An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.
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.
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.
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.
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).
Compounds that inhibit cell production of DNA or RNA.
Compounds or factors that act on a specific enzyme to increase its activity.
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.
Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.
An antitumor antibiotic produced by Streptomyces sparsogenes. It inhibits protein synthesis in 70S and 80S ribosomal systems.
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.
The biosynthesis of PEPTIDES and PROTEINS on RIBOSOMES, directed by MESSENGER RNA, via TRANSFER RNA that is charged with standard proteinogenic AMINO ACIDS.
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.
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).
Middle portion of the hypothalamus containing the arcuate, dorsomedial, ventromedial nuclei, the TUBER CINEREUM and the PITUITARY GLAND.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
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.
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)
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.
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.
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.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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.
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)
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)

Anisomycin is known to inhibit protein synthesis and induce ribotoxic stress. In this study, we investigated whether anisomycin treatment could modulate TRAIL-mediated apoptosis in human renal carcinoma Caki cells. We found that anisomycin treatment (10-15 nM) alone had no effect on the level of apoptosis, but a combination treatment of anisomycin and TRAIL significantly increased the level of apoptosis in human renal carcinoma (Caki, ACHN and A498), human glioma (U251MG), and human breast carcinoma (MDA-MB-361 and MCF7) cells. Anisomycin treatment led to the down-regulation of Bcl-2 expression at the transcriptional level, and the over-expression of Bcl-2 inhibited the apoptosis induced by the combination treatment of anisomycin and TRAIL. Furthermore, anisomycin treatment resulted in the down-regulation of c-FLIP(L) and Mcl-1 at the post-transcriptional level, and the over-expression of c-FLIP(L) and Mcl-1 blocked the induction of apoptosis caused by the combination treatment of anisomycin ...
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 ...
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.
High purity Anisomycin (#A-520) is a protein synthesis inhibitor from Alomone Labs. A natural & biologically active compound. New lots are biologically tested. Lyophilized. Free samples available. Global shipping at room temperature. Join the thousands of researchers using our products.
Tumor develops through a multistep procedure in which regular cells improvement to malignant tumors via the progression of their genomes due to the acquisition of mutations in malignancy driver genes. and 12 previously unfamiliar CISs marking fresh candidate tumor genes. Users of the and gene family members were generally mutated inside a mutually special fashion. The sequence data we generated yielded also info within the clonality of insertions in individual tumors, allowing us to develop a data-driven model of MMTV-induced tumor development. Insertional mutations near and genes mark the Anisomycin earliest initiating events in MMTV induced tumorigenesis, whereas genes are targeted later on during tumor progression. Our data demonstrates insertional mutagenesis can be used to discover the mutational networks, the timing of mutations, and the genes that initiate and travel tumor evolution. Intro With the arrival of next-generation DNA sequencing systems the mutational panorama of several tumor ...
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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 ...
Whereas other studies on the molecular processes underlying reconsolidation have mainly focused on consolidated memories a long time (days to weeks) after training (Nader et al., 2000; Abel and Lattal, 2001; Milekic and Alberini, 2002), here we investigated reconsolidation processes in an earlier time window (6-24 h) after acquisition. In this earlier time window of consolidated memory, we identified phase-dependent differences in the requirement for protein synthesis and PKA activity for memory reconsolidation after retrieval. Our study shows that translation-dependent processes are required for reconsolidation at both 6 and 24 h. This supports the notion that translation-dependent processes are critical for reconsolidation independently of the time of retrieval, at least within the time window investigated here. However, this is not the case for the function of PKA in reconsolidation in the same time window. Our direct measurements show that memory retrieval at 6 h after training, but not at ...
In the yeast Saccharomyces cerevisiae this methylation is important for resistance towards hydrogen peroxide and the antibiotic anisomycin.
Legendary investor Warren Buffett advises to be fearful when others are greedy, and be greedy when others are fearful. One way we can try to measure the level of fear in a given stock is through a technical analysis indicator called the Relative Strength Index, or RSI, which m
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 ...
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 ...
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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 ...
