Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bacteriochlorophyll a reaction-center complex I from Chlorobium limicola f. thiosulfatophilum 6230 (Tassajara) was incubated in 2 M guanidine - HCl and then chromatographed on cross-linked dextran or agarose gel. Two principal components were separated: a larger component with photochemical activity (bacteriochlorophyll a reaction-center complex II) and a smaller component without activity (bacteriochlorophyll a protein). Complex II contains carotenoid, bacteriochlorophyll a, reaction center(s), and cytochromes b and c, but lacks the well characterized bacteriochlorophyll a protein contained in Complex I. Complex II carries out a light-induced reduction of cytochrome b along with an oxidation of cytochrome c.
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PMID:An enriched reaction center preparation from green photosynthetic bacteria. 99 Feb 92

A particulate fraction consisting of heavy organelles such as nuclei and mitochondria was prepared from Ehrlich ascites tumor cells. From this fraction we have purified a GTP-binding protein with a molecular mass of 33 kDa (MTG33) by guanidine hydrochloride extraction followed by four steps of column chromatography. The Kd value of MTG33 for GTP was 17 nM. [alpha-32P]GTP-binding to MTG33 was inhibited by GTP and GDP, but not appreciably by ATP, CTP, UTP, or GMP. MTG33 hydrolyzed GTP to GDP at a rate of 4.5 mmol/min/mol protein. Subcellular fractionation analysis of mouse liver revealed that the heavy mitochondrial fraction contained the highest level of MTG33. Furthermore, dual immunofluorescence examination indicated that the staining of NIH 3T3 cells with anti-MTG33 antibody is coincident with the distribution of mitochondrial succinate dehydrogenase. Of the mouse organs examined, the heart contained the highest level of MTG33. These results strongly suggest that MTG33 is a GTP-binding protein located in mitochondria.
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PMID:Purification of a GTP-binding protein localized in mitochondria. 811 21

Guanidine-induced alterations in substrate dependent kinetics of hepatic and renal succinate dehydrogenase (SDH) have been investigated under in vitro conditions. Guanidine hydrochloride (GuHCl) induced a mixed type of inhibition by decreasing the maximal velocity (Vmax) and increasing the Michaelis-Menten constant (Km). The competitive (Ki) and non-competitive (Ki) inhibitory constants were calculated. The values showed that the inhibitory influence of GuHCl is more due to decreased enzyme substrate affinity rather than reduction in the active site density of the enzyme as revealed by low Ki values.
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PMID:Inhibitory kinetic studies on rat hepatic and renal succinate dehydrogenase with guanidine. 920 72

In an experiment with rats system and intracellular energy metabolism was assessed by cell reactions to chronic injection of beta-guanidine propionic acid (beta-GPA) stimulating AMP-dependent protein kinase (AMPK). Suspension was shown to inhibit the succinate dehydrogenase (SDH) activity, reduce glycogen in both types of muscle fibers, and stimulate the activity of alpha-glycerophosphate dehydrogenase (alpha-GPDH) in fast fibers. Supplementing the rat chow with beta-GPA did not modify these parameters during suspension; however, the blood urea level increased considerably in the suspended and control rats. In the controls, beta-GPA as well as suspension, stimulates growth of the aspartate aminotranspherase activity (AST) in blood. Yet, the suspension and beta-GPA injection had no additive effect. Moreover, their effects were opposite in rats subjected to suspension + beta-GPA. Glucose concentration was observed to become lowered in blood of resting rats treated with beta-GPA. This effect can be associated with a more intensive insulin-dependent glucose transport to muscles. The additional glucose, because of increased demand by fibers, underwent to oxidation and did not replenish the intracellular carbohydrate deposits These data suggest energy metabolism shifting toward activation of the processes of disintegration of substrates for energy production due to a sharp growth of energy demand.
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PMID:[Effects of creatine phosphokinase competitive inhibitor on system and tissue energy metabolism in rats in the norm and during unloading]. 1914 Apr 71

123 I-meta-iodo benzyl guanidine (MIBG) scans are considered the gold standard imaging in neuroblastoma; however, flouro deoxy glucose positron emission tomography (FDG-PET) scans have increased sensitivity in adults with pheochromocytoma/paraganglioma. We describe a pediatric patient initially considered to have localized neuroblastoma based on anatomical imaging and 123 I-MIBG scan, but subsequent investigations revealed germline succinate dehydrogenase complex iron sulfur subunit B (SDHB) mutation-associated pheochromocytoma with multiple FDG-avid skeletal metastases. We then compared 123 I-MIBG and FDG-PET scans in children with metastatic pheochromocytoma/paraganglioma. FDG-PET was superior to 123 I-MIBG scan for the detection of skeletal metastases (median number of skeletal lesions detected 10 [range 1-30] vs. 2 [range 1-26], respectively; P = 0.005 by t-test). FDG-PET should be considered the functional scan of choice in children with pheochromocytoma/paraganglioma.
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PMID:Failure of MIBG scan to detect metastases in SDHB-mutated pediatric metastatic pheochromocytoma. 2840 92