Mechanisms involved in the metabotropic glutamate receptor-enhancement of NMDA-mediated motoneurone responses in frog spinal cord. (1/268)

1. The metabotropic glutamate receptor (mGluR) agonist trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD) (10-100 microM) depolarized isolated frog spinal cord motoneurones, a process sensitive to kynurenate (1.0 mM) and tetrodotoxin (TTX) (0.783 microM). 2. In the presence of NMDA open channel blockers [Mg2+; (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK801); 3,5-dimethyl-1-adamantanamine hydrochloride (memantine)] and TTX, trans-ACPD significantly potentiated NMDA-induced motoneurone depolarizations, but not alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionate (AMPA)- or kainate-induced depolarizations. 3. NMDA potentiation was blocked by (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) (240 microM), but not by alpha-methyl-(2S,3S,4S)-alpha-(carboxycyclopropyl)-glycine (MCCG) (290 microM) or by alpha-methyl-(S)-2-amino-4-phosphonobutyrate (L-MAP4) (250 microM), and was mimicked by 3,5-dihydroxyphenylglycine (DHPG) (30 microM), but not by L(+)-2-amino-4-phosphonobutyrate (L-AP4) (100 microM). Therefore, trans-ACPD's facilitatory effects appear to involve group I mGluRs. 4. Potentiation was prevented by the G-protein decoupling agent pertussis toxin (3-6 ng ml(-1), 36 h preincubation). The protein kinase C inhibitors staurosporine (2.0 microM) and N-(2-aminoethyl)-5-isoquinolinesulphonamide HCI (H9) (77 microM) did not significantly reduce enhanced NMDA responses. Protein kinase C activation with phorbol-12-myristate 13-acetate (5.0 microM) had no effect. 5. Intracellular Ca2+ depletion with thapsigargin (0.1 microM) (which inhibits Ca2+/ATPase), 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetracetic acid acetyl methyl ester (BAPTA-AM) (50 microM) (which buffers elevations of [Ca2+]i), and bathing spinal cords in nominally Ca2+-free medium all reduced trans-ACPD's effects. 6. The calmodulin antagonists N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W7) (100 microM) and chlorpromazine (100 microM) diminished the potentiation. 7. In summary, group I mGluRs selectively facilitate NMDA-depolarization of frog motoneurones via a G-protein, a rise in [Ca2+]i from the presumed generation of phosphoinositides, binding of Ca2+ to calmodulin, and lessening of the Mg2+-produced channel block of the NMDA receptor.  (+info)

Effects of varying the expression level of recombinant human mGlu1alpha receptors on the pharmacological properties of agonists and antagonists. (2/268)

1. Different expression levels of the human type 1alpha metabotropic glutamate (mGlu1alpha) receptor were obtained in transfected Chinese hamster ovary cells using an isopropyl beta-D-thiogalactopyranoside (IPTG) inducible system. Expression of mGlu1alpha receptors could not be detected using immunoblotting or immunocytochemical approaches in non-induced cells, however, controlled expression could be induced following IPTG addition in a time- and concentration-dependent manner. 2. In induced cells (100 microM IPTG, 20 h) the agonists L-quisqualate or 1-aminocyclopentane-1S,3R-dicarboxylic acid stimulated large increases in [3H]-inositol (poly)phosphate (in the presence of Li+) and inositol, 1,4,5-trisphosphate levels. 3. Induction with 1-100 microM IPTG allowed the receptor density to be increased incrementally and this not only resulted in an increase in the maximum response to L-quisqualate, 1-aminocyclopentane-1S,3R-dicarboxylic acid and (S)-3,5-dihydroxy-phenylglycine, but also in an increase in the respective potencies of each agent to activate phosphoinositide hydrolysis. 4. The intrinsic activity of the partial agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid dramatically increased with increasing receptor expression. 5. The activities of the competitive mGlu1alpha receptor antagonists (S)-alpha-methyl-4-carboxyphenylglycine and (S)-4-carboxy-3-hydroxyphenylglycine for inhibition of the effects of L-quisqualate or (S)-3,5-dihydroxyphenylglycine were found to be independent of the receptor expression level. 6. When the mGlu1alpha receptor was expressed at very high levels, no evidence for receptor constitutive activity could be detected, and none of the antagonists tested revealed either any intrinsic activity or negative efficacy. 7. These data demonstrate that both the potency and efficacy of mGlu1alpha receptor agonists are influenced by expression level, whilst mGlu1alpha receptor antagonist activities are independent of expression level.  (+info)

