Anisomycin: An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.Protein Synthesis Inhibitors: Compounds which inhibit the synthesis of proteins. They are usually ANTI-BACTERIAL AGENTS or toxins. Mechanism of the action of inhibition includes the interruption of peptide-chain elongation, the blocking the A site of ribosomes, the misreading of the genetic code or the prevention of the attachment of oligosaccharide side chains to glycoproteins.p38 Mitogen-Activated Protein Kinases: A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.Emetine: The principal alkaloid of ipecac, from the ground roots of Uragoga (or Cephaelis) ipecacuanha or U. acuminata, of the Rubiaceae. It is used as an amebicide in many different preparations and may cause serious cardiac, hepatic, or renal damage and violent diarrhea and vomiting. Emetine inhibits protein synthesis in EUKARYOTIC CELLS but not PROKARYOTIC CELLS.Mitogen-Activated Protein Kinases: A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).Nucleic Acid Synthesis Inhibitors: Compounds that inhibit cell production of DNA or RNA.Enzyme Activators: Compounds or factors that act on a specific enzyme to increase its activity.JNK Mitogen-Activated Protein Kinases: A subgroup of mitogen-activated protein kinases that activate TRANSCRIPTION FACTOR AP-1 via the phosphorylation of C-JUN PROTEINS. They are components of intracellular signaling pathways that regulate CELL PROLIFERATION; APOPTOSIS; and CELL DIFFERENTIATION.Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.PyrrolidinesSparsomycin: An antitumor antibiotic produced by Streptomyces sparsogenes. It inhibits protein synthesis in 70S and 80S ribosomal systems.Puromycin: A cinnamamido ADENOSINE found in STREPTOMYCES alboniger. It inhibits protein synthesis by binding to RNA. It is an antineoplastic and antitrypanosomal agent and is used in research as an inhibitor of protein synthesis.Protein Biosynthesis: The biosynthesis of PEPTIDES and PROTEINS on RIBOSOMES, directed by MESSENGER RNA, via TRANSFER RNA that is charged with standard proteinogenic AMINO ACIDS.Trichodermin: Antifungal metabolite from several fungi, mainly Trichoderma viride; inhibits protein synthesis by binding to ribosomes; proposed as antifungal and antineoplastic; used as tool in cellular biochemistry.Imidazoles: Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).Hypothalamus, Middle: Middle portion of the hypothalamus containing the arcuate, dorsomedial, ventromedial nuclei, the TUBER CINEREUM and the PITUITARY GLAND.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Pactamycin: Antibiotic produced by Streptomyces pactum used as an antineoplastic agent. It is also used as a tool in biochemistry because it inhibits certain steps in protein synthesis.Calcium-Calmodulin-Dependent Protein Kinases: A CALMODULIN-dependent enzyme that catalyzes the phosphorylation of proteins. This enzyme is also sometimes dependent on CALCIUM. A wide range of proteins can act as acceptor, including VIMENTIN; SYNAPSINS; GLYCOGEN SYNTHASE; MYOSIN LIGHT CHAINS; and the MICROTUBULE-ASSOCIATED PROTEINS. (From Enzyme Nomenclature, 1992, p277)Mitogen-Activated Protein Kinase Kinases: A serine-threonine protein kinase family whose members are components in protein kinase cascades activated by diverse stimuli. These MAPK kinases phosphorylate MITOGEN-ACTIVATED PROTEIN KINASES and are themselves phosphorylated by MAP KINASE KINASE KINASES. JNK kinases (also known as SAPK kinases) are a subfamily.MAP Kinase Kinase 4: A mitogen-activated protein kinase kinase with specificity for JNK MITOGEN-ACTIVATED PROTEIN KINASES; P38 MITOGEN-ACTIVATED PROTEIN KINASES and the RETINOID X RECEPTORS. It takes part in a SIGNAL TRANSDUCTION pathway that is activated in response to cellular stress.Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory.Amnesia: Pathologic partial or complete loss of the ability to recall past experiences (AMNESIA, RETROGRADE) or to form new memories (AMNESIA, ANTEROGRADE). This condition may be of organic or psychologic origin. Organic forms of amnesia are usually associated with dysfunction of the DIENCEPHALON or HIPPOCAMPUS. (From Adams et al., Principles of Neurology, 6th ed, pp426-7)Arsenites: Inorganic salts or organic esters of arsenious acid.

SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activation and myeloid cell survival. (1/511)

SHIP is an inositol 5' phosphatase that hydrolyzes the PI3'K product PI(3,4,5)P3. We show that SHIP-deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy, and myeloid infiltration of vital organs. Neutrophils and bone marrow-derived mast cells from SHIP-/- mice are less susceptible to programmed cell death induced by various apoptotic stimuli or by growth factor withdrawal. Engagement of IL3-R and GM-CSF-R in these cells leads to increased and prolonged PI3'K-dependent PI(3,4,5)P3 accumulation and PKB activation. These data indicate that SHIP is a negative regulator of growth factor-mediated PKB activation and myeloid cell survival.  (+info)

Ischemic preconditioning depends on interaction between mitochondrial KATP channels and actin cytoskeleton. (2/511)

Both mitochondrial ATP-sensitive K+ (KATP) channels and the actin cytoskeleton have been proposed to be end-effectors in ischemic preconditioning (PC). For evaluation of the participation of these proposed end effectors, rabbits underwent 30 min of regional ischemia and 3 h of reperfusion. PC by 5-min ischemia + 10-min reperfusion reduced infarct size by 60%. Diazoxide, a mitochondrial KATP-channel opener, administered before ischemia was protective. Protection was lost when diazoxide was given after onset of ischemia. Anisomycin, a p38/JNK activator, reduced infarct size, but protection from both diazoxide and anisomycin was abolished by 5-hydroxydecanoate (5-HD), an inhibitor of mitochondrial KATP channels. Isolated adult rabbit cardiomyocytes were subjected to simulated ischemia by centrifuging the cells into an oxygen-free pellet for 3 h. PC was induced by prior pelleting for 10 min followed by resuspension for 15 min. Osmotic fragility was assessed by adding cells to hypotonic (85 mosmol) Trypan blue. PC delayed the progressive increase in fragility seen in non-PC cells. Incubation with diazoxide or pinacidil was as protective as PC. Anisomycin reduced osmotic fragility, and this was reversed by 5-HD. Interestingly, protection by PC, diazoxide, and pinacidil could be abolished by disruption of the cytoskeleton by cytochalasin D. These data support a role for both mitochondrial KATP channels and cytoskeletal actin in protection by PC.  (+info)

On the complexities of ceramide changes in cells undergoing apoptosis: lack of evidence for a second messenger function in apoptotic induction. (3/511)

The generation of cellular ceramides as a second messenger has been implicated as a regulatory and required step for the induction of apoptosis. In this study, we have applied a recently developed mass spectrometric technique to the determination of changes in physiological ceramide levels during apoptosis induced by tumor necrosis factor plus cycloheximide in U937 cells and the chemical agents anisomycin or geranylgeraniol in HL-60 cells. The mass spectrometric method has significant advantages over traditional methods for ceramide quantitation in that it determines the relative abundance of all ceramide species present in complex biological lipid mixtures individually and simultaneously. We quantitiated ceramides ranging from C14 to C26, finding that their basal levels and relative distribution varied significantly, both within and between different cell types. However, we were not able to detect any significant changes in either total ceramide content or species distribution until 1 h or more post-stimulation with any of these treatments, by which time the cells were in an advanced stage of apoptosis. Differences were also seen between all three treatments in the ceramide species distribution observed in these late stages of apoptosis. These data indicate that in vivo ceramide generation occurs as a consequence of apoptosis rather than as an essential second messenger involved in its induction. They also pose new questions about the potential roles that certain ceramide species may play in the late stages of apoptosis, and demonstrate a clear need to utilize the resolving power of mass spectrometry-based assays in any future investigations into the biological function of ceramides.  (+info)

