A paralytic condition of the legs caused by ingestion of lathyrogens, especially BETA-AMINOPROPIONITRILE or beta-N-oxalyl amino-L-alanine, which are found in the seeds of plants of the genus LATHYRUS.
Cyanomethylamine.

Synergistic induction of apoptosis in human leukemia cells (U937) exposed to bryostatin 1 and the proteasome inhibitor lactacystin involves dysregulation of the PKC/MAPK cascade. (1/44)

Cotreatment with a minimally toxic concentration of the protein kinase C (PKC) activator (and down-regulator) bryostatin 1 (BRY) induced a marked increase in mitochondrial dysfunction and apoptosis in U937 monocytic leukemia cells exposed to the proteasome inhibitor lactacystin (LC). This effect was blocked by cycloheximide, but not by alpha-amanitin or actinomycin D. Qualitatively similar interactions were observed with other PKC activators (eg, phorbol 12-myristate 13-acetate and mezerein), but not phospholipase C, which does not down-regulate the enzyme. These events were examined in relationship to functional alterations in stress (eg, SAPK, JNK) and survival (eg, MAPK, ERK) signaling pathways. The observations that LC/BRY treatment failed to trigger JNK activation and that cell death was unaffected by a dominant-interfering form of c-JUN (TAM67) or by pretreatment with either curcumin or the p38/RK inhibitor, SB203580, suggested that the SAPK pathway was not involved in potentiation of apoptosis. In marked contrast, perturbations in the PKC/Raf/MAPK pathway played an integral role in LC/BRY-mediated cell death based on evidence that pretreatment of cells with bisindolylmaleimide I, a selective PKC inhibitor, or geldanamycin, a benzoquinone ansamycin, which destabilizes and depletes Raf-1, markedly suppressed apoptosis. Furthermore, ERK phosphorylation was substantially prolonged in LC/BRY-treated cells compared to those exposed to BRY alone, and pretreatment with the highly specific MEK inhibitors, PD98059, U0126, and SL327, opposed ERK activation while protecting cells from LC/BRY-induced lethality. Together, these findings suggest a role for activation and/or dysregulation of the PKC/MAPK cascade in modulation of leukemic cell apoptosis following exposure to the proteasome inhibitor LC. (Blood. 2001;97:2105-2114)  (+info)

Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms. (2/44)

Mapping inducible transcription factors has shown that the Edinger-Westphal nucleus is preferentially sensitive to alcohol intoxication. Herein, we characterize the pharmacological and signal transduction mechanisms related to alcohol-induced c-Fos expression in Edinger-Westphal neurons. Using immunohistochemistry, we show that pretreatment with gamma-aminobutyric acid (GABA)-ergic antagonists (4 mg/kg bicuculline and 45 mg/kg pentylenetetrazole) attenuates induction of c-Fos expression by alcohol (2.4 g/kg, intraperitoneal). In addition, 10 mg/kg 2-(2,3-dihydro-2-methoxy-1,4-benzodioxin-2-yl)4,5-dihydro-1H-imidazole (RX 821002), an alpha(2A/D)-adrenoceptor antagonist, and 20 mg/kg haloperidol, a dopamine antagonist, also block alcohol-induced c-Fos expression in Edinger-Westphal neurons. No effects were seen in alcohol-induced c-Fos after the pretreatment of 20 mg/kg propranolol (beta-adrenoceptor antagonist), 10 mg/kg 2-(2-(4-(2-methoxyphenyl)piperazin-1-yl) ethy)-4,4-dimethyl-1,3-(2H,4H)-isoquinolindione dihydrochloride (ARC 239) (alpha(2B/C)-adrenoceptor antagonist), or 30 mg/kg naltrexone (opioid antagonist). Although positive modulators for the GABA(A) receptor (20 mg/kg 3alpha-hydroxy-5alpha-pregnan-20-one and 10-30 mg/kg chlordiazepoxide) and opioid receptor (10 mg/kg morphine) produced significant elevations, agonists for alpha(2)-adrenoceptors (clonidine) and dopamine receptors (apomorphine) had no effect on Edinger-Westphal c-Fos expression. These findings suggest that alcohol-induced c-Fos expression in Edinger-Westphal results from direct interactions with GABA(A) receptors, which are modified by alpha(2A/D)-adrenoceptors and dopamine receptors. Also using immunohistochemistry to identify potential intracellular mechanisms associated with alcohol-induced c-Fos expression in Edinger-Westphal, we show time-dependent increases in serine 727 phospho-signal transducer and activator of transcription 3 (Stat3) but no changes in phospho-cAMP response element-binding protein and phospho-Elk1. Time-dependent increases in phospho-extracellular signal-regulated kinase (ERK) 1/2 were found to occur simultaneously with increases in serine 727 phospho-Stat3. Finally, blockade of ERK 1/2 phosphorylation with the mitogen-activated protein kinase (MEK) 1/2 inhibitor SL327 blocked alcohol-induced c-Fos expression, suggesting that alcohol induces c-Fos in Edinger-Westphal neurons through activation of the MEK1/2-ERK1/2-Stat3 pathway.  (+info)