The main finding of this study is that CB1R signaling critically modulates memory reconsolidation processes necessary for subsequent drug context-induced cocaine-seeking behavior in an instrumental model of drug relapse. Furthermore, memory retrieval induces CB1R-dependent changes in IEG expression, glutamate receptor subunit phosphorylation, and excitatory synaptic transmission in the BLA during memory reconsolidation.. Systemic CB1R antagonism during cocaine-memory reconsolidation (i.e., immediately after memory retrieval) reduced drug context-induced cocaine-seeking behavior 3 d later, relative to VEH (Fig. 1). The CB1R antagonist, AM251 does not alter inhibitory avoidance (Gobira et al., 2013) or grooming behaviors (Hodge et al., 2008) at similar doses, suggesting it is not aversive. Furthermore, AM251 alone did not alter the expression of drug-seeking behavior despite its long half-life (i.e., 22 h; McLaughlin et al., 2003; Fig. 2). These observations suggest that CB1R signaling is ...
As outlined in Chap. 1, any polymeric object is actually a composite, containing a number of ingredients with different functions. Of course, the
MAPKAPK5-AS1 - (untagged)-Homo sapiens, clone MGC:15178 IMAGE:4122851, complete cds available for purchase from OriGene - Your Gene Company.
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
Test reagents. Recombinant human GDNF (PeproTech) and TNF-α (Biomol) were used at 100 ng/ml (7, 16). The p38 MAPK inhibitor SB202190 was used at 30 μM (Calbiochem) and anisomycin (Sigma-Aldrich) was used at 60 μM to activate p38 MAPK (16).. Human tissue samples. Human tissue samples were obtained from patients suffering from IBD with an indication for surgical resection. Tissue samples from patients with CD (n = 9) derived from the terminal ileum. They were taken from the center of the inflamed parts of the resection specimens and from the periphery where no inflammation was seen. In patients with ulcerative pancolitis (n = 9) a sample of the affected colon was taken. Since the whole colon was inflamed in these patients, no uninflamed tissue was collected. Control tissue samples (colon or terminal ileum) from patients not suffering from IBD derived from patients that required right or left hemi-colectomy due to colon carcinoma in which the surgical resection routinely involved a part of the ...
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.
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 ...
Propranolol administered immediately after learning or after recall has been found to impair memory consolidation or reconsolidation (respectively) in animals, but less reliably so in humans. Since reconsolidation impairment has been proposed as a treatment for mental disorders that have at their core an emotional memory, it is desirable to understand how to reliably reduce the strength of pathogenic memories in humans. We postulated that since humans (unlike experimental animals) typically receive propranolol orally, this introduces a delay before this drug can exert its memory impairment effects, which may render it less effective. As a means to test this, in two double-blind placebo-controlled experiments, we examined the capacity of propranolol to impair consolidation and reconsolidation as a function of timing of ingestion in healthy subjects. In Experiment 1, (n=36), propranolol administered immediately after learning or recall failed to impair the consolidation or reconsolidation of the ...
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 ...
TASHIRO Etsu , HIRONIWA Naoka , KITAGAWA Mitsuhiro , FUTAMURA Yushi , SUZUKI Shin-ichi , NISHIO Maki , IMOTO Masaya J. Antibiot. (Tokyo) 60(9), 547-553, 2007-09-25 Ichushi Web References (28) Cited by (4) ...
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 ...
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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, ...
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
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... 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 is used as a component of Martin Lewis agar, an in vitro diagnostic product which is used extensively in the United ...
Anisomycin inhibits the production of proteins. In tests where it is delivered to the lateral and basal nuclei in the amygdala ... "Anisomycin - an overview , ScienceDirect Topics". www.sciencedirect.com. Retrieved 2022-05-05. Doyère, Valérie; Dębiec, Jacek; ...
Schaefer, John P; Wheatley, Peter J (1967). "The Structure of Anisomycin". Chemical Communications. London: 578-79. "cremation ... Schaefer on the structure of anisomycin. Wheatley's last position was in the Department of Physical Chemistry at Cambridge. ...
These include anisomycin, cycloheximide, chloramphenicol, tetracycline, streptomycin, erythromycin, and puromycin. Prokaryotic ...
Sensitivity to novobiocin, bacitracin, anisomycin, aphidicolin, and rifampicin have been observed. However, no sensitivity has ...
When anisomycin is applied to the hippocampus, active memories are unable to fully consolidate and are lost. When anisomycin is ... 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 ...