Trichothecene mycotoxins trigger a ribotoxic stress response that activates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase and induces apoptosis. (4/511)

The trichothecene family of mycotoxins inhibit protein synthesis by binding to the ribosomal peptidyltransferase site. Inhibitors of the peptidyltransferase reaction (e.g. anisomycin) can trigger a ribotoxic stress response that activates c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinases, components of a signaling cascade that regulates cell survival in response to stress. We have found that selected trichothecenes strongly activate JNK/p38 kinases and induce rapid apoptosis in Jurkat T cells. Although the ability of individual trichothecenes to inhibit protein synthesis and activate JNK/p38 kinases are dissociable, both effects contribute to the induction of apoptosis. Among trichothecenes that strongly activate JNK/p38 kinases, induction of apoptosis increases linearly with inhibition of protein synthesis. Among trichothecenes that strongly inhibit protein synthesis, induction of apoptosis increases linearly with activation of JNK/p38 kinases. Trichothecenes that inhibit protein synthesis without activating JNK/p38 kinases inhibit the function (i.e. activation of JNK/p38 kinases and induction of apoptosis) of apoptotic trichothecenes and anisomycin. Harringtonine, a structurally unrelated protein synthesis inhibitor that competes with trichothecenes (and anisomycin) for ribosome binding, also inhibits the activation of JNK/p38 kinases and induction of apoptosis by trichothecenes and anisomycin. Taken together, these results implicate the peptidyltransferase site as a regulator of both JNK/p38 kinase activation and apoptosis.  (+info)

Translational homeostasis: eukaryotic translation initiation factor 4E control of 4E-binding protein 1 and p70 S6 kinase activities. (5/511)

Eukaryotic translation initiation factor 4E (eIF4E) is the mRNA 5' cap binding protein, which plays an important role in the control of translation. The activity of eIF4E is regulated by a family of repressor proteins, the 4E-binding proteins (4E-BPs), whose binding to eIF4E is determined by their phosphorylation state. When hyperphosphorylated, 4E-BPs do not bind to eIF4E. Phosphorylation of the 4E-BPs is effected by the phosphatidylinositol (PI) 3-kinase signal transduction pathway and is inhibited by rapamycin through its binding to FRAP/mTOR (FK506 binding protein-rapamycin-associated protein or mammalian target of rapamycin). Phosphorylation of 4E-BPs can also be induced by protein synthesis inhibitors. These observations led to the proposal that FRAP/mTOR functions as a "sensor" of the translational apparatus (E. J. Brown and S. L. Schreiber, Cell 86:517-520, 1996). To test this model, we have employed the tetracycline-inducible system to increase eIF4E expression. Removal of tetracycline induced eIF4E expression up to fivefold over endogenous levels. Strikingly, upon induction of eIF4E, 4E-BP1 became dephosphorylated and the extent of dephosphorylation was proportional to the expression level of eIF4E. Dephosphorylation of p70(S6k) also occurred upon eIF4E induction. In contrast, the phosphorylation of Akt, an upstream effector of both p70(S6k) and 4E-BP phosphorylation, was not affected by eIF4E induction. We conclude that eIF4E engenders a negative feedback loop that targets a component of the PI 3-kinase signalling pathway which lies downstream of PI 3-kinase.  (+info)

Tri-iodothyronine increases insulin-like growth factor binding protein-2 expression in cultured hepatocytes from hypothyroid rats. (6/511)

Previous evidence suggests the existence of a thyroid hormone-IGF axis in the liver and changes in hepatic insulin-like growth factor binding protein (IGFBP) expression in rats with altered thyroid status have been previously reported. The aim of this study was to check if the higher IGFBP-2 mRNA levels observed in liver of hypothyroid rats could be due to a direct effect of thyroid hormone on the IGFBP-2 gene. In our experiments, cultured hepatocytes isolated from normal and hypothyroid adult rats were used. Northern blot analysis revealed barely detectable IGFBP-2 mRNA in normal rat hepatocytes, but easily detectable signal in hypothyroid rat cells. Therefore, the effect of tri-iodothyronine (T3) was investigated using cultured hepatocytes from hypothyroid rats as an in vitro model. The IGFBP-2 message was increased in a dose-dependent manner in hepatocytes cultured for 12-24 h in the presence of T3. A similar increase occurred in accumulation of IGFBP-2 in the culture medium, as measured by RIA. The effect of T3 on IGFBP-2 transcript levels appeared to consist of enhanced gene transcription and was independent of ongoing protein synthesis, but it was completely abolished by the incubation of hepatocytes with insulin. The latter result confirmed the dominant role of insulin in regulating IGFBP-2 expression by cultured hepatocytes. In vivo experiments confirmed an increase in hepatic IGFBP-2 mRNA and serum IGFBP-2 levels in hypothyroid rats and demonstrated, in addition, a significant increase in these measures in T3-treated rats. Taken together, our in vitro and in vivo results support a role for a thyroid hormone-IGF axis in the liver and suggest that other factors, such as insulin, interact in vivo with thryoid hormone in regulating hepatic IGFBP-2 expression.  (+info)

MEK kinase 3 directly activates MKK6 and MKK7, specific activators of the p38 and c-Jun NH2-terminal kinases. (7/511)

Mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase kinase kinase 3 (MEKK3) activates the c-Jun NH2-terminal kinase (JNK) pathway, although no substrates for MEKK3 have been identified. We have examined the regulation by MEKK3 of MAPK kinase 7 (MKK7) and MKK6, two novel MAPK kinases specific for JNK and p38, respectively. Coexpression of MKK7 with MEKK3 in COS-7 cells enhanced MKK7 autophosphorylation and its ability to activate recombinant JNK1 in vitro. MKK6 autophosphorylation and in vitro activation of p38alpha were also observed following coexpression of MKK6 with MEKK3. MEKK2, a closely related homologue of MEKK3, also activated MKK7 and MKK6 in COS-7 cells. Importantly, immunoprecipitates of either MEKK3 or MEKK2 directly activated recombinant MKK7 and MKK6 in vitro. These data identify MEKK3 as a MAPK kinase kinase specific for MKK7 and MKK6 in the JNK and p38 pathways. We have also examined whether MEKK3 or MEKK2 activates p38 in intact cells using MAPK-activated protein kinase-2 (MAPKAPK2) as an affinity ligand and substrate. Anisomycin, sorbitol, or the expression of MEKK3 in HEK293 cells enhanced MAPKAPK2 phosphorylation, whereas MEKK2 was less effective. Furthermore, MAPKAPK2 phosphorylation induced by MEKK3 or cellular stress was abolished by the p38 inhibitor SB-203580, suggesting that MEKK3 is coupled to p38 activation in intact cells.  (+info)

Use of a drug-resistant mutant of stress-activated protein kinase 2a/p38 to validate the in vivo specificity of SB 203580. (8/511)

Stress-activated protein kinase 2a, also called p38, is inhibited by SB 203580 and this drug has been used widely to implicate this enzyme in the regulation of many physiological processes. Here, we introduce a novel method of general application, which can be used to establish whether the effects of SB 203580 are mediated via inhibition of stress-activated protein kinase 2a/p38 or whether they result from 'non-specific' effects. Four events thought to occur upon activation of stress-activated protein kinase 2a/p38 have been established unequivocally. These are the activation of mitogen-activated protein kinase-activated protein kinase-2 and mitogen- and stress-activated protein kinase-1 and the phosphorylation of their presumed substrates, heat shock protein 27 and the transcription factor cyclic AMP response element binding protein, respectively. In contrast, the SB 203580-induced activation of c-Raf is independent of stress-activated protein kinase 2a/p38 inhibition.  (+info)

*Memory consolidation

... by means of immediate amygdala infusions of the protein synthesis inhibitor anisomycin, but not by infusions made six hours ... the protein synthesis inhibitor anisomycin) and both require the transcription factor CREB. However, recent amygdala research ...