Significant neuroprotection against ischemic brain injury by inhibition of the MEK1 protein kinase in mice: exploration of potential mechanism associated with apoptosis. (3/44)

MEK1/2 is a serine/threonine protein kinase that phosphorylates and activates extracellular signal-responsive kinase (ERK)1/2. In the present study we explored the role of MEK1/2 in ischemic brain injury using a selective MEK1/2 inhibitor, SL327, in mice. C57BL/6 mice were subjected to a 30-min occlusion of the middle cerebral artery (MCAO) followed by reperfusion. Western blot analysis demonstrated the immediate activation of MEK/ERK after reperfusion (within the first 10 min) in the ischemic brain; this activation was dose dependently blocked by SL327 (10-100 mg/kg, i.p.). A single dose of SL327 (100 mg/kg) administered 15 min before or 25 min after the onset of ischemia resulted in 63.6% (n = 18, p < 0.001) and 50.7% (n = 18, p < 0.01) reduction in infarct size, respectively, compared with vehicle-treated mice. Similarly, SL327 significantly reduced neurological deficits 1 to 3 days after reperfusion (n = 12, p < 0.01). The salutary effect of SL327-induced neuroprotection was independent of mitochondrial cytochrome c release or caspase-8-mediated apoptosis; however, SL327 markedly suppressed the levels of active caspase-3 and DNA fragmentation (as a measure of apoptosis) after ischemia/reperfusion. Our data suggest that the inhibition of MEK1/2 results in neuroprotection from reperfusion injury and that this protection may be associated with the reduction in apoptosis.  (+info)

A role for ERK MAP kinase in physiologic temporal integration in hippocampal area CA1. (4/44)

Recent studies demonstrate a requirement for the Extracellular signal Regulated Kinase (ERK) mitogen-activated protein kinase (MAPK) cascade in both the induction of long-lasting forms of hippocampal synaptic plasticity and in hippocampus-dependent associative and spatial learning. In the present studies, we investigated mechanisms by which ERK might contribute to synaptic plasticity at Schaffer collateral synapses in hippocampal slices. We found that long-term potentiation (LTP) induced with a pair of 100-Hz tetani does not require ERK activation in mice whereas it does in rats. However, in mice, inhibition of ERK activation blocked LTP induced by two LTP induction paradigms that mimicked the endogenous theta rhythm. In an additional series of studies, we found that mice specifically deficient in the ERK1 isoform of MAPK showed no impairments in tests of hippocampal physiology. To investigate ERK-dependent mechanisms operating during LTP-inducing stimulation paradigms, we monitored spike production in the cell body layer of the hippocampus during the period of theta-like LTP-inducing stimulation. Theta-burst stimulation (TBS) produced a significant amount of postsynaptic spiking, and the likelihood of spike production increased progressively over the course of the three trains of TBS independent of any apparent increase in Excitatory Post-Synaptic Potential (EPSP) magnitude. Inhibition of ERK activation dampened this TBS-associated increase in spiking. These data indicate that, for specific patterns of stimulation, ERK may function in the regulation of neuronal excitability in hippocampal area CA1. Overall, our data indicate that the progressive increase in spiking observed during TBS represents a form of physiologic temporal integration that is dependent on ERK MAPK activity.  (+info)

