Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The BCL2 (B cell lymphoma/leukemia-2) and C-HA-RAS oncogenes encode membrane-associated proteins of 26 and 21 kilodaltons, respectively. Although RAS proteins have long been known for their ability to bind and hydrolyze GTP, recent investigations suggest that BCL2 encodes a novel GTP-binding protein (S.
Haldar
, C. Beatty, Y. Tsujimoto, and C. M. Croce, Nature [London] 342:195-198, 1989). Cotransfection of BCL2 and HA-RAS oncogenes resulted in morphological transformation of early-passage rodent fibroblasts, rendering these cells tumorigenic in animals and enabling them to grow in semisolid medium. In contrast, cotransfection of BCL2 with oncogenes that encode nuclear proteins (E1A and C-MYC) did not produce malignant transformation, whereas HA-RAS did complement with these genes. These findings suggest that proteins encoded by oncogenes such as BCL2 and HA-RAS, although having similar subcellular locations and perhaps similar biochemical properties, can regulate distinct complementary pathways involved in cellular transformation.
Mol
Cell Biol 1990 Aug
PMID:Complementation by BCL2 and C-HA-RAS oncogenes in malignant transformation of rat embryo fibroblasts. 219 51
The incorporation of the membrane form and the soluble form of variant surface glycoprotein (mfVSG and sVSG) from Trypanosoma brucei brucei into liposomes has been investigated. It was found that selective incorporation of mfVSG into liposomes was possible in the presence of 8 M urea as a denaturing agent; sVSG, by contrast, was incorporated only poorly into liposomes. After proteolysis of mfVSG incorporated into liposomes, a compound was isolated from the liposomes which carries with it constituents of the glyophospholipid membrane anchor: ethanolamine, di-14:0-diglyceride and phosphatidylinositol were identified by electron impact and fast atom bombardment mass spectrometry, thus providing direct confirmation of the earlier findings of Holder [Holder, A.A. (1983) Biochem. J. 209, 261-262] and Ferguson et al. [Ferguson, M.A.J.,
Haldar
, K. and Cross, G.A.M. (1985) J. Biol. Chem. 260, 4963-4968; Ferguson, M.A.J., Low, M.G. and Cross, G.A.M. (1985) J. Biol. Chem. 260, 14547-14555].
Mol
Biochem Parasitol 1986 Aug
PMID:A study of the membrane attachment site of the membrane-form variant surface glycoprotein from Trypanosoma brucei brucei using lipid vesicles as a model of the plasma membrane. 352 49
Liposomal lipid peroxidation and peroxide induced DNA damage were investigated. Inhibition of lipid peroxidation was studied using 400 microM uric acid, beta-carotene, alpha-tocopherol, curcumin and butylated hydroxyanisole (BHA).
Curcumin
, the active principle of turmeric (
Curcuma
longa), was as effective an antioxidant as BHA. An aqueous extract of turmeric was also found to be an effective inhibitor. The inhibition obtained using this aqueous extract, incorporated into the liposome itself, was 70% at 300 ng/microliter. This indicates the presence of yet another antioxidant in turmeric besides the lipophilic curcumin. The aqueous antioxidant extended 80% protection to DNA against peroxidative injury at 100 ng/microliter. This component of turmeric is being characterised and investigated as an antioxidant/anticlastogen and as an antipromoter.
Mol
Cell Biochem 1987 Sep
PMID:Lipid peroxide induced DNA damage: protection by turmeric (Curcuma longa). 369 62
Curcumin
protects hemoglobin from nitrogen dioxide induced oxidation.
Curcumin
was also found to scavenge nitrogen dioxide in a concentration dependent way. The study also explains the ability of curcumin to protect hemoglobin from nitrite induced oxidation, where nitrogen dioxide is a key intermediate.
Mol
Cell Biochem 1995 May 10
PMID:Curcumin inhibits nitrogen dioxide induced oxidation of hemoglobin. 765 74
The spice principles curcumin (from turmeric) and eugenol (from cloves) are good inhibitors of lipid peroxidation. Lipid peroxidation is known to be initiated by reactive oxygen species. The effect of curcumin and eugenol on the generation of reactive oxygen species in model systems were investigated. Both curcumin and eugenol inhibited superoxide anion generation in xanthine-xanthine oxidase system to an extent of 40% and 50% at concentrations of 75 microM and 250 microM respectively.