*Anisomycin

... interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system. Anisomycin ... Injection of anisomycin into the hippocampus has been proposed for selective removal of memories. Despite anisomycin's wide ... Butler, K. (1966). "Anisomycin. II.1 Biosynthesis of Anisomycin". The Journal of Organic Chemistry. 31 (1): 317-20. doi:10.1021 ... Anisomycin can activate stress-activated protein kinases, MAP kinase and other signal transduction pathways. Anisomycin is ...

*Translation (biology)

These include anisomycin, cycloheximide, chloramphenicol, tetracycline, streptomycin, erythromycin, and puromycin. Prokaryotic ...

*Haloferax larsenii

Sensitivity to novobiocin, bacitracin, anisomycin, aphidicolin, and rifampicin have been observed. However, no sensitivity has ...

*De novo protein synthesis theory of memory formation

When anisomycin is applied to the hippocampus, active memories are unable to fully consolidate and are lost. Interestingly, ... In research, commonly used PSI's include anisomycin, cycloheximide, and puromycin - although the use of puromycin has stopped ... anisomycin has been shown to cause a substantial catecholamine release that co-occurs with neural suppression, which has not ... Anisomycin administered at a dose that inhibits 95% of protein synthesis and associated electrical activity is not the highest ...

*ELK3

Ducret C, Maira SM, Dierich A, Wasylyk B (2000). "The net repressor is regulated by nuclear export in response to anisomycin, ...

*Anoikis

Anisomycin achieved this anti-metastatic activity in part by decreasing the abundance of the death receptor inhibiting protein ... showed that anisomycin can sensitize metastatic epithelial cells to anoikis and reduce circulating tumor cell implantation in ... September 2007). "A chemical screen identifies anisomycin as an anoikis sensitizer that functions by decreasing FLIP protein ...

*Animal cognition

... but not medium-term retention of olfactory memory in honeybees is impaired by actinomycin D and anisomycin". European Journal ...

*Long-term potentiation

Frey U, Krug M, Reymann K, Matthies H (1988). "Anisomycin, an inhibitor of protein synthesis, blocks late phases of LTP ...

*Streptomyces griseolus

... and the antibiotics anisomycin and sinefungin. Xu, Wenping; Tao, Liming; Gu, Xuebin; Shen, Xiaoxia; Yuan, Sheng (September 2009 ...

*Hippocampal memory encoding and retrieval

After receiving post-retrieval an intra-amygdalar infusion of a known amnesic agent, anisomycin, rats failed to recall a ...

*Protein biosynthesis

The capacity of disabling or inhibiting translation in protein biosynthesis is used by some antibiotics such as anisomycin, ...

*Kaang Bong-kiun

... the infusion of proteasome inhibitors into the CA1 of the hippocampus immediately after retrieval prevented anisomycin-induced ...

*ZAK

2005). "Complete inhibition of anisomycin and UV radiation but not cytokine induced JNK and p38 activation by an aryl- ...

*List of MeSH codes (D03)

... anisomycin MeSH D03.383.773.107 --- bepridil MeSH D03.383.773.165 --- clemastine MeSH D03.383.773.170 --- 3,4-dichloro-n-methyl ...

*P53 upregulated modulator of apoptosis

... the death effector TRAIL or chemical drugs such as anisomycin. PUMA protein is degraded in a proteasome dependent manner and ...

*Fermentek

Anisomycin, Thiolutin, Wortmannin, K252a, Staurosporine, K252C, Bafilomycin, Alamethicin, Leptomycin, A23187, Chelerythrine, ... Anisomycin, Thapsigargin, cyclopamine, Thiostrepton, Staurosporine, Mithramycin, Midostaurin, Wortmannin, K252a, Geldanamycin ...

*List of biomolecules

Anabolic steroid Anethole Angiotensinogen Anisomycin Antidiuretic hormone (ADH) Arabinose Arginine Ascomycin Ascorbic acid ( ...