Glutamate regulates IP3-type and CICR stores in the avian cochlear nucleus. (3/268)

Neurons of the avian cochlear nucleus, nucleus magnocellularis (NM), are activated by glutamate released from auditory nerve terminals. If this stimulation is removed, the intracellular calcium ion concentration ([Ca2+]i) of NM neurons rises and rapid atrophic changes ensue. We have been investigating mechanisms that regulate [Ca2+]i in these neurons based on the hypothesis that loss of Ca2+ homeostasis causes the cascade of cellular changes that results in neuronal atrophy and death. In the present study, video-enhanced fluorometry was used to monitor changes in [Ca2+]i stimulated by agents that mobilize Ca2+ from intracellular stores and to study the modulation of these responses by glutamate. Homobromoibotenic acid (HBI) was used to stimulate inositol trisphosphate (IP3)-sensitive stores, and caffeine was used to mobilize Ca2+ from Ca2+-induced Ca2+ release (CICR) stores. We provide data indicating that Ca2+ responses attributable to IP3- and CICR-sensitive stores are inhibited by glutamate, acting via a metabotropic glutamate receptor (mGluR). We also show that activation of C-kinase by a phorbol ester will reduce HBI-stimulated calcium responses. Although the protein kinase A accumulator, Sp-cAMPs, did not have an effect on HBI-induced responses. CICR-stimulated responses were not consistently attenuated by either the phorbol ester or the Sp-cAMPs. We have previously shown that glutamate attenuates voltage-dependent changes in [Ca2+]i. Coupled with the present findings, this suggests that in these neurons mGluRs serve to limit fluctuations in intracellular Ca2+ rather than increase [Ca2+]i. This system may play a role in protecting highly active neurons from calcium toxicity resulting in apoptosis.  (+info)

The protein phosphatase inhibitor cantharidin induces head and foot formation in buds of Cassiopea andromeda (Rhizostomae, Scyphozoa). (4/268)

The polyps of Cassiopea andromeda produce spindle shaped, freely swimming buds which do not develop a head (a mouth opening surrounded by tentacles) and a foot (a sticky plate at the opposite end) until settlement to a suited substrate. The buds, therewith, look very similar to the planula larvae produced in sexual reproduction. With respect to both, buds and planulae, several peptides and the phorbolester TPA have been found to induce the transformation into a polyp. Here it is shown that cantharidin, a serine/threonine protein phosphatase inhibitor, induces head and foot formation in buds very efficiently in a 30 min treatment, the shortest yet known efficient treatment. Some resultant polyps show malformations which indicate that a bud is ordinary polyp tissue in which preparatory steps of head and foot formation mutually block each other from proceeding. Various compounds related to the transfer of methyl groups have been shown to affect head and foot formation in larvae of the hydrozoon Hydractinia echinata. These compounds including methionine, homocysteine, trigonelline, nicotinic acid and cycloleucine are shown to also interfere with the initiation of the processes which finally lead to head and foot formation in buds of Cassiopea andromeda.  (+info)

Cardiovascular response to group I metabotropic glutamate receptor activation in NTS. (5/268)

Glutamate is the proposed neurotransmitter of baroreceptor afferents at the level of the nucleus tractus solitarius (NTS). Exogenous glutamate in the NTS activates neurons through ionotropic and metabotropic glutamate receptors (mGluRs). This study tested the hypothesis that group I mGluRs in the NTS produce depressor, bradycardic, and sympathoinhibitory responses. In urethan-anesthetized rats, unilateral 30-nl microinjections of the group I-selective mGluR agonist 3,5-dihydroxyphenylglycine (DHPG) into the NTS decreased mean arterial pressure, heart rate, and lumbar sympathetic nerve activity. The dose of drug that produced 50% of the maximal response (ED50) was 50-100 microM. The response to microinjection of equal concentrations of DHPG or the general mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (ACPD) produced similar cardiovascular effects. The cardiovascular response to injection of DHPG or ACPD was abolished by NTS blockade of mGluRs with alpha-methyl-4-carboxyphenylglycine (MCPG). Blockade of ionotropic glutamate receptors with kynurenic acid did not attenuate the response to DHPG or ACPD injection. These data suggest that DHPG and ACPD activate mGluRs in the NTS and do not require ionotropic glutamate receptors to produce their cardiovascular response. In the NTS the group I mGluRs produce responses that are consistent with excitation of neurons involved in reducing sympathetic outflow, heart rate, and arterial pressure.  (+info)