Ducret C, Maira SM, Dierich A, Wasylyk B (2000). "The net repressor is regulated by nuclear export in response to anisomycin, ...
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 ...
It is resistant to many antibiotics, including Vancomycin and Tetracycline, but can be killed by Anisomycin. This organism does ...
Frey U, Krug M, Reymann KG, Matthies H (June 1988). "Anisomycin, an inhibitor of protein synthesis, blocks late phases of LTP ...
The rats that were injected with anisomycin after consolidation had taken place, retained the fear reaction to the tone. ... Groups of rats were then injected with anisomycin, an antibiotic that restricts protein synthesis, at different points in time ... 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 ...
Frey, Uwe; Krug, Manfred; Reymann, Klaus G.; Matthies, Hansjuergen (1988). "Anisomycin, an inhibitor of protein synthesis, ... as proven by injecting anisomycin into a dendritic spine and observing the resulting absence of late LTP. To achieve ...
"Inhibition of protein synthesis and JNK activation are not required for cell death induced by anisomycin and anisomycin ...
... but not medium-term retention of olfactory memories in honeybees is impaired by actinomycin D and anisomycin". The European ...
... and the antibiotics anisomycin and sinefungin. Tohyama, Shigehiro; Kakinuma, Katsumi; Eguchi, Tadashi (January 2006). "The ...
After receiving post-retrieval an intra-amygdalar infusion of a known amnesic agent, anisomycin, rats failed to recall a ...
... the infusion of proteasome inhibitors into the CA1 of the hippocampus immediately after retrieval prevented anisomycin-induced ...
2005). "Complete inhibition of anisomycin and UV radiation but not cytokine induced JNK and p38 activation by an aryl- ...
The molecular formula C14H19NO4 (molar mass: 265.31 g/mol, exact mass: 265.1314 u) may refer to: Anisomycin, also known as ...
... anisomycin MeSH D03.383.773.107 - bepridil MeSH D03.383.773.165 - clemastine MeSH D03.383.773.170 - 3,4-dichloro-n-methyl-n-(2 ...
Anisomycin Drug Enforcement Administration October 2000. The Hallucinogen PMA: Dancing With Death Shulgin, Alexander Theodore; ...
... the death effector TRAIL or chemical drugs such as anisomycin. PUMA protein is degraded in a proteasome dependent manner and ...
Anisomycin, Thiolutin, Wortmannin, K252a, Staurosporine, K252C, Bafilomycin, Alamethicin, Leptomycin, A23187, Chelerythrine, ... Anisomycin, Thapsigargin, cyclopamine, Thiostrepton, Staurosporine, Mithramycin, Midostaurin, Wortmannin, K252a, Geldanamycin ...
... "fungicidal substances of the anisomycin group".[citation needed] This bacterium can also be used to determine the nutrient ...
Androgen Anethole Angiotensinogen Anisomycin Antidiuretic hormone (ADH) Anti-Müllerian hormone (AMH) Arabinose Arginine ...
... and anisomycin treatment or JDP2 is also regulated by other kinases such as p38 MAPK and doublecortin like protein kinase. ...
Stafford, J. M., & Lattal, K. M. (2009). Direct comparisons of the size and persistence of anisomycin-induced consolidation and ... Stafford, JM & Lattal, KM 2009, Direct comparisons of the size and persistence of anisomycin-induced consolidation and ... Direct comparisons of the size and persistence of anisomycin-induced consolidation and reconsolidation deficits. Learning and ... Direct comparisons of the size and persistence of anisomycin-induced consolidation and reconsolidation deficits. In: Learning ...
Dive into the research topics of Behavioral impairments caused by injections of the protein synthesis inhibitor anisomycin ... Behavioral impairments caused by injections of the protein synthesis inhibitor anisomycin after contextual retrieval reverse ...
Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of ... Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of ... Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of ... Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of ...
Anisomycin * 3,4-dihydroxyphenylglycol Grant support * R01 NS051255/NS/NINDS NIH HHS/United States ...
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.
DB07374, Anisomycin. DB08437, Puromycin. Genetic variation databases. BioMuta curated single-nucleotide variation and disease ...
Phosphorylated ATF-2 Control Cell Extracts: Total extracts from NIH/3T3 cells, treated with Anisomycin #2222 at 25 ug/ml for 30 ...