*Jun dimerization protein

... and anisomycin treatment or JDP2 is also regulated by other kinases such as p38 MAPK and doublecortin like protein kinase. ...
The protein synthesis inhibitor anisomycin features a unique benzylpyrrolidine system and exhibits diverse biological and pharmacologic activities. Its biosynthetic origin has remained obscure for more than 60 y, however. Here we report the identification of the biosynthetic gene cluster (BGC) of anisomycin in Streptomyces hygrospinosus var. beijingensis by a bioactivity-guided high-throughput screening method. Using a combination of bioinformatic analysis, reverse genetics, chemical analysis, and in vitro biochemical assays, we have identified a core four-gene ensemble responsible for the synthesis of the pyrrolidine system in anisomycin: aniQ, encoding a aminotransferase that catalyzes an initial deamination and a later reamination steps; aniP, encoding a transketolase implicated to bring together an glycolysis intermediate with 4-hydroxyphenylpyruvic acid to form the anisomycin molecular backbone; aniO, encoding a glycosyltransferase that catalyzes a cryptic glycosylation crucial for ...
It is generally accepted that memory formation involves an irreversible passage via labile phases to the stable form of long-term memory impervious to amnestic agents such as protein synthesis inhibitors. However, recent experiments demonstrate that reactivation of memory by way of a reminder renders it labile to such inhibitors, suggesting that such retrieval is followed by a so-called reconsolidation process similar or identical in its cellular and molecular correlates to that occurring during the initial consolidation. We compared the effects of the protein synthesis inhibitor anisomycin and the glycoprotein synthesis inhibitor 2-deoxygalactose on the temporal dynamics and pharmacological sensitivity of initial consolidation and memory expression following a reminder in a one-trial passive-avoidance task in day-old chicks. This comparison revealed three differences between the action of the inhibitors on newly formed compared with reactivated memory. First, the recall deficit after the ...
Memory traces, once established, are no longer sensitive to disruption by metabolic inhibitors. However, memories reactivated by reminder are once again vulnerable, in a time-dependent manner, to amnestic treatment. To determine whether the metabolic events following a reminder recapitulate those following initial training we examined the temporal dynamics of amnesia induced by the protein synthesis inhibitor anisomycin and the glycosylation inhibitor 2-deoxygalactose. The effects of both were transient and dependent on time of reminder post-training and time of injection relative to reminder, and differed from those following initial training. 2-[C-14]-deoxyglucose uptake increased in two brain regions, the intermediate medial hyperstriatum ventrale (IMHV) and lobus parolfactorius (LPO) following reminder as it did following training, but the increase was bilateral rather than confined to the left hemisphere and was more marked in LPO than IMHV. C-fos expression after reminder was increased ...
BioAssay record AID 327182 submitted by ChEMBL: Inhibition of JNK1 in rat H9c2 cells assessed as inhibition of anisomycin-induced cJun phosphorylation after 30 mins.
In this paper, we report that (+)-preussin, a pyrrolidinol alkaloid originally identified as an antifungal agent, has growth-inhibitory and cytotoxic effects on human cancer cells. Preussin was found to be a potent inhibitor of cyclin E kinase (CDK2-cyclin E) in vitro (50% inhibitory concentration; approximately 500 nM) and to inhibit cell cycle progression into S phase. In agreement with these findings, the level of the cyclin-dependent kinase inhibitor p27(KIP-1) is increased in response to preussin treatment while the expression of both cyclin A and the transcription factor E2F-1 is down-regulated. Preussin also induces programmed cell death (apoptosis), which requires caspase activation and involves the release of cytochrome c from mitochondria. This induction of apoptosis is not blocked by high levels of Bcl-2, which usually confers resistance to chemotherapeutic agents. Taken together, our data indicate that preussin could be a promising lead compound for the development of a new class of potent
Buy Anisomycin (CAS 22862-76-6), a protein synthesis inhibitor. Join researchers using high quality Anisomycin from Abcam and achieve your mission, faster.
Anisomycin is a pyrrolidine antibiotic, acts as an anti-fungal antibiotic which inhibits Protein Synthesis, also is a potent activator of SAPKs/JNKs. ...Quality confirmed by NMR,HPLC & MS.
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The data presented here demonstrate that blocking dopaminergic signaling within the BLA either at the D1R with SCH23390 or at the D2R with raclopride prevented the amnesia that normally follows post-reactivation protein synthesis inhibition. Therefore, the CS−sucrose memory, retrieved and behaviorally expressed during the memory reactivation session, did not require protein synthesis in order to restabilize and subsequently persist-consistent with the hypothesis that activity at either D1Rs or D2Rs is required for destabilization of the CS−sucrose memory. That the memorys persistence was independent of protein synthesis cannot be attributed to the parameters of the memory reactivation session, since rats having received intra-amygdala vehicle infusions prior to reactivation were subsequently amnesic at test following post-reactivation administration of the protein synthesis inhibitor anisomycin. Furthermore, nonselective antagonism at dopamine receptors with α-flupenthixol did not block ...
In the yeast Saccharomyces cerevisiae this methylation is important for resistance towards hydrogen peroxide and the antibiotic anisomycin.
Focus Biomolecules is a supplier of Anisomycin, Trichostatin A, Latrunculin a, IBMX, DMOG, 1400W, ampk activators, pde inhibitors and many other biomolecules for research. From the industry experience they set out to refine the practices of small molecule based life sciences companies and eliminate the challenges too often found by customers.. ...
Studies were performed to investigate whether electrically-induced long-term depression (LTD) within rat hippocampal slices in vitro shares any common cellular features with LTD in the intact animal, with particular emphasis being placed on mechanisms required for its late maintenance. Our initial studies have led to the development of stimulation protocols which are able to reliably produce different forms of LTD. Depending on the induction protocol applied, we are able to demonstrate a transient protein synthesis-independent early-LTD with a duration of up to 3-4 h, together with a de novo protein synthesis-dependent late-LTD lasting for at least 8 h. Furthermore, we are able to show input-specific LTD within the CA1 region, with expression shown only by those synapses specifically stimulated by a low-frequency protocol. These studies are important pre-requisites to investigate mechanisms of synaptic tagging and late-associativity during LTD ...
In innate immune responses, induction of type‐I interferons (IFNs) prevents virus spreading while viral replication is delayed by protein synthesis inhibition. We asked how cells perform these apparently contradictory activities. Using single fibroblast monitoring by flow cytometry and mathematical modeling, we demonstrate that type‐I IFN production is linked to cells ability to enter dsRNA‐activated PKR‐dependent translational arrest and then overcome this inhibition by decreasing eIF2α phosphorylation through phosphatase 1c cofactor GADD34 (Ppp1r15a) expression. GADD34 expression, shown here to be dependent on the IRF3 transcription factor, is responsible for a biochemical cycle permitting pulse of IFN synthesis to occur in cells undergoing protein synthesis inhibition. Translation arrest is further demonstrated to be key for anti‐viral response by acting synergistically with MAVS activation to amplify TBK1 signaling and IFN‐β mRNA transcription, while GADD34‐dependent protein ...
Cells respond to diverse stimuli, which include physiological agents such as growth factors (reviewed in Bravo, 1990; Marshall, 1994) and cytokines (Freshney et al., 1994; Sluss et al., 1994), pharmacological compounds such as anisomycin (Edwards and Mahadevan, 1992; Hazzalin et al., 1998, and references therein), phorbol esters and okadaic acid (reviewed in Cohen, 1990; Cano et al., 1995) and stresses such as UV radiation (Hibi et al., 1993; Kyriakis et al., 1994), hyperosmotic (Han et al., 1994; Rosette and Karin, 1996) and heavy metal stress (Rouse et al., 1994, and references therein) by initiating intracellular signalling mechanisms that rapidly elicit transcription of a subset of genes in the nucleus (reviewed in Karin, 1994; Cano and Mahadevan, 1995; Treisman, 1996; Hazzalin et al., 1998). These genes, called immediate‐early (IE) genes, are activated directly and require no new transcription or translation for their induction (Greenberg et al., 1986; Almendral et al., 1988; reviewed in ...
Memory, Taste, Amygdala, Anisomycin, Rats, Learning, Inhibition, Long-term Memory, Dopamine, Short-term Memory, Administration, Animals, Association, Glutamate, Microdialysis, Hippocampus, Temporal Lobe, Brain, Saccharin, Time
Protein kinase B (PKB) isoforms became activated [and glycogen synthase kinase-3 (GSK3) became inhibited] when mouse Swiss 3T3 fibroblasts were exposed to oxidative stress (H2O2) or heat shock, but not when they were exposed to osmotic shock (0.5 M sorbitol or 0.7 M NaCl), chemical stress (sodium arsenite), the protein-synthesis inhibitor anisomycin, or UV radiation. In contrast, all seven stimuli activated mitogen-activated protein kinase-activated protein kinase-2 (MAPKAP-K2). The activation of MAPKAP-K2 was suppressed by the drug SB 203580, but not by inhibitors of phosphoinositide (phosphatidylinositide, PI) 3-kinase. In contrast, the activation of PKB isoforms and the inhibition of GSK3 by oxidative stress or heat shock were prevented by inhibitors of PI 3-kinase, but not by SB 203580. Thus the activation of PKB by oxidative stress or heat shock is mediated by PI 3-kinase and not by MAPKAP-K2. PKBα and PKBγ were also activated by heat shock and oxidative stress in human embryonic kidney ...
MAPKAPK5-AS1 - (untagged)-Homo sapiens, clone MGC:15178 IMAGE:4122851, complete cds available for purchase from OriGene - Your Gene Company.
The ribotoxic stress response, which is conserved between prokaryotes and eukaryotes, is a cellular reaction to cytotoxic interference with the function of the 3′-end of the large (23 S/28 S) ribosomal RNA. The 3′-end of the large rRNA is directly involved in the three sequential steps of translational elongation: the aminoacyl-tRNA binding, the peptidyl transfer, and the ribosomal translocation. In mammalian cells, the ribotoxic stress response involves activation of the stress-activated protein kinase/c-Jun NH2-terminal kinase and the p38 mitogen-activated protein kinase and transcriptional induction of immediate early genes such as c-fos and c-jun. Active ribosomes are essential mediators of the ribotoxic stress response. We demonstrate here that the transcriptional response of mammalian cells to ultraviolet radiation (UV response) displays the characteristics of a ribotoxic stress response, inasmuch as (i) the activation of stress kinases and gene expression in response to UV requires the
Several studies have demonstrated that the intrinsic catalytic activity of cell surface glucose transporters is highly regulated in 3T3-L1 adipocytes expressing GLUT1 (erythrocyte/brain) and GLUT4 (adipocyte/skeletal muscle) glucose transporter isoforms. For example, inhibition of protein synthesis in these cells by anisomycin or cycloheximide leads to marked increases in hexose transport without a change in the levels of cell surface glucose transporter proteins (Clancy, B. M., Harrison, S. A., Buxton, J. M., and Czech, M. P. (1991) J. Biol. Chem. 266, 10122-10130). In the present work the exofacial hexose binding sites on GLUT1 and GLUT4 in anisomycin-treated 3T3-L1 adipocytes were labeled with the cell-impermeant photoaffinity reagent [2-3H]2-N-[4-(1-azitrifluoroethyl)benzoyl]-1,3-bis- (D-mannos-4-yloxy)-2-propylamine [( 2-3H] ATB-BMPA) to determine which isoform is activated by protein synthetic blockade. As expected, a 15-fold increase in 2-deoxyglucose uptake in response to insulin was associated
Animals and protocols. Sixty adult male Long-Evans rats (8 weeks of age; raised within our stock) were used in four experiments. First, the level of PSI after an intracortical injection of anisomycin (ANI) was assessed at three different time points in motor cortex and at one time point in parietal cortex and cerebellum (n = 3 in each group). Second, the spread of the injected volume of anisomycin in motor cortex, parietal cortex, and cerebellum was simulated by injections of India ink (five rats per site) (Berman and Dudai, 2001). Third, motor skill learning was evaluated after inducing PSI in contralateral motor cortex or in ipsilateral cerebellum (relative to the trained forelimb) by injection of ANI immediately after training sessions (days) 1 and 2. At identical time points, control groups received vehicle injections into motor cortex or ANI injections into contralateral parietal cortex (n = 6 per group). Skill training was continued until session 8. The investigator training the animals ...
