Interaction of a rat kidney endoplasmic reticulum fraction with glycolytic enzymes

1963 ◽  
Vol 71 ◽  
pp. 277-284 ◽  
Author(s):  
Vernon D Jones ◽  
John L Norris ◽  
Erwin J Landon
Keyword(s):  
Endoplasmic Reticulum ◽  
Rat Kidney ◽  
Glycolytic Enzymes ◽  
Endoplasmic Reticulum Fraction

A characterization of heam uptake and intracellular distribution by isolated hepatocytes

1985 ◽  
Vol 5 (7) ◽  
pp. 609-614 ◽  
Author(s):  
A. Lodola
Keyword(s):  
Endoplasmic Reticulum ◽  
Specific Binding ◽  
Isolated Hepatocytes ◽  
Intracellular Distribution ◽  
Distribution Data ◽  
Temperature Dependent ◽  
Rat Hepatocyte ◽  
Isolated Rat ◽  
Endoplasmic Reticulum Fraction

The uptake and intracellular distribution of haem by isolated rat hepatocyte suspensions was studied. An increase in cell haem content occurred after a challenge with 5, 10 or 20 μM haem, supplied as methaemalbumin. The rate of haem uptake was temperature dependent; no non-specific binding occurred. Intracellular haem distribution data are consistent with a rapid association of haem with the endoplasmic reticulum fraction prior to its accumulation in the cytosol and at the mitochondrion.

Restraint stress aggravates rat kidney injury caused by a crush injury through endoplasmic reticulum stress

2013 ◽  
Vol 75 (5) ◽  
pp. 798-806 ◽  
Author(s):  
Jing Geng ◽  
Xiao Jing Zhang ◽  
Chun Ling Ma ◽  
Ying Min Li ◽  
Guo Zhong Zhang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Restraint Stress ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Crush Injury

Metabolomics and Lipidomics Profiling of a Combined Mitochondrial Plus Endoplasmic Reticulum Fraction of Human Fibroblasts: A Robust Tool for Clinical Studies

2017 ◽  
Vol 17 (1) ◽  
pp. 745-750 ◽  
Author(s):  
Charlotte Veyrat-Durebex ◽  
Cinzia Bocca ◽  
Stéphanie Chupin ◽  
Judith Kouassi Nzoughet ◽  
Gilles Simard ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Clinical Studies ◽  
Human Fibroblasts ◽  
Endoplasmic Reticulum Fraction

scholarly journals Phosphatidylinositol kinase and diphosphoinositide kinase of rat kidney cortex: properties and subcellular localization

1976 ◽  
Vol 160 (1) ◽  
pp. 97-105 ◽  
Author(s):  
P H Cooper ◽  
J N Hawthorne
Keyword(s):  
Endoplasmic Reticulum ◽  
Golgi Complex ◽  
Brush Border ◽  
Rat Kidney ◽  
Subcellular Fractionation ◽  
Kidney Cortex ◽  
Marker Enzymes ◽  
Rat Kidney Cortex ◽  
Phosphatidylinositol Kinase ◽  
Golgi Membranes

The properties of phosphatidylinositol kinase and diphosphoinositide kinase from rat kidney cortex were studied. The enzymes were completely Mg2+-dependent. Cutscum detergent activated phosphatidylinositol kinase, but diphosphoinositide kinase was inhibited by all detergents tested. The pH optima were 7.7 for phosphatidylinositol kinase and 6.5 for diphosphoinositide kinase. On subcellular fractionation of kidney-cortex homogenates by differential centriflgation, the distribution of phosphatidylinositol kinase resembled that of the marker enzymes for brush-border, endoplasmic-reticulum and Golgi membranes. Diphosphoinositide kinase distribution resembled that of thiamin pyrophosphatase (assayed in the absence of ATP), diphosphoinositide phosphatase and triphosphoinositide phosphatase. Activities of both kinases were low in purified brush-border fragments. Diphosphoinositide kinase is probably localized in the Golgi complex.