Preparation of (cyanomethylene)trimethylphosphorane as a new Mitsunobu-type reagent. (5/44)

(Cyanomethylene)trimethylphosphorane (CMMP) mediates Mitsunobu-type reactions, which are a versatile method for the alkylation of various nucleophiles (HA) with alcohols (ROH) to give RA. CMMP is quite effective for the reaction of carbon nucleophiles whose pK(a) value are higher than 13. CMMP, which is very sensitive to air and moisture, was synthesized in two steps starting from chloroacetonitrile.  (+info)

The role of the extracellular signal-regulated kinase signaling pathway in mood modulation. (6/44)

The neurobiological underpinnings of mood modulation, molecular pathophysiology of manic-depressive illness, and therapeutic mechanism of mood stabilizers are largely unknown. The extracellular signal-regulated kinase (ERK) pathway is activated by neurotrophins and other neuroactive chemicals to produce their effects on neuronal differentiation, survival, regeneration, and structural and functional plasticity. We found that lithium and valproate, commonly used mood stabilizers for the treatment of manic-depressive illness, stimulated the ERK pathway in the rat hippocampus and frontal cortex. Both drugs increased the levels of activated phospho-ERK44/42, activated phospho-ribosomal protein S6 kinase-1 (RSK1) (a substrate of ERK), phospho-CREB (cAMP response element-binding protein) and phospho-B cell lymphoma protein-2 antagonist of cell death (substrates of RSK), and BDNF. Inhibiting the ERK pathway with the blood-brain barrier-penetrating mitogen-activated protein kinase (MAP kinase)/ERK kinase (MEK) kinase inhibitor SL327, but not with the nonblood-brain barrier-penetrating MEK inhibitor U0126, decreased immobility time and increased swimming time of rats in the forced-swim test. SL327, but not U0126, also increased locomotion time and distance traveled in a large open field. The behavioral changes in the open field were prevented with chronic lithium pretreatment. SL327-induced behavioral changes are qualitatively similar to the changes induced by amphetamine, a compound that induces relapse in remitted manic patients and mood elevation in normal subjects. These data suggest that the ERK pathway may mediate the antimanic effects of mood stabilizers.  (+info)

Sustained extracellular signal-regulated kinase 1/2 phosphorylation in neonate 6-hydroxydopamine-lesioned rats after repeated D1-dopamine receptor agonist administration: implications for NMDA receptor involvement. (7/44)

Extracellular signal-regulated kinase (ERK) 1/2, a well known regulator of gene expression, is likely to contribute to signaling events underlying enduring neural adaptations. Phosphorylated (phospho)-ERK was examined immunohistochemically after both single and repeated (i.e., sensitizing) doses of the partial D1-dopamine (DA) receptor agonist SKF-38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benazepine HCl) to adult rats lesioned as neonates (neonate lesioned) with 6-hydroxydopamine. Remarkably, prolonged phospho-ERK accumulated primarily in layers II-III of medial prefrontal cortex (MPC), where it declined gradually yet remained significantly elevated for at least 36 d after repeated doses of SKF-38393. Sustained (> or =7 d) phospho-ERK was observed for shorter periods in various other cortical regions but was not detectable in striatum or nucleus accumbens. At 36 d, an additional injection of SKF-38393 to sensitized rats restored phospho-ERK to maximal levels only in MPC when examined 7 d later. Phosphorylated cAMP response element-binding protein (CREB), examined 7 d after the sensitizing regimen, was observed exclusively in MPC, where it was abundant throughout all layers. Systemic injections of SL327 (alpha-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitri le), an inhibitor of the upstream ERK activator mitogen ERK kinase, attenuated both ERK and CREB phosphorylation in layers II-III of MPC. Pretreatment with the D1 antagonist SCH-23390 ((R)-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-OL maleate) inhibited the prolonged increase in MPC phospho-ERK, whereas the 5-HT2 receptor antagonist ketanserin (3-[2-[4-(4-fluorobenzoyl)-1-piperidinyl]ethyl]-2,4(1H,3H)-quinazolinedione tartrate) was ineffective. Competitive and noncompetitive NMDA receptor antagonists also blocked sustained ERK phosphorylation. Collectively, the present results demonstrate coupling of D1 and NMDA receptor function reflected in sustained activation of the ERK signaling pathway in MPC of SKF-38393-sensitized neonate-lesioned rats. Ultimately, long-lasting phosphorylation of ERK and CREB in MPC may play a pivotal role in any permanent adaptive change(s) in these animals.  (+info)