La proteína quinasa 2 activada por MAP quinasas (MAPKAPK2) es una enzima codificada en humanos por el gen HGNC MAPKAPK2 .[1]​[2]​ Esta proteína pertenece a la familia de las serina/treonina quinasas. MAPKAPK2 es regulada por medio de una fosforilación directa llevada a cabo por la MAP quinasa p38. Esta quinasa, junto con p38, parece estar implicada en multitud de procesos celulares incluyendo repuestas a estrés y a inflamación, exportación nuclear, regulación de la expresión génica y proliferación celular. La proteína de choque térmico Hsp27 ha demostrado ser uno de los sustratos de MAPKAPK2 en ensayos in vivo. Se han descrito dos variantes transcripcionales del gen que codifica esta quinasa, las cuales codifican dos isoformas de la enzima.[3]​ La proteína MAPKAPK2 ha demostrado ser capaz de interaccionar con: MAPK14[4]​[5]​ AKT1[4]​ PHC2[6]​ SHC1[6]​ SB 203580, suprime la activación de MAPKAPK2. Zu YL, Wu F, Gilchrist A, Ai Y, Labadia ME, Huang CK (Jun de 1994). ...
In this episode of the Wise Counsel Podcast, Bruce Ecker describes the core treatment method of Coherence Therapy. Ecker relates this method to emerging neuropsychological research on memory reconsolidation, a naturally occurring phenomena through which emotional memories can be dissolved and erased. Reconsolidation studies by brain scientists have shown that under special circumstances, the physical storage of emotional memories is unlocked by reactivation of the stored knowledge and is then reconsolidated back into a stable condition after a few hours. During that window, it is possible for new learnings to revise and even erase the existing emotional knowledge and the behavioral responses that it drives. Ecker maintains that the same reconsolidation process demonstrated in contemporary neuroscience research seems to be at work in coherence therapy and accounts for clinical observations of profound change and lasting relief from longstanding symptoms of many kinds.
Hi,. Would really appreciate if somone could help me understand the role of treating cells with cycloheximide? Is this a protein synthesis inhibitor ? If for example, a particular treatment (e.g. treatment X) decreases beta-catenin protein levels, investigators treat cells with treatment X alone or in combination with Cycloheximide to determine if beta-catenin inhibition is a result of degradation? Why do they mention degradation if Cycloheximide is a protein synthesis inhibitor? The journals mention that beta catenin is down regulated after treatmemnt with X and also in combination Cycloheximide, therefore suggesting inhibition of beta catenin is a result of increased degradation? I thought MG132 is used to determine degradation by proteasome?. ...
Apoptosis is important for tissue homeostasis and is the mechanism of cell death induced by many anticancer agents. The apoptotic machinery is present in all cells, such that tight regulation must exist to prevent untimely cell and tissue death. To avert apoptotic death, cells utilize survival signaling pathways including the PI3 kinase/Akt and MEK/ERK pathways. Inhibitors of serine/threonine protein phosphatases can inhibit drug-induced apoptosis, implicating these phosphatases in regulation of apoptotic pathways. Here, we determined which protein phosphatases (PP) are critical for this protection from apoptosis, and investigated the relationship between phosphatases and survival pathways. An apoptotic signal can be delivered through a receptor pathway or via drug-induced stress that triggers death via mitochondrial events. Chemical inhibitors of protein phosphatases, calyculin A, okadaic acid and tautomycin, prevented anisomycin-induced apoptosis, a model of the latter pathway. Concentrations ...
Apoptosis is important for tissue homeostasis and is the mechanism of cell death induced by many anticancer agents. The apoptotic machinery is present in all cells, such that tight regulation must exist to prevent untimely cell and tissue death. To avert apoptotic death, cells utilize survival signaling pathways including the PI3 kinase/Akt and MEK/ERK pathways. Inhibitors of serine/threonine protein phosphatases can inhibit drug-induced apoptosis, implicating these phosphatases in regulation of apoptotic pathways. Here, we determined which protein phosphatases (PP) are critical for this protection from apoptosis, and investigated the relationship between phosphatases and survival pathways. An apoptotic signal can be delivered through a receptor pathway or via drug-induced stress that triggers death via mitochondrial events. Chemical inhibitors of protein phosphatases, calyculin A, okadaic acid and tautomycin, prevented anisomycin-induced apoptosis, a model of the latter pathway. Concentrations ...
Despite advances in anti-inflammatory therapy, the US cattle industry now loses over $1 billion annually due to Gram-negative infections. In light of reduced lymphocyte proliferation concurrent with decreased cyclooxygenase-2 and matrix metalloproteinase-9 expression in bovine lactoferrin (bLF)-supplemented cells, we intended to show that bLF and the lactoferricin B (LFcin B) peptide, proven antibiotic agents, can also serve as low-risk anti-inflammatory agents, and hypothesized their ability to influence p38 MAPK signaling which is critical in macrophage-mediated inflammation. While LF is present in neutrophils, it is anticipated that enzymatic activity within infective sites will heighten local LFcin B concentrations.. Following pre-treatment with either bLF, the selective p38 MAPK inhibitor SB203580 (SB), or LFcin B, monocytes isolated from healthy 1 wk. to 5 mo old cattle stimulated with either lipopolysaccharide (LPS) or anisomycin (Aniso), were evaluated for iNOS, IL-1β and TNF-α ...
Protein synthesis machinery, including ribosomes, is somewhat different in bacteria compared to mammalian cells. This accounts for the selectivity of this group of drugs for bacteria. Some textbooks and instructors make a point of having students know which ribosomal subunit a class of drugs binds to. However, this is not of primary importance. If you already know it, try not to forget it. If you are struggling with the antimicrobials at this point, save this fact for later. These drugs require binding to an intracellular protein (ribosomal subunit). Therefore, the drugs need to gain entry into the cell. A major route of resistance for the bacteria is to block the movement of the drugs into the cell. ...
Reference: Polikarpova L.I., Effect of protein synthesis inhibitors on the hormonal induction of alanine and aspartate aminotransferases in the liver of sexually mature male rats, Voprosy meditsinskoi khimii, 1974, vol: 20(2), 215-217 ...
Memory can be divided according to different temporal phases: acquisition, consolidation, and retrieval. The consolidation phase is divided into molecular consolidation (range of hours after acquisition) and system consolidation (range of weeks and months after acquisition) (Dudai, 2004). Molecular consolidation is thought to be a protein synthesis-dependent process (Alberini, 2008; Costa-Mattioli et al., 2009). The clear effect of protein synthesis inhibitors on long-term memory was studied extensively mainly in the context of late-phase long-term potentiation (LTP) (Abraham and Williams, 2008). Similar molecular mechanisms were proposed for maintenance of long-term synaptic modifications and learning processes (Davis and Squire, 1984; Costa-Mattioli et al., 2009). However, long-term memory is not supported only by modulation of synaptic strength; modifications in intrinsic neuronal properties also subserve learning-related behavioral changes (Saar and Barkai, 2003; Zhang and Linden, 2003; ...
Summary: During the past 15 years, the memory research field has increased interest in examining the consequences of retrieving a memory. The finding that inhibition of protein synthesis after retrieval was able to impair the original memory led to the construction of the destabilization-reconsolidation theory. There is accumulating evidence that, under certain conditions, retrieval can result in memory reconsolidation. However, for an associative memory, retrieval can also engage extinction of the original association. Recently, a handful of studies have started to identify the boundaries between reconsolidation and extinction with quite surprising results. In addition, there is also new evidence that indicates that memory expression might not be a required condition for reconsolidation to occur. In this symposium, we will discuss these subjects with pioneering scientists that have actively tried to identified the system, cellular and molecular establishment of the boundaries between ...
Mapkapk2 - Mapkapk2 (Myc-DDK-tagged) - Mouse MAP kinase-activated protein kinase 2 (Mapkapk2) available for purchase from OriGene - Your Gene Company.
Mouse monoclonal antibody raised against recombinant MAPKAPK5. Recombinant protein corresponding to human MAPKAPK5. (MAB10404) - Products - Abnova
Fear memories, here defined as learned associations between a stimulus and a physiological fear reaction, are formed through fear conditioning. In animals, fear memories, present in the lateral amygdala, undergo reconsolidation after recall. Moreover, this reconsolidation process can be disrupted both pharmacologically and behaviourally, resulting in a reduced fear response to the stimulus. This thesis examines the attenuation of fear memories by disrupting reconsolidation in humans, using measures of both the central and peripheral nervous system activity. Serotonergic and dopaminergic genes have previously been tied to both fear conditioning and anxiety disorders, where fear conditioning mechanisms are important. In order to evaluate the possible role of fear memory reconsolidation mechanims in the effect on fear and anxiety by these genes, this thesis also compare the reconsolidation disruption effect between different serotonergic and dopaminergic genotypes.. Study I examined the ...
The inhibition of protein synthesis in eukaryotic cells will prevent them from entering mitosis. Emetine inhibits peptide elongation. When it was added to asynchronous populations of Chinese hamster ovary (CHO) cells, the mitotic index decreased sharply 30 to 40 min later. It was found that the inhibitory effect of emetine could be reversed when it was removed and the reversibility was dependent on both the initial concentration of emetine and the pH of the medium. Cell populations that were blocked by emetine for up to 2h showed a four- to fivefold increase in mitotic index approximately 1 h after the emetine was removed. These results indicate that there is a point or period in G2 phase at which critical mitotic proteins are being synthesized, and if their synthesis is interrupted cells will fail to enter mitosis. ...
TY - JOUR. T1 - Exploratory synthetic studies of the α-methoxylation of amides via cuprous ion-promoted decomposition of o-diazobenzamides. AU - Han, Gyoonhee. AU - LaPorte, Matthew G.. AU - McIntosh, Mathias C.. AU - Weinreb, Steven M.. AU - Parvez, Masood. PY - 1996/12/27. Y1 - 1996/12/27. N2 - A convenient nonelectrochemical amide oxidation method has been developed. The process involves a cuprous ion-promoted decomposition of o-diazobenzamides like 4, generated in situ from the corresponding o-aminobenzamides, to give N-acyliminium ion intermediate 9 via a 1,5-H-atom transfer, followed by metal-catalyzed oxidation of the resulting α-amidyl radical. The transformation produces α-methoxybenzamides 15 in good yields. An attempt was made to apply this oxidation method to a total synthesis of the alkaloid (-)-anisomycin (16). Scalemic o-aminobenzamide pyrrolidine derivatives 18a/18b underwent oxidation to give α-methoxylated amide substrates 19a/19b, respectively, in good yields. However, ...
Contact Us. Tel:732-484-9848. Fax:888-484-5008. Email:[email protected]. Add:1 Deer Park Dr, Suite Q,. Monmouth Junction, NJ 08852, USA. ...
Despite substantial therapeutic advances, Posttraumatic Stress Disorder (PTSD) remains difficult to treat. One promising new area of research is in post-reactivation pharmacologic intervention, which is based upon the concept of blockade of memory reconsolidation. Recent animal research suggests that reactivation (retrieval) of a stored memory can return it to a labile (alterable) state from which it must be restabilized in order to persist. This process is called reconsolidation, and various drugs have been found to block it in animals. This blockade may lead to a weakening of the original memory trace.. The aim of this study is to pilot the effect of mifepristone on physiologic responding during traumatic imagery. Although mifepristone is widely and safely used to cause a medical abortion, it is also a powerful stress hormone receptor blocker. These stress hormones, called glucocorticoids, may enhance memory (re)consolidation. Indeed, a recent study in animals reported that mifepristone ...
The trichothecenes, a group of sesquiterpenoid mycotoxins commonly encountered as food contaminants worldwide, have been etiologically linked to human and anima...
Mouse monoclonal antibody raised against a full length recombinant MAPKAPK2. MAPKAPK2 (NP_116584, 266 a.a. ~ 352 a.a) full length recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. (H00009261-M02) - Products - Abnova
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies. ...