Indomethacin induces endoplasmic reticulum stress, but not apoptosis, in the rat kidney

2015 ◽  
Vol 761 ◽  
pp. 199-205 ◽  
Author(s):  
Arumugam Suriyam Nagappan ◽  
Joe Varghese ◽  
Jithu V. James ◽  
Molly Jacob
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Rat Kidney

Ultrastructure of Isolated Mitochondria from the Renal Cortex after Reversible and Irreversible Ischemia in the Rat

1977 ◽  
Vol 35 ◽  
pp. 412-413
Author(s):  
S. E. Coleman ◽  
J. Duggan ◽  
R. L. Hackett
Keyword(s):  
Endoplasmic Reticulum ◽  
Renal Cortex ◽  
Rat Kidney ◽  
Renal Ischemia ◽  
Mitochondrial Matrix ◽  
Isolated Mitochondria ◽  
Initial Damage ◽  
Inner Cortex ◽  
Rat Kidneys

Complete renal ischemia causes a series of subcellular changes including chromatin clumping, dilation of endoplasmic reticulum and condensation of mitochondrial matrix followed by swelling of the mitochondria and unfolding of the cristae (1). Most mitochondria are condensed by 15 minutes and half are condensed and half swollen by 30 minutes with the majority of the mitochondria swollen by 60 minutes of ischemia.In this study we have looked at the ability of mitochondria isolated from ischemic rat kidneys to undergo structural energy transformations in the presence of substrate and ADP. Mitochondria were isolated from the inner cortex of rat kidney where initial damage from ischemia occurs. The tissue was diced in the cold, homogenized with a Dounce homogenizer, spun twice at 600 g, and the supernatant at 15,000 g for pelleting of mitochondria.

scholarly journals Isolation of membrane-bound renal enzymes that metabolize kinins and angiotensins

1976 ◽  
Vol 157 (3) ◽  
pp. 643-650 ◽  
Author(s):  
P E Ward ◽  
E G Erdös ◽  
C D Gedney ◽  
R M Dowben ◽  
R C Reynolds
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Proximal Tubule ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Rat Kidney ◽  
Surface Membrane ◽  
Renal Kallikrein ◽  
Proximal Tubular ◽  
Kallikrein Activity

Cortex of rat kidney was homogenized and fractions enriched in plasma membrane, endoplasmic reticulum or brush border were prepared by several techniques of differential centrifugation. The identity and homogeneity of the membrane fragments were investigated by assaying marker enzymes and by transmission and scanning electron microscopy. Kallikrein was present in both plasma-membrane- and endoplasmic-reticulum-enriched fractions isolated by two fractionation procedures. Kallikrein was highly concentrated in a plasma-membrane fraction but was absent from the brush-border membrane of proximal tubular cells. Cells of transplanted renal tumours of the rat, originating from the proximal tubule, had no kallikrein activity. Kininase activity, angiotensin I-converting enzyme (kininase II) and angiotensinase were found in a plasma-membrane-enriched fraction and especially in the fraction containing isolated brush border. It is suggested that after renal kallikrein is synthesized on endoplasmic reticulum, it is subsequently reoriented to a surface membrane for activation and release. Renal kallikrein may enter the tubular filtrate distal to the proximal tubules. The brush-border membrane of proximal tubule is the major site of inactivation of kinins and angiotensin II..

RNA Polymerase Stimulation: Effect of Aldosterone and Other Adrenocorticoids on RNA Turnover in Rat Kidney

1975 ◽  
Vol 53 (1) ◽  
pp. 70-78 ◽  
Author(s):  
Ram K. Mishra ◽  
L. A. W. Feltham
Keyword(s):  
Endoplasmic Reticulum ◽  
Rna Polymerase ◽  
Smooth Endoplasmic Reticulum ◽  
Rat Kidney ◽  
Polymerase Activity ◽  
Daily Administration ◽  
Aldosterone Receptor ◽  
Rna Polymerase Activity ◽  
Adrenocortical Hormone ◽  
Dna Template

The results of steroid hormone stimulation of aggregate RNA polymerase activity in kidney can be interpreted in terms of either template or enzyme alterations. In order to discover the effect of aldosterone on enzyme or DNA template, the RNA polymerases were purified from kidney nuclei of normal, adrenalectomized or adrenalectomized plus aldosterone treated rats and the activity was determined using different sources of DNA. It was found that the DNA from aldosterone treated rats was transcribed more efficiently than from other sources. Aldosterone does not seem to have a direct effect on the RNA polymerase. Fractionation of ([14C]aldosterone injected) kidney chromatin revealed the presence of radioactivity in the non-histone acidic proteins and DNA, suggesting the possible binding of aldosterone or aldosterone–receptor complex to these chromatin fractions which may result in enhanced template activity.Turnover of RNA was also studied in various subcellular fractions: nuclei, mitochondria, rough endoplasmic reticulum, smooth endoplasmic reticulum, polysomes, ribosomes and sRNA, in normal, adrenalectomized, and adrenalectomized plus adrenocortical hormone treated rat kidney, by following the loss of radioactivity after a single injection of [14C]-orotic acid. Daily administration of aldosterone or deoxycorticosterone reversed the effects of adrenalectomy. Daily administration of corticosterone was without effect.

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