Differential effects of metabotropic glutamate receptor antagonists on bursting activity in the amygdala. (6/268)

Differential effects of metabotropic glutamate receptor antagonists on bursting activity in the amygdala. Metabotropic glutamate receptors (mGluRs) are implicated in both the activation and inhibition of epileptiform bursting activity in seizure models. We examined the role of mGluR agonists and antagonists on bursting in vitro with whole cell recordings from neurons in the basolateral amygdala (BLA) of amygdala-kindled rats. The broad-spectrum mGluR agonist 1S,3R-1-aminocyclopentane dicarboxylate (1S,3R-ACPD, 100 microM) and the group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG, 20 microM) evoked bursting in BLA neurons from amygdala-kindled rats but not in control neurons. Neither the group II agonist (2S,3S,4S)-alpha-(carboxycyclopropyl)-glycine (L-CCG-I, 10 microM) nor the group III agonist L-2-amino-4-phosphonobutyrate (L-AP4, 100 microM) evoked bursting. The agonist-induced bursting was inhibited by the mGluR1 antagonists (+)-alpha-methyl-4-carboxyphenylglycine [(+)-MCPG, 500 microM] and (S)-4-carboxy-3-hydroxyphenylglycine [(S)-4C3HPG, 300 microM]. Kindling enhanced synaptic strength from the lateral amygdala (LA) to the BLA, resulting in synaptically driven bursts at low stimulus intensity. Bursting was abolished by (S)-4C3HPG. Further increasing stimulus intensity in the presence of (S)-4C3HPG (300 microM) evoked action potential firing similar to control neurons but did not induce epileptiform bursting. In kindled rats, the same threshold stimulation that evoked epileptiform bursting in the absence of drugs elicited excitatory postsynaptic potentials in (S)-4C3HPG. In contrast (+)-MCPG had no effect on afferent-evoked bursting in kindled neurons. Because (+)-MCPG is a mGluR2 antagonist, whereas (S)-4C3HPG is a mGluR2 agonist, the different effects of these compounds suggest that mGluR2 activation decreases excitability. Together these data suggest that group I mGluRs may facilitate and group II mGluRs may attenuate epileptiform bursting observed in kindled rats. The mixed agonist-antagonist (S)-4C3HPG restored synaptic transmission to control levels at the LA-BLA synapse in kindled animals. The different actions of (S)-4C3HPG and (+)-MCPG on LA-evoked bursting suggests that the mGluR1 antagonist-mGluR2 agonist properties may be the distinctive pharmacology necessary for future anticonvulsant compounds.  (+info)

On the respective roles of nitric oxide and carbon monoxide in long-term potentiation in the hippocampus. (7/268)

Perfusion of hippocampal slices with an inhibitor nitric oxide (NO) synthase blocked induction of long-term potentiation (LTP) produced by a one-train tetanus and significantly reduced LTP by a two-train tetanus, but only slightly reduced LTP by a four-train tetanus. Inhibitors of heme oxygenase, the synthetic enzyme for carbon monoxide (CO), significantly reduced LTP by either a two-train or four-train tetanus. These results suggest that NO and CO are both involved in LTP but may play somewhat different roles. One possibility is that NO serves a phasic, signaling role, whereas CO provides tonic, background stimulation. Another possibility is that NO and CO are phasically activated under somewhat different circumstances, perhaps involving different receptors and second messengers. Because NO is known to be activated by stimulation of NMDA receptors during tetanus, we investigated the possibility that CO might be activated by stimulation of metabotropic glutamate receptors (mGluRs). Consistent with this idea, long-lasting potentiation by the mGluR agonist tACPD was blocked by inhibitors of heme oxygenase but not NO synthase. Potentiation by tACPD was also blocked by inhibitors of soluble guanylyl cyclase (a target of both NO and CO) or cGMP-dependent protein kinase, and guanylyl cyclase was activated by tACPD in hippocampal slices. However, biochemical assays indicate that whereas heme oxygenase is constitutively active in hippocampus, it does not appear to be stimulated by either tetanus or tACPD. These results are most consistent with the possibility that constitutive (tonic) rather than stimulated (phasic) heme oxygenase activity is necessary for potentiation by tetanus or tACPD, and suggest that mGluR activation stimulates guanylyl cyclase phasically through some other pathway.  (+info)

Group I mGluR activation causes voltage-dependent and -independent Ca2+ rises in hippocampal pyramidal cells. (8/268)