Anisomycin | AbcamAnisomycin | Abcam

Join researchers using high quality Anisomycin from Abcam and achieve your mission, faster. ... Anisomycin activates p38 MAP kinase to induce LTD in mouse primary visual cortex.. Brain Res 1085:68-76 (2006). Read more ( ... Anisomycin-activated protein kinases p45 and p55 but not mitogen-activated protein kinases ERK-1 and -2 are implicated in the ... The cells were incubated at 37°C for 6h in media containing different concentrations of ab120495 (anisomycin) in DMSO, fixed ...
more infohttp://www.abcam.com/anisomycin-ab120495.html

Anisomycin|Flagecidin;Wuningmeisu C|CAS 22862-76-6 Buy Anisomycin from supplier medchemexpress.comAnisomycin|Flagecidin;Wuningmeisu C|CAS 22862-76-6 Buy Anisomycin from supplier medchemexpress.com

Anisomycin is a pyrrolidine antibiotic, acts as an anti-fungal antibiotic which inhibits Protein Synthesis, also is a potent ... Anisomycin causes an increase in the number of apoptotic cells in MDA-MB-468 cultures, but not in MDA16 cultures. Anisomycin ... Target: antibiotic in vitro: Anisomycin inhibits EAC cell proliferation in concentration-dependent manner. [2] Anisomycin (3 μM ... Anisomycin (Synonyms: Flagecidin; Wuningmeisu C). Cat. No.: HY-18982 Purity: 98.03% Data Sheet SDS Handling Instructions ...
more infohttp://www.medchemexpress.com/Anisomycin.html

AID 327182 - Inhibition of JNK1 in rat H9c2 cells assessed as inhibition of anisomycin-induced cJun phosphorylation after 30...AID 327182 - Inhibition of JNK1 in rat H9c2 cells assessed as inhibition of anisomycin-induced cJun phosphorylation after 30...