Curcumin
and eugenol also inhibited the generation of hydroxyl radicals (.OH) to an extent of 76% and 70% as measured by deoxyribose degradation. The .OH-radical formation measured by the hydroxylation of salicylate to 2,3-dihydroxy benzoate was inhibited to an extent of 66% and 46%, respectively, by curcumin and eugenol at 50 microM and 250 microM. These spice principles also prevented the oxidation of Fe2+ in Fentons reaction which generates .OH radicals.
Mol
Cell Biochem 1994 Aug 17
PMID:Studies on the inhibitory effects of curcumin and eugenol on the formation of reactive oxygen species and the oxidation of ferrous iron. 784 73
The effect of retinol deficiency and curcumin and turmeric feeding on brain microsomal Na(+)-K(+)ATPase activity was investigated. The brain Na(+)-K(+)ATPase activity registered an increase of 148.5% as compared to the control group. Upon treating retinol deficient rats with curcumin or turmeric, the abnormally elevated activity showed a decrease of 36.9 and 47.1%, respectively, when compared to the retinol deficient group. An increase in Vmax by 67% and Km by 66% for ATP was observed in the retinol deficient group.
Curcumin
or turmeric fed retinol-deficient groups reduced the Vmax by 25 and 33%, while Km was reduced by 25 and 31%, respectively, compared to the retinol deficient group. Arrhenius plot of Na(+)-K(+) ATPase showed a typical bi-phasic pattern in all the groups. Cholesterol:Phospholipid ratio showed a decrease in the retinol-deficient group by 67.8%, which showed a marked increase in curcumin or turmeric treated groups. Detergents could increase the Na(+)-K(+) ATPase activity more in the control group than in the retinol deficient groups.
Curcumin
or turmeric improved the detergent action on the enzyme. Subsequent freezing and thawing over a period of 30 min decreased the enzyme activity by 22.8% in the retinol deficient group compared to 15.9% decrease in the control group.
Curcumin
or turmeric treated groups showed a decrease in the enzyme activity by 22.0 and 19.2%, respectively, when compared to the zero time in each group. In the presence of concanavalin-A (Con-A) there was only 52.4% stimulation in the enzyme activity in retinol deficient groups, compared to 108.0% in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol
Cell Biochem 1994 Aug 31
PMID:Effect of retinol deficiency and curcumin or turmeric feeding on brain Na(+)-K+ adenosine triphosphatase activity. 784 84
The effect of curcumin on the biochemical changes induced by isoproterenol (ISO) administration in rats was examined. ISO (300 mg Kg-1 administered subcutaneously twice at an interval of 24 h) caused a decrease in body weight and an increase in heart weight, water content as well as in the levels of serum marker enzymes viz creatine kinase (CK), lactate dehydrogenase (LDH) and LDH1 isozyme. It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation.
Curcumin
at a concentration of 200 mg.Kg-1, when administered orally, showed a decrease in serum enzyme levels and the electrocardiographic changes got restored towards normalcy. Myocardial infarction was accompanied by the disintegration of membrane polyunsaturated fatty acids expressed by increase of thiobarbituric acid reactive substance (TBARS), a measure of lipid peroxides and by the impairment of natural scavenging, characterized by the decrease in the levels of superoxide dismutase, catalase, glutathione peroxidase, ceruloplasmin, alpha tocopherol, reduced glutathione (GSH) and ascorbic acid. The oral pretreatment with curcumin two days before and during ISO administration decreased the effect of lipid peroxidation. It was shown to have a membrane stabilizing action by inhibiting the release of beta-glucuronidase from nuclei, mitochondria, lysosome and microsome.
Curcumin
pre- and co-treatment decreased the severity of pathological changes and thus, could have a protective effect against the damage caused by myocardial infarction (MI).
