Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.11 (AMPK)
 12,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cell-free extract from wheat germ contains an inhibitor interfering with translation of a natural template (BMV RNA). The inhibitor affects neither the translation of poly(U) nor the aminoacylation of tRNA. It exhibits the activity of protein kinase (ATP:protein phosphotransferase, EC 2.7.1.37). The inhibitor is found in lipoprotein aggregates which can be separated from ribosomes on Sepharose 2B column. Ribosomes purified on the Sepharose are several times more active in translation of BMV RNA than those isolated by conventional methods.
Acta Biochim Pol 1979
PMID:Isolation of wheat ribosomes free of high molecular weight inhibitors of the natural messenger translation. 50 12

Apomorphine produced biphasic changes in the activity of an endogenous, specific inhibitor of cAMP-dependent protein kinase (type I inhibitor). Small doses of apomorphine (50-100 micrograms/kg) induced an increase while high doses (1-10 mg/kg) produced a dose-dependent decrease of the type I inhibitor activity in the striatum of control rats. Prolonged treatment with nomifensin markedly reduced the response of the type I inhibitor both to low and high doses of apomorphine and shifted the dose-response curves to the right. The apomorphine-induced increase of the type I inhibitor activity in nomifensin-pretreated rats was blocked by aminophylline and by small, presynaptically active doses of haloperidol. This suggests that small doses of apomorphine stimulate presynaptic D2 receptor. The apomorphine-induced decrease of the type I inhibitor activity in nomifensin pretreated animals was enhanced by aminophylline and by presynaptically active dose of haloperidol. In contrast, this action of apomorphine was blocked by high, postsynaptically active, dose of haloperidol. It suggested postsynaptic site of action of high doses of apomorphine. Prolonged pretreatment with nomifensin resulted in subsensitivity of both presynaptic D2 and postsynaptic D1 receptors.
Pol J Pharmacol Pharm
PMID:The responsiveness of the endogenous inhibitor of cAMP-dependent protein kinase to apomorphine in rat striatum after prolonged treatment with nomifensin. 407 79

Isoprenaline produced a dose-dependent decrease in the activity of an endogenous, specific inhibitor of cAMP-dependent protein kinase (type I inhibitor) in rat hippocampus, brain stem and pineal gland. Prolonged, 21-days treatment with some antidepressant (imipramine, nomifensin and mianserin) markedly reduced the response of the type I inhibitor activity to isoprenaline. To obtain the significant decrease of the type I inhibitor activity, five times higher dose of isoprenaline had to be used in these animals than in control rats. Mianserin is known to produce a decrease of the activity of adenylate cyclase coupled to beta-adrenergic receptors without changing the number of receptor binding sites. In the present study we have shown that also mianserin after prolonged treatment produces subsensitivity of beta-adrenergic receptors when measured by the response of the type I inhibitor activity to isoprenaline. Single doses of imipramine, nomifensin and mianserin did not change the isoprenaline-induced decrease of the type I inhibitor activity. It seems that the isoprenaline-induced decreased of the type I inhibitor activity can be used as an index of beta-adrenergic receptor reactivity.
Pol J Pharmacol Pharm
PMID:Isoprenaline-induced changes in type I inhibitor activity as an index of beta-adrenergic receptor subsensitivity. 608 61

Isoprenaline and adrenaline produced an increase of cAMP content and a decrease of the activity of the endogenous inhibitor of cAMP-dependent protein kinase (type I inhibitor) in human lymphocytes and in rat heart. The maximal effect was seen at a concentration of 10(-6) M. Noradrenaline and dopamine required much higher concentration to elicite the same effect. The decrease of type I inhibitor activity was mediated through beta-adrenergic receptors because propranolol, but not phentolamine, blocked the effects produced by isoprenaline. Stimulation of beta-adrenergic receptors did not influence the activity of type II inhibitor.
Acta Physiol Pol
PMID:The effect of beta-receptor stimulation on the activity of the inhibitor of cAMP-dependent protein kinase. 612 59

The cytosol fraction of the cells of Saccharomyces cerevisiae contains a low-molecular-mass, heat-stable inhibitor for endogenous cAMP-independent protein kinase. The inhibitor (Mr 15 000) is specific toward the protein kinase of A type, while the protein kinase of G type and the catalytic subunit of cAMP-dependent protein kinase are not affected. The following results suggest a protein structure of the inhibitor: 1. preincubation of the inhibitor with trypsin totally abolished its activity; 2. the inhibitor can be labelled by reductive alkylation of the amino acids with [14C]formaldehyde and sodium cyanoborohydride. The kinetic experiments have shown that the inhibitor is a competitive effector of the protein kinase of A type with respect to the protein substrate.
Acta Biochim Pol 1982
PMID:Endogenous inhibitor of a cyclic AMP-independent (A type) protein kinase. 629 92