ERK kinase inhibition stabilizes the aryl hydrocarbon receptor: implications for transcriptional activation and protein degradation. (8/44)

The ultimate carcinogen and metabolite of benzo-[a]pyrene-7,8-dihydrodiol, benzo[a]pyrene-r-7,t-8-dihydrodiol-t-9,10-epoxide (+/-), stimulates apoptosis, and this process can be blocked by extracellular signal-regulated kinase (Erk) kinase inhibitors. However, we show here that Erk kinase inhibitors were unable to prevent B[a]P-7,8-dihydrodiol-induced apoptosis, leading us to speculate that Erk kinases are linked to regulation of the aryl hydrocarbon (Ah) receptor. Cotreatment of hepa1c1c7 cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and Erk kinase inhibitor PD98059, U0126, or SL327 led to enhanced nuclear accumulation of Ah receptor but with a reduced capacity to complement TCDD induction of Cyp1a1. This is explained in part by the ability of Erk kinase inhibitors to alter the steady-state levels of cellular Ah receptor, a result that leads to a dramatic induction in detectable receptor levels. These changes in cellular Ah receptor levels are associated with delayed degradation of the Ah receptor because TCDD-initiated degradation is reversed when cells are co-treated with TCDD and Erk kinase inhibitors. Erk kinase is linked to Ah receptor expression, as demonstrated by reductions in total Ah receptor levels after overexpression of constitutively active MEK1. In addition, Erk kinase activity modulates the transcriptional response because MEK1 overexpression enhances TCDD-initiated transactivation potential of the receptor. Thus, Erk kinase activity facilitates ligand-initiated transcriptional activation while targeting the Ah receptor for degradation. Immunoprecipitation experiments of the Ah receptor indicate that Erk kinase activity is associated with the receptor. It is interesting that the carboxyl region of the Ah receptor is associated with the transactivation region as well as the site for ubiquitination, indicating that Erk kinase-dependent phosphorylation targets the carboxyl region of the receptor.  (+info)

Lathyrism is a neurological disorder caused by the consumption of large amounts of food sources containing a toxin called β-N-oxalyl-L-α,β-diaminopropionic acid (ODAP), which is found in certain legumes of the genus Lathyrus, particularly in grass peas (L. sativus). This disorder is characterized by the irreversible spastic paralysis of lower limbs due to damage in the upper motor neurons of the spinal cord. The onset and severity of lathyrism depend on the amount and duration of ODAP-containing food intake, with higher doses and longer exposure leading to more severe symptoms. Lathyrism is more prevalent in regions where grass peas are a staple food and access to diverse nutrition is limited.

Aminoacetonitrile is a chemical compound with the formula NH₂CH₂CN. It is an organic compound that contains both an amino group (-NH₂) and a cyano group (-CN). This colorless liquid is used in organic synthesis and as a building block for the production of certain pharmaceuticals and agrochemicals.

It's important to note that Aminoacetonitrile itself is not a medication or a drug, but it can be used in the synthesis of certain drugs and chemicals. It is not a naturally occurring compound and must be produced through chemical reactions.

As with any chemical compound, Aminoacetonitrile should be handled with care, following appropriate safety guidelines, to minimize the risk of exposure and potential health effects.