Mol
Cell Biochem 1996 Jun 21
PMID:Protective role of curcumin against isoproterenol induced myocardial infarction in rats. 885 58
Curcumin
(diferuloyl methane) is the major active yellow pigment of turmeric and curry. Studies in recent years have indicated that curcumin is a potent inhibitor of the initiation and promotion of chemical carcinogen-induced skin carcinogenesis in mice. When COLO205 colorectal carcinoma cells were treated with curcumin (60 microM), the appearance of apoptotic DNA ladders was delayed about 5 h, and G1 arrest was detected. Further analysis of the endonuclease activities in these cells revealed that the activity of Ca(+2)-dependent endonuclease in COLO205 cells was profoundly inhibited and that the extent of inhibition depended on the degree of calcium depletion. The reduction of p53 gene expression was accompanied by the induction of HSP70 gene expression in the curcumin-treated cells. These findings suggest that curcumin may induce the expression of the HSP70 gene through the initial depletion of intracellular Ca(+2), followed by the suppression of p53 gene function in the target cells.
Mol
Carcinog 1996 Dec
PMID:Induction of HSP70 gene expression by modulation of Ca(+2) ion and cellular p53 protein by curcumin in colorectal carcinoma cells. 898 16
Streptozotocin-induced diabetic rats were maintained on 0.5% curcumin containing diet for 8 weeks. Blood cholesterol was lowered significantly by dietary curcumin in these diabetic animals. Cholesterol decrease was exclusively from LDL-VLDL fraction. Significant decrease in blood triglyceride and phospholipids was also brought about by dietary curcumin in diabetic rats. In a parallel study, wherein diabetic animals were maintained on a high cholesterol diet, the extents of hypercholesterolemia and phospholipidemia were still higher compared to those maintained on control diet.
Curcumin
exhibited lowering of cholesterol and phospholipid in these animals also. Liver cholesterol, triglyceride and phospholipid contents were elevated under diabetic conditions. Dietary curcumin showed a distinct tendency to counter these changes in lipid fractions of liver. This effect of curcumin was also seen in diabetic animals maintained on high cholesterol diet. Dietary curcumin also showed significant countering of renal cholesterol and triglycerides elevated in diabetic rats. In order to understand the mechanism of hypocholesterolemic action of dietary curcumin, activities of hepatic cholesterol-7a-hydroxylase and HMG CoA reductase were measured. Hepatic cholesterol-7a-hydroxylase activity was markedly higher in curcumin fed diabetic animals suggesting a higher rate of cholesterol catabolism.
Mol
Cell Biochem 1997 Jan
PMID:Hypolipidemic action of curcumin, the active principle of turmeric (Curcuma longa) in streptozotocin induced diabetic rats. 904 34
There are only a small number of molecular markers currently proven to be useful for phylogenetic inference within the flowering plants. We demonstrate that the 5' end of the 26S ribosomal DNA (ca. 1100 bp) is of great value for investigating generic to subfamilial relationships. We analyzed DNA sequences from 31 species of the Ranunculaceae and four species of the Berberidaceae to test phylogenetic relationships within the Ranunculaceae. The inferred phylogeny strongly supports the concept that the Thalictrum chromosome group is not monophyletic, but consists of three independent lineages: (1)
Hydrastis
, (2) Xanthorhiza and Coptis, and (3) Thalictrum, Aquilegia, and Enemion. Based on comparison with conventional taxonomic characters, we propose a hypothesis that the third group also includes the rest of the Thalictrum chromosome taxa that have a base chromosome number of seven. For the Ranunculus chromosome group, our study suggests several relationships that have not been recognized by conventional systematics. The inferred 26S rDNA topology is compared with results from two previously published molecular data sets: DNA sequences from rbcL, atpB, and 18S rDNA genes and restriction fragment length polymorphism data from chloroplast DNA. The three topologies are highly congruent and agree with karyological characters, but not with fruit type, both of which have often been used for the higher classification of the Ra- nunculaceae.
Mol
Phylogenet Evol 1997 Oct
PMID:Molecular phylogenetic study of the Ranunculaceae: utility of the nuclear 26S ribosomal DNA in inferring intrafamilial relationships. 929 18
1
2
3
4
5
6
7
8
9
10
Next >>