Inhibition of JNK1 in rat H9c2 cells assessed as inhibition of anisomycin-induced cJun phosphorylation after 30 mins. ...
more infohttps://pubchem.ncbi.nlm.nih.gov/bioassay/327182

The effects of anisomycin (a protein synthesis inhibitor) on spatial 
learning and memory in CA1 region of rats hippocampusThe effects of anisomycin (a protein synthesis inhibitor) on spatial learning and memory in CA1 region of rats hippocampus

Anisomycin inhibits the late maintenance of long-term depression in rat hippocampal slices in vitro.. Sajikumar S, Frey JU.. ... Anisomycin. Neurosci Lett 2003 Feb 27;338(2):147-50. Related Articles, Links ...
more infohttp://anisomycin.noneto.com/a3.htm

Ribosome-translocon complex mediates calcium leakage from endoplasmic reticulum stores | Journal of Cell ScienceRibosome-translocon complex mediates calcium leakage from endoplasmic reticulum stores | Journal of Cell Science

Anisomycin (a peptidyl transferase inhibitor) inhibits the puromycin reaction (Ioannou et al., 1998). Anisomycin alone did not ... Anisomycin prevents puromycin-induced luminal calcium release. To be sure that puromycin induces a decrease in [Ca2+]ER by ... Anisomycin at 200 μM was also used (Fig. 3B). During the dye loading and throughout the experiment, the cells were in the ... Anisomycin blocks the calcium leak from intracellular stores induced by puromycin. (A,B) The intracellular stores of LNCaP ...
more infohttp://jcs.biologists.org/content/117/18/4135

Most recent papers with the keyword cryptical biosynthesis | Read by QxMDMost recent papers with the keyword cryptical biosynthesis | Read by QxMD

Here we report the identification of the biosynthetic gene cluster (BGC) of anisomycin in Streptomyces hygrospinosus var. ... Biosynthesis of the pyrrolidine protein synthesis inhibitor anisomycin involves novel gene ensemble and cryptic biosynthetic ... The protein synthesis inhibitor anisomycin features a unique benzylpyrrolidine system and exhibits diverse biological and ... we have identified a core four-gene ensemble responsible for the synthesis of the pyrrolidine system in anisomycin: aniQ, ...
more infohttps://www.readbyqxmd.com/keyword/95129

Reminder effects: the molecular cascade following a reminder in young chicks does not recapitulate that following training on a...Reminder effects: the molecular cascade following a reminder in young chicks does not recapitulate that following training on a...

... following initial training we examined the temporal dynamics of amnesia induced by the protein synthesis inhibitor anisomycin ...
more infohttp://oro.open.ac.uk/6714/

Anisomycin - wikidocAnisomycin - wikidoc

Anisomycin, also known as Flagecidin (IUPAC name: 3,4-Pyrrolidinediol, 2-[(4-methoxyphenyl)methyl]-, 3-acetate, (2R,3S,4S)-) is ... Mode of action of anisomycin". J. Biol. Chem. 242 (13): 3226-33. PMID 6027796.. Check date values in: ,date=. (help) Free text ... Anisomycin is also mentioned as a potential psychiatric drug, as it may erase "short-range memory" [2]. ... Anisomycin interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system. ...
more infohttps://www.wikidoc.org/index.php?title=Anisomycin&printable=yes

Anisomycin | PromoCellAnisomycin | PromoCell

Anisomycin. Activator of p54 and MAP kinases; induces apoptosis e.g. in the human monoblastoid cell line ...
more infohttps://www.promocell.com/product/anisomycin/

Anisomycin - WikipediaAnisomycin - Wikipedia

Anisomycin interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system. Anisomycin ... Injection of anisomycin into the hippocampus has been proposed for selective removal of memories. Despite anisomycins wide ... Butler, K. (1966). "Anisomycin. II.1 Biosynthesis of Anisomycin". The Journal of Organic Chemistry. 31 (1): 317-20. doi:10.1021 ... Anisomycin can activate stress-activated protein kinases, MAP kinase and other signal transduction pathways. Anisomycin is ...
more infohttps://en.wikipedia.org/wiki/Anisomycin

DON shares a similar mode of action as the ribotoxic stress inducer anisomycin while TBTO shares ER stress patterns with the ER...DON shares a similar mode of action as the ribotoxic stress inducer anisomycin while TBTO shares ER stress patterns with the ER...

... anisomycin), ER stress (thapsigargin) and T cell activation (ionomycin). Genes affected by anisomycin and the majority of genes ... DON shares a similar mode of action as the ribotoxic stress inducer anisomycin while TBTO shares ER stress patterns with the ER ... DON did not affect other genes than anisomycin indicating the effect of DON to be restricted to ribotoxic stress. This study ...
more infohttp://library.wur.nl/WebQuery/wurpubs/478370

AnisomycinAnisomycin

... ,(2R,3S,4S)-2-[(4-Methoxyphenyl)methyl]-3,4-pyrrolidinediol 3-acetate,[2R-(2alpha,3alpha,4beta)]-2-[(4-methoxyphenyl) ... Literature References: Prepn from anisomycin: Nickell et al., US 2935444 (1960 to Pfizer). ...
more infohttp://www.druglead.com/cds/anisomycin.html

Anisomycin - PI3K and MEK Inhibitors in Breast CancerAnisomycin - PI3K and MEK Inhibitors in Breast Cancer

Tag Archive: Anisomycin. Objective Platelets play essential assignments in the pathophysiology of thrombosis and. biotech May ... Conclusions Our data claim that platelet years produced prior to the acute event Anisomycin… Read more ... 31, 2017 H+-ATPase Anisomycin, Gja4 Objective Platelets play essential assignments in the pathophysiology of thrombosis and ...
more infohttp://www.biotech-angels.com/tag/anisomycin/

Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells 
to Fas mediated apoptosis.Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis.

Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis.. Curtin JF, Cotter TG.. ... Anisomycin. Br J Cancer 2002 Nov 4;87(10):1188-94. Related Articles, Links ... Using anisomycin, a potent JNK agonist, we have demonstrated a role for JNK in Fas mediated apoptosis in DU 145 cells. ...
more infohttp://anisomycin.noneto.com/a5.htm

1C) in 50-week-old primary WT tumor cells treated with anisomycin | AKT inhibitor|AKT pathway1C) in 50-week-old primary WT tumor cells treated with anisomycin | AKT inhibitor|AKT pathway

When comparing anisomycin PD0325901 in vitro effect on scAR (lane 1 versus 2; P = 0.04) and siAR (lane 3 versus 4; P = 0.01) ... 1C) in 50-week-old primary WT tumor cells treated with anisomycin. Posted on August 2, 2018 by admin ... anisomycin reduces anoikis in the 50-week-old WT mice scramble (sc)-treated hepatic cells (57% ± 8% to 39% ± 4%; P = 0.04). ... 1C) in 50-week-old primary WT tumor cells treated with anisomycin, we tested AR and p38 effects on cell anoikis. As shown in ...
more infohttp://cellbasedassayblog.com/1c-in-50-week-old-primary-wt-tumor-cells-treated-with-anisomycin-2