... is the organic compound with the formula NCCH2NH2. The compound is a colorless liquid. It is unstable at room ... Using radio astronomy, aminoacetonitrile was discovered in the Large Molecule Heimat, a giant gas cloud near the Galactic ... Aminoacetonitrile derivatives are useful antihelmintics. They act as nematode specific ACh agonists causing a spastic paralysis ... Tauber, Johannes; Opatz, Till (2015). "2-Aminoacetonitrile". E-EROS Encyclopedia of Reagents for Organic Synthesis: 1-4. doi: ...
drugs: benzimidazoles, levamisole, macrocyclic lactones, amino acetonitrile derivatives and spiroindoles. Narrow spectrum drugs ...
Experimental investigation of nitrile formation from VUV photochemistry of interstellar ices analogs: acetonitrile and amino acetonitrile ...
2008), "Detection of amino acetonitrile in Sgr B2(N)", Astronomy & Astrophysics, 482 (1): 179-196, arXiv:0801.3219, Bibcode: ...
Many species of molecule, including aminoacetonitrile (a molecule related to glycine), ethyl formate, and butyronitrile, have ...
For instance, 2-methyl-5-aminothiazoles were prepared via condensation and cyclization of aminoacetonitrile and ... 5-amino-2-benzylthiazole and 5-amino-4-carbethoxy-2-benzylthiazole by reacting dithiophenylacetic acid with aminoacetonitrile ...
... aminoacetonitrile) + H2O NH2-CH2-CN + 2H2O → NH3 + NH2-CH2-COOH (glycine) Furthermore, water and formaldehyde can react, via ...
In 2008, the Max Planck Institute for Radio Astronomy discovered the spectral lines of a glycine precursor (aminoacetonitrile) ...
... aminoacetonitrile MeSH D02.640.529.175 - chloramphenicol MeSH D02.640.529.175.850 - thiamphenicol MeSH D02.640.529.240 - ...
... can react with ammonia to give aminoacetonitrile, which can be hydrolysed to give glycine: HOCH2CN + NH3 → ...
... formally an aminoacetonitrile derivative of isoindolinone with two moles of HCN. When substituted 2-formylbenzoic acid, ...
This is especially true of nematodes, and has helped spur development of aminoacetonitrile derivatives for treatment against ... aminoacetonitrile class) - effective against a variety of nematodes including those resistant to other anthelmintic classes ...
Aminoacetonitrile is the organic compound with the formula NCCH2NH2. The compound is a colorless liquid. It is unstable at room ... Using radio astronomy, aminoacetonitrile was discovered in the Large Molecule Heimat, a giant gas cloud near the Galactic ... Aminoacetonitrile derivatives are useful antihelmintics. They act as nematode specific ACh agonists causing a spastic paralysis ... Tauber, Johannes; Opatz, Till (2015). "2-Aminoacetonitrile". E-EROS Encyclopedia of Reagents for Organic Synthesis: 1-4. doi: ...
the amino-acetonitrile derivative monepantel [1, 2]. Nevertheless, the effectiveness of the accessible anthelmintics over time ... the amino-acetonitrile derivative monepantel [1, 2]. Nevertheless, the effectiveness of the accessible anthelmintics over time ... Uncategorized , the amino-acetonitrile derivative monepantel [1, 2]. Nevertheless, the effectiveness of the accessible ...
Aminoacetonitrile derivatives. *Arecoline (Arecaline, Arecholine, Arecolin, Arecoline base, Arekolin, Methylarecaidin.). * ...
Aminoacetonitriles with Arylboronic Acids. Angew. Chem. Int. Ed. 2014, 53, 10510. ...
We have prepared a series of achiral aminoacetonitriles, bearing tri-ring benzamide moieties and an aminocyclohexanecarboxylate ...
Selye, H.; Nielsen, K. 1957: Factors influencing skeletal changes induced by aminoacetonitrile; effect of alizarin and ...
