukh V. Patel ◽  
Karl B. Freeman
Keyword(s):  
Malate Dehydrogenase ◽  
Rat Liver ◽  
Specific Binding ◽  
Liver Mitochondria ◽  
Scatchard Plot ◽  
Rat Liver Mitochondria ◽  
Isolated Mitochondria ◽  
Plot Analysis ◽  
Scatchard Plot Analysis ◽  
Mitochondrial Malate Dehydrogenase

The binding of 14C-labelled bovine and porcine malate dehydrogenase (EC 1.1.1.37) to rat liver mitochondria and mitoplasts was examined. The bovine enzyme was found to associate nonspecifically with isolated mitochondria and sonicated mitoplasts. Scatchard plot analysis suggested a specific binding to mitoplasts of the order of 5 pmol malate dehydrogenase per milligram of mitoplast protein. Porcine malate dehydrogenase dimer but not monomer exhibited a similar binding. The results are discussed in relation to the mechanism of uptake of the enzyme by mitochondria after synthesis on cytosolic ribosomes.

Oestrogen receptors in endometrial cytosol of gilts on days 10-13 of oestrous cycle and pregnancy

1994 ◽  
Vol 42 (3) ◽  
pp. 217-223
Author(s):  
J. Van Der Meulen ◽  
F.A. Helmond ◽  
C.P.J. Oudenaarden
Keyword(s):  
Oestrous Cycle ◽  
Endometrial Tissue ◽  
Scatchard Plot ◽  
Oestrogen Receptors ◽  
Reproductive State ◽  
Dextran Coated Charcoal ◽  
Plot Analysis ◽  
Scatchard Plot Analysis

Cytosolic oestrogen receptors (ER(c)) were determined with a Dextran-coated charcoal assay and Scatchard plot analysis in endometrial tissue of non-pregnant and pregnant gilts on Days 10-13 after standing oestrus. The Kd of the ER(c) was 0.40 +/- 0.04 nM (mean +/- SEM) and was not affected by day or reproductive state. The endometrial ER(c) concentration was affected by day and reproductive state (P

Prolactin permits the expression of a circadian variation in insulin receptor profile in hepatocytes of the golden hamster (Mesocricetus auratus)

1985 ◽  
Vol 106 (2) ◽  
pp. 177-181 ◽  
Author(s):  
A. H. Cincotta ◽  
A. H. Meier
Keyword(s):  
Insulin Receptor ◽  
Circadian Variation ◽  
Prolactin Release ◽  
High Affinity ◽  
Plot Analysis ◽  
Receptor Profile ◽  
Scatchard Plot Analysis ◽  
High Affinity Receptor ◽  
Receptor Number ◽  
Affinity Receptor

ABSTRACT Insulin receptor profile was determined in freshly isolated hamster hepatocytes at two times (07.00 and 16.00 h) during a 14-h daily photoperiod (08.00–22.00 h). The hamsters were pretreated for 5 days with bromocriptine (to inhibit prolactin release), bromocriptine and prolactin replacement, or control saline injections. The insulin receptor profile was determined by Scatchard plot analysis. The insulin receptor number (high and low affinity) was three times greater at 07.00 than at 16.00 h among saline-injected controls. However, their affinities did not differ. Bromocriptine pretreatment reduced (70%) both the high and low affinity receptor numbers and increased the affinity of the high affinity receptor at 07.00 h. Prolactin replacement in bromocriptine-treated hamsters restored the receptor profile at 07.00 h to control values. These data indicate that prolactin facilitates the expression of a circadian variation in insulin receptor profile. J. Endocr. (1985) 106, 177–181

Specific Estradiol Binding in Schwannomas, Meningiomas, and Neurofibromas

Neurosurgery ◽  
1981 ◽  
Vol 9 (6) ◽  
pp. 665-671 ◽  
Author(s):  
Robert L. Martuza ◽  
David T. MacLaughlin ◽  
Robert G. Ojemann
Keyword(s):  
Binding Sites ◽  
Genetic Disorder ◽  
High Affinity ◽  
Acoustic Neuromas ◽  
Saturation Binding ◽  
Plot Analysis ◽  
Wide Range ◽  
Scatchard Plot Analysis ◽  
Range Of Values

Abstract The cytoplasmic fractions of schwannomas (acoustic neuromas), meningiomas, and neurofibromas were assayed for the presence of estrogen receptors. Specific estradiol binding was detected in 7 of 16 schwannomas, 7 of 10 meningiomas, and 1 of 6 neurofibromas. A nontumorous vestibular nerve was also studied and showed no estradiol binding. In the tumors, the concentration of the estradiol binding sites as estimated by saturation binding analysis covered a wide range of values (21 to 2430 fmol/g of tumor) but, overall, meningiomas contained the highest amount of estradiol binder. A Scatchard plot analysis of one of the schwannoma specimens demonstrated high affinity estradiol binding (Ka = 1.695 × 1010M−1). Although there were more females than males in each tumor category, the overall incidence of estradiol binding was similar in males (5 of 11. 45%) and in females (10 of 21, 48%r). In 5 cases, progestin binding was also measured and was delected in two meningiomas (both from female patients): one meningioma and two neurofibromas showed no progestin binding. A discussion is presented of the possible role of estradiol in the pathogenesis or modulation of meningeal and Schwann cell tumors as well as in the genetic disorder neurofibromatosis.

Overpressure Identification Using The Eaton Method on The Gumai Formation of Geragai Graben, Jambi Sub Basin

2020 ◽  
Author(s):  
A. O. Marnila
Keyword(s):  
Pressure Data ◽  
Stratigraphic Sequence ◽  
Fine Grained ◽  
Marine Sedimentation ◽  
Plot Analysis ◽  
Significant Reversal ◽  
Porosity And Permeability ◽  
Upper Level ◽  
Type Data ◽  
Fine Grained Sand

Geragai graben is located in the South Sumatera Basin. It was formed by mega sequence tectonic process with various stratigraphic sequence from land and marine sedimentation. One of the overpressure indication zones in the Geragai graben is in the Gumai Formation, where the sedimentation is dominated by fine grained sand and shale with low porosity and permeability. The aim of the study is to localize the overpressure zone and to analyze the overpressure mechanism on the Gumai Formation. The Eaton method was used to determine pore pressure value using wireline log data, pressure data (RFT/FIT), and well report. The significant reversal of sonic and porosity log is indicating an overpressure presence. The cross-plot analysis of velocity vs density and fluid type data from well reports were used to analyze the causes of overpressure in the Gumai Formation. The overpressure in Gumai Formation of Geragai graben is divided into two zones, they are in the upper level and lower level of the Gumai Formation. Low overpressure have occurred in the Upper Gumai Formation and mild overpressure on the Lower Gumai Formation. Based on the analyzed data, it could be predicted, that the overpressure mechanism in the Upper Gumai Formation might have been caused by a hydrocarbon buoyancy, whereas in the Lower Gumai Formation, might have been caused by disequilibrium compaction as a result of massive shale sequence.

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