The defects in RQC of the RQT mutants correlate with sensitivity to anisomycin, which stalls ribosome at the rotated form. Cryo ... a The anisomycin sensitivity of rqt and uS10-K6/8R mutants. b Ribosome short footprints were accumulated at CGA-CGA codons. The ... The yeast rqt1∆ and rqt2∆ mutant cells conferred sensitivity to deoxynivalenol, trichothecin38, and anisomycin16 (Fig. 5a), ... The sensitivity of the rqt mutants to anisomycin correlated with the defects in RQC (Figs. 2b and 5a), suggesting that Rqt1 ...
AnisomycinNew. Anisomycin (Flagecidin, Wuningmeisu C) is a bacterial antibiotic isolated from Streptomyces griseolus, which ...
Anisomycin was used to activate P38, and p-P38, p-CREB, and MMP13 were evaluated by immunofluorescence and Western blot ... The expressions of p-P38, p-CREB, and MMP13 were all upregulated in osteoarthritic cartilage or anisomycin-induced chondrocytes ... Can the P38 agonist anisomycin (ANS) induce mouse OA? ...
Sensitivity to intrahippocampal anisomycin was observed only in the protocol involving new memory encoding at the time of ... Sensitivity to intrahippocampal anisomycin was observed only in the protocol involving new memory encoding at the time of ... Sensitivity to intrahippocampal anisomycin was observed only in the protocol involving new memory encoding at the time of ... Sensitivity to intrahippocampal anisomycin was observed only in the protocol involving new memory encoding at the time of ...
But if the anisomycin has been delivered to the animal that is receiving the paired odor, the conditioned odor, the valence of ... And whether you add anisomycin, the protein synthesis inhibitor, it has no effect on the frequency of freezing. ...
Incubation of HeLa cells (50,000 cells/well) with Anisomycin for 60 min at 37°C stimulates phosphorylation of p38αβγ at T180/ ... Epidermal growth factor (EGF; PeproTech®), Interferon-alpha (INFα; ProSpec) and Anisomycin (Cayman Chemical) ...
PDB Description: structure of anisomycin resistant 50s ribosomal subunit: 23s rrna mutation a2488u ...
PDB Description: structure of anisomycin resistant 50s ribosomal subunit: 23s rrna mutation a2488u ...
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... vehicle vs anisomycin, p , 0.05, Students t test). Students t test comparing Test 1 of the anisomycin group with its relative ... vehicle vs anisomycin, p , 0.05, Students t test). B, Hippocampal injections of anisomycin 15 min before IA training disrupted ... of vehicle or anisomycin at designated time points. A, Hippocampal injections of anisomycin 15 min before IA training had no ... In contrast, anisomycin injected either at 2 d or 7 d after training had no effect on memory retention tested at 2 d, 7d, or 21 ...
Stress-induced glucose uptake in bovine chromaffin cells: a comparison of the effect of arsenite and anisomycin. Biochim ...
Anisomycin / pharmacology Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Anisomycin downregulates gap-junctional intercellular communication via the p38 MAP-kinase pathway. Journal of Cell Science 117 ...
Western blot analysis of extracts from NIH/3T3 cells, untreated (-) or treated with Anisomycin (25 μg/ml, 30 min; +), using ... Western blot analysis of extracts from NIH/3T3 cells, untreated (-) or treated with Anisomycin (25 μg/ml, 30 min; +), using ... Flow cytometric analysis of THP-1 cells, untreated (blue) or Anisomycin treated (green), using Phospho-ATF-2 (Thr71)/ATF-7 ( ... Flow cytometric analysis of THP-1 cells, untreated (blue) or Anisomycin treated (green), using Phospho-ATF-2 (Thr71)/ATF-7 ( ...
Antibiotic anisomycin selectively targets leukemia cell lines and patient samples through suppressing Wnt/β-catenin signaling. ...
A Short Synthetic Approach to Enantiomerically Pure (-)-Anisomycin. Hidemi Yoda,* Tomohito Nakajima, Hiroyasu Yamazaki, and ... A convenient enantiomerically pure route to an antibiotic, natural (-)-anisomycin has been developed in a short number of steps ...