Application of the metabotropic glutamate receptor (mGluR) agonist (1S, 3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) or the selective group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG) depolarized both CA3 and CA1 pyramidal cells in guinea pig hippocampal slices. Simultaneous recordings of voltage and intracellular Ca2+ levels revealed that the depolarization was accompanied by a biphasic elevation of intracellular Ca2+ concentration ([Ca2+]i): a transient calcium rise followed by a delayed, sustained elevation. The transient [Ca2+]i rise was independent of the membrane potential and was blocked when caffeine was added to the perfusing solution. The sustained [Ca2+]i rise appeared when membrane depolarization reached threshold for voltage-gated Ca2+ influx and was suppressed by membrane hyperpolarization. The depolarization was associated with an increased input resistance and persisted when either the transient or sustained [Ca2+]i responses was blocked. mGluR-mediated voltage and [Ca2+]i responses were blocked by (+)-alpha-methyl-4-carboxyphenylglycine (MCPG) or (S)-4-carboxy-3-hydroxyphenylglycine (4C3HPG). These data suggest that in both CA3 and CA1 hippocampal cells, activation of group I mGluRs produced a biphasic accumulation of [Ca2+]i via two paths: a transient release from intracellular stores, and subsequently, by influx through voltage-gated Ca2+ channels. The concurrent mGluR-induced membrane depolarization was not caused by the [Ca2+]i rise.  (+info)