Amino-Acetonitrile Derivatives (AADs or orange). *Choosing and Using Products. *Application Methods for Cattle *Pour-on for ...
Zolvix Plus is a unique combination drench that contains monepantel, the only member of the amino-acetonitrile derivative or ...
Amino acetonitrile detected (2) Mar 2008 Extrasolar planetary methane Mar 2008 Spitzer finds organics and water in planet- ...
Aminoacetonitrile. Iprodione. Diacetylmorphine. Dextranase. Potassium Salicylate. Porphyropsin. Ammonium Cobaltous Sulfate. ...
Contents 1Definitions 1.1Challenge 1.2Descriptive 1.3Physics 1.4Living systems 1.5Death 1.6Viruses 2History of study 2.1Materialism 2.2Hylomorphism 2.3Spontaneous generation 2.4Vitalism 3Devel...
Aminoacetonitrile sulfate. *4 -Phenylacetophenone. *Methylacetophenone Chemical. *Nitroacetophenone Chemical. *Nitroacetoph ...
amino acetonitrile hydrochloride *Glycinamide hydrochloride *amino acetonitrile sulfate *Ethanolamine hydrochloride *methlyene ...
Home Chemical Groups and Actives Amino-Acetonitrile Derivatives (AADs or orange) Amino-Acetonitrile Derivatives (AADs or ... Types of amino-acetonitrile derivative. A guide to the different actives and the pests they affect are in Table 1. See the ...
... Structural Formula: CH2=N-CH2-CN. Appearance: White to white-like crystal. Content: ≥98.5%. ...
MeSH Terms: Aminoacetonitrile/analogs & derivatives; Apoptosis; Blotting, Western; Butadienes/pharmacology; Cell Line; Cell ...
Aminoacetonitrile Preferred Term Term UI T001825. Date01/01/1999. LexicalTag NON. ThesaurusID ... Aminoacetonitrile Preferred Concept UI. M0000933. Registry Number. 3739OQ10IJ. Related Numbers. 540-61-4. Scope Note. ... Aminoacetonitrile. Tree Number(s). D02.626.080.085. Unique ID. D000607. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/ ...
Cyanation of Phenol Derivatives with Aminoacetonitriles by Nickel Catalysis. Ryosuke Takise, Kenichiro Itami and Junichiro ...
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Aminoacetonitrile - Preferred Concept UI. M0000933. Scope note. Cyanomethylamine. Preferred term. Aminoacetonitrile Entry term( ...
The direct Strecker reaction of formaldehyde and ammonium cyanide produces methylene amino acetonitrile, which must be ... Amination of chloroacetic acid and the hydrolysis of aminoacetonitrile are the favored methods of production. ... DL-SerineHydantoinhydracideAMINOACETONITRILEBarium acetateteryleneBiuretSILKMethylenaminoacetonitrileAminoacetonitrile sulfate ...
N0000007838 Amino Alcohols N0000008208 Amino Sugars N0000168141 Amino-Acid N-Acetyltransferase N0000166568 Aminoacetonitrile ...
EFFECT OF GROWTH HORMONE AND AMINOACETONITRILE ON THE MITOTIC RATE OF EPIPHYSICAL CARTILAGE IN HYPOPHYSECTOMIZED RATS. PMID- ...
Some of these species are of prebiotic interest such as glycolaldehyde, the simplest sugar, or aminoacetonitrile, a possible ...
... pregnenolone-16α-carbonitrile and aminoacetonitrile on dialkyinitrosamine metabolism and mutagenicity in vitro, Chemico- ...
Aminoacetonitrile sulfate. *4 -Phenylacetophenone. *Methylacetophenone Chemical. *Nitroacetophenone Chemical. *Nitroacetoph ...
Aminoacetonitrile [D02.626.080.085] * Acrylonitrile [D02.626.095] * Aminopropionitrile [D02.626.151] * Amygdalin [D02.626.175] ...
Aminoacetonitrile Aminoacridines Aminoacylation Aminoacyltransferases Aminobenzoates Aminobiphenyl Compounds Aminobutyrates ...
Sulfur Amino Acyl-tRNA Synthetases Amino Alcohols Amino Sugars Amino-Acid N-Acetyltransferase Aminoacetonitrile Aminoacridines ...

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