Anisomycin was then added for 30 minutes to prevent de novo protein synthesis and to activate cellular stress responses. Cells ... Anisomycin was then added for 30 minutes to prevent de novo protein synthesis and to activate cellular stress responses. Cells ... Cells were pretreated with SBI-0089410 for 3 to 9 hours, before stimulation with anisomycin. SBI-0089410 inhibited ATF2 ... Cells were pretreated with SBI-0089410 for 3 to 9 hours, before stimulation with anisomycin. SBI-0089410 inhibited ATF2 ...
Lee, P. T., Chao, P. K., Ou, L. C., Chuang, J. Y., Lin, Y. C., Chen, S. C., Chang, H. F., Law, P. Y., Loh, H. H., Chao, Y. S., Su, T. P. & Yeh, S. H., 12月 1 2014, 於: Nucleic Acids Research. 42, 21, p. 13012-13025 14 p.. 研究成果: 雜誌貢獻 › 文章 › 同行評審 ...
... anisomycin, and vancomycin (Legionella MWY Selective Supplement SR118, Oxoid Ltd., Hampshire, England). Plates were incubated ...
Anisomycin Preferred Term Term UI T002463. Date01/01/1999. LexicalTag NON. ThesaurusID ... Anisomycin Preferred Concept UI. M0001251. Registry Number. 6C74YM2NGI. Related Numbers. 22862-76-6. Scope Note. An antibiotic ... 91(75); was see under PYRROLIDINES 1975-90; FLAGECIDIN was see ANISOMYCIN 1975-95. Date Established. 1991/01/01. Date of Entry ... 91; was see under PYRROLIDINES 1975-90; FLAGECIDIN was see ANISOMYCIN 1975-95. History Note. ...
... this virus-specific RNA synthesis was not induced in the presence of the protein synthesis inhibitor anisomycin. A new RNA- ...
  • Originally discovered by Sobin and Tanner in 1954, Anisomycin was identified as an antibiotic active against protozoa such as Trichomonas and fungi and yeasts, and was considered as a potential human anti-candidal and anti-amoebic drug. (fermentek.com)
  • Anisomycin, a new antiprotozoa antibiotic. (fermentek.com)
  • Anisomycin is an antibiotic isolated from Streptomyces griseolus that inhibits protein synthesis. (discofinechem.com)
  • Anisomycin ReadyMade™ Solution ( A226 ) is a natural alkaloid anti-protozoal pyrrolidine antibiotic. (toku-e.com)
  • 2008 Nov-Dec;31(9):858-70 In the field of cell-signaling research, Anisomycin is used as an activator of kinase cascades in mammalian cells, especially the stress-activated Protein Kinase (SAPK2/p38MAPK) and p46/54JNK Anisomycin is a selective ingredientof Martin Lewis Agar, a bacteriological solid medium used for isolation of pathogenic Neisseria species. (fermentek.com)
  • Anisomycin can activate stress-activated protein kinases, MAP kinase and other signal transduction pathways. (ichacha.net)
  • In the present experiments, anisomycin was infused into either the hippocampus or the amygdala 20 min before inhibitory avoidance training. (syr.edu)
  • In contrast, intra-amygdala injections of anisomycin impaired memory tested at 0.5, 4, and 48 hr after training, revealing no evidence for spared memory at short times after training. (syr.edu)
  • The distinct temporal properties for amnesia following anisomycin injections into the hippocampus or amygdala may reflect different consequences for memory of perturbations of the neural system in which the manipulation is made. (syr.edu)
  • Canal, CE & Gold, PE 2007, ' Different Temporal Profiles of Amnesia After Intra-hippocampus and Intra-Amygdala Infusions of Anisomycin ', Behavioral Neuroscience , vol. 121, no. 4, pp. 732-741. (syr.edu)
  • 1956 Sep-Dec;21(7-10):114-5 Anisomycin is also proposed as a potential psychiatric drug, as it is shown to affect protein synthesis an Amygdala, a brain part involved in memory(1). (fermentek.com)
  • MEFs from MKP-2(-/-) mice also showed enhanced apoptosis when stimulated with anisomycin correlated with increased caspase-3 cleavage and gamma H2AX phosphorylation. (strath.ac.uk)
  • Similar to previous findings, intra-hippocampus injections of anisomycin impaired memory tested 48 hr after training yet spared memory tested 4 hr after training. (syr.edu)
  • We also show that learning during this paradigm activated Arc/Arg3.1 mRNA expression in the hippocampus and that stereotactic injection of anisomycin into this region impairs memory consolidation. (jneurosci.org)