TY - JOUR. T1 - The effect of cycloleucine on SFV A7(74) infection in mice. AU - Amor, S. AU - Webb, H E. PY - 1987/4. Y1 - 1987/4. N2 - Cycloleucine (CL), a non-metabolizable amino acid analogue, was found to reduce thymus and spleen weights in Semliki Forest virus (SFV) strain A7(74) infected and control mice. The maximum effects were seen when three daily doses of CL were given to mice 24 h after an SFV A7(74) infection. In these mice thymus atrophy led to abolition of thymus dependent immune responses and changes in the pathological features of the viral infection--the most striking feature being prevention of demyelination. In addition virus titres in the brains of CL treated infected mice were increased and prolonged. These results show that demyelination following an SFV A7(74) infection is not a result of direct virus action, but of a T-cell mediated mechanism.. AB - Cycloleucine (CL), a non-metabolizable amino acid analogue, was found to reduce thymus and spleen weights in Semliki ...
In this study, the regulation of striatal cyclic-3,5-adenosine monophosphate (cAMP) formation and GABA release by dopamine D1 and metabotropic glutamate receptors (mGluR) was studied in brain slices. In the absence of adenosine A2 receptor blockade, the mGluR agonist, 1-aminocyclopentane-1S,3R-dicarboxylic acid (1S,3R-ACPD) stimulated cAMP accumulation through a pertussis toxin-insensitive mechanism that could be blocked by L-serine-o-phosphate, but not by L(+)-2-amino-3-phosphonopropionic acid. However, in the presence of the adenosine antagonist, 3-isobutyl-1-methylxanthine, 1S,3R-ACPD had no significant effect on basal cAMP, but it inhibited cAMP formation stimulated by the D1 agonist, SKF 38393. This inhibitory response was prevented by pertussis toxin pretreatment and mimicked by L(+)-2-amino-3-phosphonopropionic acid, but it was unaffected by L-serine-o-phosphate. Thus, 1S,3R-ACPD was determined to activate distinct mGluRs in the striatum that mediate either inhibition or activation of ...
Metabotropic glutamate receptors (mGluRs) are coupled to effector systems through GTP-binding proteins (G-proteins) and appear to mediate slow synaptic responses in the CNS. Although mGluR-mediated increases in phosphoinositide hydrolysis have been well characterized, other mechanisms for signal transduction employed by mGluRs are poorly understood. We recently reported that the selective mGluR agonist 1- aminocyclopentane-1 S,3R-dicarboxylic acid (1S,3R-ACPD) increases cAMP accumulation in rat hippocampal slices. We have now investigated the mechanisms involved in this response. A number of G-protein-linked receptors that are not directly coupled to adenylate cyclase increase cAMP accumulation by potentiating cAMP responses to other agonists. Furthermore, previous studies suggest that glutamate increases cAMP accumulation by a mechanism that is dependent upon the presence of endogenous adenosine. Therefore, we tested the hypothesis that 1S,3R- ACPD-stimulated increases in cAMP accumulation in ...
We have studied the expression of metabotropic glutamate receptor (mGluR) mRNA by Northern blot analysis with a specific cDNA probe (the pmGR1 probe). In 1-day-old rats, the steady state levels of mRNA were higher in the hypothalamus and olfactory bulb, with intermediate levels in the cerebellum and low levels in the hippocampus and cerebral cortex. In the olfactory bulb, hypothalamus, and cerebral cortex, the expression of mGluR mRNA remained constant at 8 and 30 days of postnatal life. In contrast, in the cerebellum and hippocampus, mRNA levels increased progressively with age. There was no correlation between levels of mGluR mRNA and stimulation of polyphosphoinositide hydrolysis by 1-aminocyclopentane-1S,3R-dicarboxylic acid (trans-ACPD), which was much greater in brain slices from 8-day-old rats and was nearly absent in the adult cerebellum and olfactory bulb, where we have found the highest levels of mRNA. In addition, mGluR mRNA was detectable in cultured cerebellar granule cells but not ...
How is RS)-alpha-methyl-4-carboxy-phenylglycine abbreviated? M4CPG stands for RS)-alpha-methyl-4-carboxy-phenylglycine. M4CPG is defined as RS)-alpha-methyl-4-carboxy-phenylglycine rarely.
Metabotropic glutamate receptors (mGluRs) are coupled to effector systems through GTP-binding proteins (G-proteins) and appear to mediate slow synaptic responses in the CNS. Although mGluR-mediated increases in phosphoinositide hydrolysis have been well characterized, other mechanisms for signal transduction employed by mGluRs are poorly understood. We recently reported that the selective mGluR agonist 1- aminocyclopentane-1 S,3R-dicarboxylic acid (1S,3R-ACPD) increases cAMP accumulation in rat hippocampal slices. We have now investigated the mechanisms involved in this response. A number of G-protein-linked receptors that are not directly coupled to adenylate cyclase increase cAMP accumulation by potentiating cAMP responses to other agonists. Furthermore, previous studies suggest that glutamate increases cAMP accumulation by a mechanism that is dependent upon the presence of endogenous adenosine. Therefore, we tested the hypothesis that 1S,3R- ACPD-stimulated increases in cAMP accumulation in ...
A family of metabotropic glutamate receptors (mGluRs) has been elucidated by molecular cloning. To study the possible modulatory role of mGluRs in synaptic transmission, we tested the effect of a mGluR agonist, (±)-l-aminocyclopentane-trans-l,3-dicarboxylic acid (trans-ACPD), on the excitatory post-synaptic currents (EPSCS) recorded from neurons in thin slices of rat visual cortex, by using the whole-cell patch-clamp method. We found that trans-ACPD) markedly suppressed the evoked EPSCS without affecting the mean amplitude of spontaneous miniature EPSCS. This effect on the evoked EPSCS was blocked by a potassium channel blocker, 4-aminopyridine (4-AP) in a dose-dependent manner We suggest that trans-ACPD presynaptically inhibits EPSCS by a mechanism involving the 4-AP-sensitive channels. ...