Potassium in the structure of Structure of Anisomycin Resistant 50S Ribosomal Subunit: 23S Rrna Mutation G2482C (pdb 3ccu)Potassium in the structure of Structure of Anisomycin Resistant 50S Ribosomal Subunit: 23S Rrna Mutation G2482C (pdb 3ccu)

Structure of Anisomycin Resistant 50S Ribosomal Subunit: 23S Rrna Mutation G2482C ... Potassium in the structure of Structure of Anisomycin Resistant 50S Ribosomal Subunit: 23S Rrna Mutation G2482C (pdb 3ccu). ... The binding sites of Potassium atom in the structure of Structure of Anisomycin Resistant 50S Ribosomal Subunit: 23S Rrna ...
more infohttp://potassium.atomistry.com/pdb3ccu.html

4UJZ CRYSTAL STRUCTURE OF ANISOMYCIN BOUND TO THE YEAST 80S RIBOSOME | 4UJZ L | P15056 | BRAF | Serine/threonine-protein kinase...4UJZ CRYSTAL STRUCTURE OF ANISOMYCIN BOUND TO THE YEAST 80S RIBOSOME | 4UJZ L | P15056 | BRAF | Serine/threonine-protein kinase...

Fullscreen (supported by IE11, latest versions of Firefox, Chrome, Safari (not including iOS Safari), Edge, Chrome for Android, Samsung Internet) ...
more infohttps://cansarblack.icr.ac.uk/target/P15056/3d/4UJZ_L

The Neurocritic: July 2007The Neurocritic: July 2007

... attenuated anisomycin-induced amnesia. In addition, similar to the effects on memory seen with anisomycin, intraamygdala ... ANISOMYCIN IS STRONG In yesterdays story, EVERYTHING IS WRONG [...about protein synthesis and memory formation], The ... No anisomycin necessary. At this stage, one can only speculate on the significance of these findings for the future of PTSD ... Intraamygdala injections of anisomycin before inhibitory avoidance training impaired memory in rats tested 48 h later. Release ...
more infohttps://neurocritic.blogspot.com/2007/07/

Griffin:Antibody Related Solutions & Recipes - OpenWetWareGriffin:Antibody Related Solutions & Recipes - OpenWetWare

Anisomycin. 0.25 mg/ml overnight Camptothecin. 4.0 uM for 4 hours CoCl2. 75 micromolar CoCl2 for 4 hours at 37C ...
more infohttps://openwetware.org/wiki/?title=Griffin:Antibody_Related_Solutions_%252526_Recipes&oldid=546952

AntibioticsAntibiotics

BioVision develops and offers a wide variety of products including assay kits, antibodies, recombinant proteins & enzymes, and other innovative research tools for studying Apoptosis, Metabolism, Cell Proliferation, Cellular Stress, Cell Damage and Repair, Diabetes, Obesity and Metabolic Syndrome, Stem Cell Biology, Gene Regulation, Signal Transduction, etc. BioVisions products are currently being sold in more than 60 countries worldwide.
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Apoptosis InducersApoptosis Inducers

BioVision develops and offers a wide variety of products including assay kits, antibodies, recombinant proteins & enzymes, and other innovative research tools for studying Apoptosis, Metabolism, Cell Proliferation, Cellular Stress, Cell Damage and Repair, Diabetes, Obesity and Metabolic Syndrome, Stem Cell Biology, Gene Regulation, Signal Transduction, etc. BioVisions products are currently being sold in more than 60 countries worldwide.
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Antibiotics- AG ScientificAntibiotics- AG Scientific

Anisomycin (Flagecidin). A-1049. Options. 10 mg $39.99. 50 mg $99.99. 100 mg $149.99. 500 mg $349.99. ...
more infohttps://www.agscientific.com/molecular-biology/antibiotics.html

Carbenicillin | CAS 4800-94-6 | Gene Selection Antibiotic | AG Sci.Carbenicillin | CAS 4800-94-6 | Gene Selection Antibiotic | AG Sci.

Find the best deals in the life science marketplace on carbenicillin. AG Scientific has over 20 years of experience in biochemical supplies!
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Dual Roles for c-Jun N-Terminal Kinase in Developmental and Stress Responses in Cerebellar Granule Neurons | Journal of...Dual Roles for c-Jun N-Terminal Kinase in Developmental and Stress Responses in Cerebellar Granule Neurons | Journal of...

Lysates of anisomycin-treated 1 DIV neurons were also blotted for c-Jun protein and Ser-63 phosphorylation. Although anisomycin ... 1B). Anisomycin (50 μg/ml) induced an eightfold elevation in U937 cell JNK activity as reported previously in these cells ( ... Treatment with anisomycin lead to a 399 ± 59% increase in p38 activity in neurons, comparable with that in U937 cells of 302 ± ... Treatment with anisomycin or osmotic shock for 45 min typically induces p38 activity in cell lines (Kyriakis and Avruch, 1996; ...
more infohttps://www.jneurosci.org/content/20/20/7602?ijkey=d68104ec7a2d4dae8dc368d4b531a9b23f8b9b08&keytype2=tf_ipsecsha
  • Finally, appropriately timed administration of the beta-adrenergic antagonist propranolol and the beta-adrenergic agonist clenbuterol attenuated (but did not eliminate) the anisomycin-induced amnesia. (blogspot.com)
  • The cells were incubated at 37°C for 6h in media containing different concentrations of ab120495 (anisomycin) in DMSO, fixed with 4% formaldehyde for 10 minutes at room temperature and blocked with PBS containing 10% goat serum, 0.3 M glycine, 1% BSA and 0.1% tween for 2h at room temperature. (abcam.com)
  • furthermore, 3-deazaneplanocin A solubility dmso anisomycin treatment of sc/siAR-infected WT primary cells (Fig. 2F) showed the anoikis between sc versus siAR RNA P = 0.003, which is consistent with our hypothesis. (cellbasedassayblog.com)
  • This suggests that UV-mediated TNFα release may occur via different p38 pathway intermediates compared to those stimulated by anisomycin. (mdpi.com)
  • The first goal of the present study was to provide final proof for these mode of actions by comparing the effects of 6 h exposure to DON and TBTO on mRNA expression to those of positive controls of ribotoxic stress (anisomycin), ER stress (thapsigargin) and T cell activation (ionomycin). (wur.nl)
  • The AR-related anisomycin suppression on cell anoikis reached statistical significance (P = 0.03). (cellbasedassayblog.com)
  • It was noted that deacetylanisomycin was a prominent product in the first few days of fermentation, suggesting that acetylation of the C-3 hydroxyl group by acetyl Co-A is the final step in the biosynthesis of anisomycin. (wikipedia.org)
  • DON did not affect other genes than anisomycin indicating the effect of DON to be restricted to ribotoxic stress. (wur.nl)
  • Anisomycin is also mentioned as a potential psychiatric drug , as it may erase "short-range memory" . (wikidoc.org)
  • Moreover, a high dose of NE injected into the amygdala before training impairs memory to an extent similar to that seen after anisomycin injections. (blogspot.com)
  • Anisomycin is also mentioned as a potential psychiatric drug, as it may inhibit the consolidation of new context-specific long-term memories, as well as long time consolidated memories rendered labile through reactivation. (wikipedia.org)
  • Additionally, blockade of amygdala beta-adrenergic receptors at the time of anisomycin injections, i.e., at the time of high release of biogenic amines, attenuates the amnesia produced by anisomycin as tested 48 h after training. (blogspot.com)