  • This discovery leads to researches on the potential use of Anisomycin in transplantation: Anisomycin inhibits the behaviors of T cells and the allogeneic skin transplantation in mice.Xing F et al,J Immunother. (fermentek.com)
  • structure of anisomycin resistant 50s ribosomal subunit: 23s rrna mutation u2535c. (berkeley.edu)
  • To detect possible fastidious bacteria PCR for amplification of the bacterial 16S rRNA gene in valve tissue was performed by real-time PCR in a LightCycler instrument using SYBR green I (Roche Diagnostics) and broad-range primers Anisomycin PSL (forward 5 ATT AGA TAC CCT GGT AGT CCA-3′) and P13P (reverse 5 CCC GGG AAC GTA TTC AC-3′) (24). (conferencedequebec.org)
  • In order to characterize the strain of detected in our patient's valve tissue the 16S-23SrRNA gene intergenic spacer region and domain name III of the 23S rRNA gene were amplified and sequenced as previously explained (11 12 and classified as Anisomycin type 1A. (conferencedequebec.org)
  • Systemic or intra-hippocampal administration of the protein synthesis inhibitor anisomycin generally leads to impairments in memory tested 24 hr or more after training but spares memory for a few hours after training. (syr.edu)
  • Anisomycin is a protein synthesis inhibitor. (fermentek.com)
  • Again, this property of Anisomycin is ascribed to its ability to inhibit protein synthesis. (fermentek.com)
  • Behavioral impairments caused by injections of the protein synthesis inhibitor anisomycin after contextual retrieval reverse with time. (btemplateseo.com)
  • The role of protein synthesis in the MeA was investigated by local application of the protein synthesis blocker anisomycin (n = 11). (haifa.ac.il)
  • Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system. (medchemexpress.com)
  • Incubation of HeLa cells (50,000 cells/well) with Anisomycin for 60 min at 37°C stimulates phosphorylation of p38αβγ at T180/Y182. (bmglabtech.com)
  • PDGF stimulation of sustained ERK phosphorylation was enhanced in MKP-2(-/-) MEFs, whereas anisomycin-induced JNK was only marginally increased. (strath.ac.uk)
  • Western blot analysis of extracts from MDA-MB-231 cells untreated or treated with Anisomycin using Rabbit anti p53 (pThr18) antibody ( AHP2668 ). (bio-rad-antibodies.com)
  • Cells were cultured in serum free media for 16-20 hours before treatment with Anisomycin (5μg/ml) for 30 minutes. (bio-rad-antibodies.com)
  • 實驗方法(Assay):Mice received subcutaneous injections of 50 or 75 mg of anisomycin/kg of body weight or an equivalent volume of saline in the first experiment. (btemplateseo.com)
  • 實驗方法(Assay):LA effective refractory period (AERP) was measured using an S1-S2 pacing protocol and atrial arrhythmias (AT/AF) were induced using burst pacing in open-chest heartsin young rabbits with (n = 4) or without (n = 5)anisomycin treatment (15 mg/kg, iv, four treatments over 9 days)and aged rabbits without anisomycin treatment (n = 6). (btemplateseo.com)
  • D ) Representative immunoblots (upper) and quantitative analyses (lower) for FasL from BV-2 cultures following actinomycin D or anisomycin treatment. (biomedcentral.com)
  • Fujita, 1999), we assessed the effect of cooling on Geph in the presence of translation elongation blocker Anisomycin (Aniso). (researchgate.net)
  • In addition, we observed that the effect of L-kynurenine was blocked by JNK agonist, anisomycin, suggesting the involvement of the JNK pathway in the signal transduction of L-kynurenine-reduced NKG2D expression. (elsevier.com)
  • 1977. Anisomycin: improved antimycotic activity in modified Thayer-Martin medium. (fermentek.com)
  • 1979 Dec;66(3):524-32 Recently, publications appear showing the immunomodulating properties on Anisomycin. (fermentek.com)
  • Results Anisomycin application to the MeA prevented the formation of long-term SRM. (haifa.ac.il)
  • After an optimistic PCR result for was attained valve tissues was reexamined in Anisomycin the pathology lab and regular acid-Schiff stain (PAS)-positive. (conferencedequebec.org)
  • As a result of the higher polarity of Anisomycin Formula glycosylated polyphenols, aqueous mixtures with a polar organic solvent have been employed to maximize their recovery. (dna-alkylating.com)