The response of an endogenous inhibitor of cAMP-dependent protein kinase (type I inhibitor) to tremorine was used as an index of sensitivity of control muscarinic M2-receptors. Tremorine induced a dose-dependent increase in type I inhibitor activity in the posterior hypothalamus and brain stem. The action of the compound was blocked by pretreatment with aminophylline and atropine. Prolonged, 28 days treatment with lysine vasopressin (1 U/kg/day ip) induced hypertension and modified the dose-response curve for tremorine. Five times higher doses of tremorine than in normotensive rats were necessary to induce statistically significant increase in type I inhibitor activity in the posterior hypothalamus and brain stem suggesting subsensitivity of M2-muscarinic receptors in the brain areas responsible for the regulation of blood pressure.
Pol J Pharmacol
PMID:The responsiveness of M2-muscarinic receptors in the posterior hypothalamus and brain stem of vasopressin hypertensive rats. 822 Jun 62

Ribosome biogenesis plays key roles in cell growth by providing increased capacity for protein synthesis. It requires coordinated production of ribosomal proteins (RP) and ribosomal RNA (rRNA), including the processing of the latter. Here, we show that, the depletion of RPS19 causes a reduction of rRNA synthesis in cell lines of both erythroid and non-erythroid origin. A similar effect is observed upon depletion of RPS6 or RPL11. The deficiency of RPS19 does not alter the stability of rRNA, but instead leads to an inhibition of RNA Polymerase I (Pol I) activity. In fact, results of nuclear run-on assays and ChIP experiments show that association of Pol I with the rRNA gene is reduced in RPS19-depleted cells. The phosphorylation of three known regulators of Pol I, CDK2, AKT and AMPK, is altered during ribosomal stress and could be involved in the observed downregulation. Finally, RNA from patients with Diamond Blackfan Anemia (DBA), shows, on average, a lower level of 47S precursor. This indicates that inhibition of rRNA synthesis could be one of the molecular alterations at the basis of DBA.
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PMID:Depletion of ribosomal protein S19 causes a reduction of rRNA synthesis. 2773 13

Type 2 diabetes mellitus (T2D) is a chronic diet-related disease which due to many dangerous complications has become a prominent health problem of the world. The aim of the study was to explore the in vitro activity of Japanese quince (Chaenomeles japonica L., family Rosaceae, JQ) fruit polyphenolic extract as modulator of carbohydrates metabolism. The research was designed to investigate the effect of JQ polyphenolic extract on glucose metabolism in human hepatoma HepG2 cell line cultured under normal non-metabolically changed and hyperglycemic conditions. Pretreatment of the cells with JQ preparation caused decrease of intracellular ROS generation and influenced mitochondrial membrane polarization which seemed to lead to AMPK activation. Further effects observed in HepG2 cells were associated with activation of the enzyme: elevation of glucose uptake and glycogen content, and alleviation of gluconeogenesis through modulation of PEPCK, PTP1B, FOXO1 and GLUT2/4 expression. These findings suggest that JQ polyphenols exhibit hypoglycemic effects via modulation of AMPK signaling in hepatocytes.
Acta Biochim Pol 2018
PMID:Japanese quince (Chaenomeles japonica L.) fruit polyphenolic extract modulates carbohydrate metabolism in HepG2 cells via AMP-activated protein kinase. 2949 9

Skeletal muscle mass responds in a remarkable manner to alterations in loading and use. It has long been clear that skeletal muscle hypertrophy can be prevented by inhibiting RNA synthesis. Since 80% of the cell's total RNA has been estimated to be rRNA, this finding indicates that de novo production of rRNA via transcription of the corresponding genes is important for such hypertrophy to occur. Transcription of rDNA by RNA Pol I is the rate-limiting step in ribosome biogenesis, indicating in turn that this biogenesis strongly influences the hypertrophic response. The present minireview focuses on 1) a brief description of the key steps in ribosome biogenesis and the relationship of this process to skeletal muscle mass and 2) the coordination of ribosome biogenesis and protein synthesis for growth or atrophy, as exemplified by the intracellular AMPK and mTOR pathways.
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PMID:Ribosome biogenesis in skeletal muscle: coordination of transcription and translation. 3121 75

Bovine tuberculosis is an airborne infectious disease caused by organisms of the Mycobacterium tuberculosis (MTB) complex. Mycolic acid (MA) is the main lipid component of the cell membrane of MTB. It is non-enzymatically reduced by NAD(P)H and further produces reactive oxygen species (ROS), which can cause oxidative stress in human cells. N-acetylcysteine (NAC) is a synthetic precursor of glutathione (GSH) and exhibits anti-ROS activity. However, the underlying mechanisms of its protective properties remain uncertain. Herein, after pre-incubation of RAW264.7 cells with NAC, the factors associated with apoptosis and autophagy were measured. Mechanistically, NAC could reduce MA-induced expression of pro-apoptotic and pro-autophagy proteins. At the mRNA level, NAC can inhibit AMPK and activate mTOR expression. The results indicate that NAC might regulate autophagy in RAW264.7 cells through the AMPK/mTOR pathway. To further prove the effect of NAC on MA, ICR mice were used to evaluate the lung injury. Hematoxylin-eosin (HE) staining was performed on the lung. The results show that NAC could reduce cell injury induced by MA. In conclusion, our research showed that NAC attenuates apoptosis and autophagy in response to incubation with mycolic acid.
Pol J Microbiol 2020 Sep
PMID:N-acetylcysteine (NAC) Attenuating Apoptosis and Autophagy in RAW264.7 Cells in Response to Incubation with Mycolic Acid from Bovine Mycobacterium tuberculosis Complex. 3254 87


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