  • These experiments showed that when experiences and performance are matched prior to anisomycin injections, consolidation deficits are generally larger and more persistent compared to reconsolidation deficits. (elsevier.com)
  • In Chinese hamster ovary cells expressing the human insulin receptor and murine 3T3L1 adipocytes, insulin specifically activated ERK with no significant effect on JNK, whereas anisomycin specifically activated JNK but was unable to activate ERK. (elsevier.com)
  • h after SFC showed reduced manifestation of interpersonal fear, indicating impaired interpersonal fear memory space, whereas anisomycin caused no effects when given 4 h after SFC. (raltegravir.info)
  • When administered near the time of training, protein synthesis inhibitors such as anisomycin impair later memory. (syr.edu)
  • Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of protein synthesis, as assessed by c-Fos immunohistochemistry. (syr.edu)
  • These findings are consistent with past evidence suggesting that anisomycin causes amnesia by initiating abnormal release of neurotransmitters in response to the inhibition of protein synthesis. (syr.edu)
  • 10 M U0126), or the cellular protein synthesis inhibitor and MAPK-inducer, anisomycin (5 M). DMOG was employed as the positive control for inhibition of plus-strand HTLV-1 transcription. (fabretp.org)
  • Inhibition of JNK conferred no protection to the anisomycin-induced infarct size [16]. (azd1152.com)
  • IP3 receptors (Xestospongin C, 2-APB), ryanodine receptors (dantrolene), and translocon (anisomycin) inhibition facilitated ER Ca2+ leak in model macrophage, with translocon inhibition also reducing resting [Ca2+]cyto. (uea.ac.uk)
  • Of this suspension, 100-µL samples were cultured without dilution and after 10- and 100-fold dilutions on buffered charcoal yeast extract agar with alpha-ketoglutarate (BCYE-alpha) and a selective supplement with dyes and the antibiotics polymyxin, anisomycin, and vancomycin (Legionella MWY Selective Supplement SR118, Oxoid Ltd., Hampshire, England). (medscape.com)
  • The exact formulation has changed over the years but includes agents active against gram-positive bacteria (vancomycin), gram-negative bacteria (colistin, trimethoprim), and fungi (nystatin, anisomycin) at concentrations that do not inhibit N gonorrhoeae. (medscape.com)
  • The specific medium consists vancomycin, an antimicrobial agent colistin, anisomycin, colistin (V-C-A inhibitor) and trimethoprim to inhibit the normal bacteria. (microbiologynote.com)
  • Phosphorylated ATF-2 Control Cell Extracts: Total extracts from NIH/3T3 cells, treated with Anisomycin #2222 at 25 ug/ml for 30 minutes to serve as a positive control. (cellsignal.com)
  • We found that systemic or intrahippocampal administration of anisomycin caused a deficit in groups receiving context conditioning (consolidation groups) or reactivation (reconsolidation groups) immediately prior to the injections. (elsevier.com)
  • Control studies confirmed that intrahippocampal infusions of anisomycin inhibited protein synthesis locally and that the spatial training protocols we used are subject to overnight protein synthesis-dependent consolidation. (ed.ac.uk)
  • Sensitivity to intrahippocampal anisomycin was observed only in the protocol involving new memory encoding at the time of retrieval. (ed.ac.uk)
  • However, recent findings support an alternative interpretation that abnormally large increases in neurotransmitter release after injections of anisomycin may be responsible for producing amnesia. (syr.edu)
  • In the present study, a local anesthetic was administered prior to anisomycin injections in an attempt to mitigate neurotransmitter actions and thereby attenuate the resulting amnesia. (syr.edu)
  • Rats received lidocaine and anisomycin injections into the amygdala 130 and 120. (syr.edu)
  • As seen previously, anisomycin injections produced large increases in release of norepinephrine in the amygdala. (syr.edu)
  • Stafford, JM & Lattal, KM 2009, ' Direct comparisons of the size and persistence of anisomycin-induced consolidation and reconsolidation deficits ', Learning and Memory , vol. 16, no. 8, pp. 494-503. (elsevier.com)
  • The defects in RQC of the RQT mutants correlate with sensitivity to anisomycin, which stalls ribosome at the rotated form. (nature.com)
  • Insulin and osmotic shock, but not anisomycin, resulted in SOS phosphorylation and disassociation of the Grb2-SOS complex, demonstrating that the JNK pathway was not involved in the insulin-stimulated feedback uncoupling of the Grb2-SOS complex. (elsevier.com)
  • C): Disruption of the expression of powerful LTP (apical pathway S2, bottom gray trace) by anisomycin (horizontal bar) did not substantially avert the interference in excess of the subsequent expression of sturdy LTD (basal pathway S1, prime grey trace). (itkinhibitor.com)
  • A, Biomarker response data are graphed for anisomycin-exposed TK6 cells versus concentration. (nih.gov)
  • The bottom middle panel shows clastogen probabilities as a function of anisomycin concentration based on 3 machine learning algorithms: LR, ANN, and RF. (nih.gov)
  • Promotes apoptosis in response to cellular stress mediated by exposure to anisomycin or UV (PubMed:24512202). (nih.gov)
  • Ideally potential experiments will obviously define the part of AHR in model systems exposure to potential Anisomycin AHR agonists. (acmbcb.org)
  • Anisomycin may block the SARS-CoV-2 infection, and it can block the macrophage inflammation which may further inhibit the cytokine storm in COVID-19 disease. (toku-e.com)
  • For instance, above expression of Macrophage inhibitory cytokine one predicted sensi tivity of ribotoxic anisomycin. (vegfinhibitors.com)
  • We identify a role for translocon-mediated ER Ca2+ leak in receptor-mediated Ca2+ signalling in both model and primary human macrophage, whereby the Ca2+ response to ADP (P2Y receptor agonist) is augmented following anisomycin treatment. (uea.ac.uk)
  • By administering a compound called anisomycin, which blocks protein synthesis within neurons, immediately after mice had formed a new memory, the researchers were able to prevent the synapses from strengthening. (diytdcs.com)
  • Anisomycin upregulates autophagy and increases apoptosis . (selleckchem.com)
  • Sadowski, RN, Canal, CE & Gold, PE 2011, ' Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala ', Neurobiology of Learning and Memory , vol. 96, no. 2, pp. 136-142. (syr.edu)
  • Open in a separate window Number 3 Anisomycin impairs the consolidation of interpersonal fear memory space when given 6 h or 8 h after interpersonal fear conditioning (SFC). (raltegravir.info)
  • Anisomycin, however, eliminated long-term memory lasting at least 1 week after nine training events. (brainstages.com)
  • If you test memory recall with natural recall triggers in an anisomycin-treated animal, it will be amnesiac, you cannot induce memory recall," Tonegawa says. (diytdcs.com)
  • This getting shows that anisomycin impaired the consolidation of interpersonal fear memories whatsoever time-points, except when given 4 h after SFC. (raltegravir.info)
  • The following experiments examined the size and persistence of these deficits after matching both the amount of experience with a context and the levels of performance in that context prior to delivery of the protein synthesis inhibitor anisomycin. (elsevier.com)
  • While at UM, Respondent falsified twenty-four (24) Western blots for phosphorylated JNK or MMK4 expression in mN/SF exposed to UV light, H2O2, cadmium, or anisomycin in the seven (7) presentations and twenty-six (26) data files in the research record, when the images were duplicated and falsely relabeled Western blots of unrelated experiments. (nih.gov)
  • Furthermore, it isn't just the total amount but also the Anisomycin intracellular area (nucleus) of CTNNB1 manifestation that is very Anisomycin important to canonical Wnt signaling that occurs. (acmbcb.org)
  • 24hrs following tetanisation (but not at earlier time-points), the titre of R14 was elevated in the dentate area ipsilateral to tetanisation and in both the ipsi- and contralateral CAL The titre of 411B was increased specifically in the target, dentate area and only at 8hrs following tetanisation, an increase which was abolished in the presence of the protein synthesis inhibitor, anisomycin. (open.ac.uk)