1 Mouse cortical wedge preparations were used in order to study the effects of metabotropic glutamate receptor (mGluR) agonists and antagonists on the depolarization induced by N-methyl-D-aspartate (NMDA) or by (S)-α-amino-4-bromo-3-hydroxy-5-isoxazolepropionic acid (AMPA). 2 (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) (30-300 μM) significantly potentiated the depolarizations induced by NMDA, leaving unchanged those mediated by AMPA. This potentiation developed slowly and lasted for up to 60 min provided that the slices were continuously perfused with the mGluR agonist. 3 Concentration-response curves to NMDA in the absence and in the presence of 1S,3R-ACPD (100 μM) indicated that the potentiation was due to increased affinity of the NMDA receptor complex for its agonist. The maximal responses to NMDA were not potentiated. 4 Selective agonists of group 1 mGluR such as quisqualate (Quis) (30 μM) or (RS)-3,5-dihydroxyphenylglycine (DHPG) (300 μM) did not potentiate NMDA ...
cyclobutane-1,1-dicarboxylic acid 5445-51-2 MSDS report, cyclobutane-1,1-dicarboxylic acid MSDS safety technical specifications search, cyclobutane-1,1-dicarboxylic acid safety information specifications ect.
TY - JOUR. T1 - Activation of metabotropic glutamate receptors induces long-term depression of GABAergic inhibition in hippocampus. AU - Liu, Y. B.. AU - Disterhoft, J. F.. AU - Slater, N. T.. PY - 1993. Y1 - 1993. N2 - 1. The long-term enhancement of synaptic excitability in CA1 hippocampal pyramidal neurons produced by activation of metabotropic glutamate receptors (mGluRs) was studied in rabbit hippocampal slices in vitro. 2. Bath application of the mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) (5-20 μM) for 20 min produced a reversible depolarization of membrane potentiatil, blockade of spike accommodation, and increase in input resistance of CA1 neurons. However, a long-lasting increase in synaptic excitability was observed: single stimuli applied to the Schaffer collateral commisural fiber pathway evoked epileptiform discharges in the presence of 1S,3R-ACPD and after the washout of 1S,3R-ACPD, persistent paroxysmal depolarization shifts (PDSs) were evoked by ...
Thank you for your interest in spreading the word about Biochemical Society Transactions.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
10,11-dihydrodibenzo[b,f]oxepine-4,6-dicarboxylic acid - chemical structural formula, chemical names, chemical properties, synthesis references
TY - JOUR. T1 - Metabotropic glutamate receptor 5 tracer [18F]-FPEB displays increased binding potential in postcentral gyrus and cerebellum of male individuals with autism. T2 - A pilot PET study. AU - Fatemi, S. Hossein. AU - Wong, Dean F.. AU - Brašić, James R.. AU - Kuwabara, Hiroto. AU - Mathur, Anil. AU - Folsom, Timothy D.. AU - Jacob, Suma. AU - Realmuto, George M.. AU - Pardo, José V.. AU - Lee, Susanne. PY - 2018/2/12. Y1 - 2018/2/12. N2 - Background: Autism is a neurodevelopmental disorder that is first manifested during early childhood. Postmortem experiments have identified significantly elevated expression of metabotropic glutamate receptor 5 (mGluR5) in cerebellar vermis and prefrontal cortex of individuals with autism. Methods: In the current study we employed the mGluR5 tracer [18F]-3-fluoro-5-[(pyridin-3-yl)ethynyl]benzonitrile ([18F]-FPEB) to quantify mGluR5 binding in vivo in adults with autism vs. healthy controls using positron emission tomography (PET). Results: We ...
The design, synthesis and evaluation of eight contrast agents for metabotropic glutamate receptors is reported. Each of the contrast agents contains a selective mGluR5 binding moiety linked to a DOTA-derived gadolinium complex. The potential of these systems was evaluated in vitro for application as respon
Anti Metabotropic Glutamate Receptor 2/3 (mGluR2/3) Antibody , Rabbit Anti-Rat Polyclonal Antibody validated in WB, IHC-P, IHC-F (ABD13051), Abgent
BioAssay record AID 252326 submitted by ChEMBL: Percentage of maximal glutamate (1 mM) response of human metabotropic glutamate receptor 2 done at 30 degree C for 1 hr.
The IUPHAR/BPS Guide to Pharmacology. mGlu4 receptor - Metabotropic glutamate receptors. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
The IUPHAR/BPS Guide to Pharmacology. mGlu5 receptor - Metabotropic glutamate receptors. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
The Report Metabotropic Glutamate Receptor 5 (GPRC1E or MGLUR5 or GRM5) - Pipeline Review, H2 2017 provides information on pricing, market analysis,...
BioAssay record AID 107086 submitted by ChEMBL: Compound was tested for its antagonist activity against Ser152 and Thr175 (Metabotropic glutamate receptor 5).
There are no specific protocols for Recombinant Human Metabotropic Glutamate Receptor 1 protein (ab114707). Please download our general protocols booklet
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CAS NO:627877-90-1; Chemical name:1H-Indole-1,3-dicarboxylic acid, 2,3-dihydro-2-oxo-3-phenyl-, diphenylester, (3S)- ; physical and chemical property of 627877-90-1, 1H-Indole-1,3-dicarboxylic acid, 2,3-dihydro-2-oxo-3-phenyl-, diphenylester, (3S)- is provided by ChemNet.com
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17 beta-hydroxy-7 alpha-methyl-5-estren-3-one: RN given refers to (7alpha,17beta)-isomer; structure given in first source; progestational hormone antagonist
16602-88-3 - ZTBPMPNPJPKIHB-UHFFFAOYSA-N - Hydrazine, 1-(alpha-methyl-3,4-methylenedioxy)phenethyl- - Similar structures search, synonyms, formulas, resource links, and other chemical information.
TY - JOUR. T1 - Molecular characterization of a novel metabotropic glutamate receptor mGluR5 coupled to inositol phosphate/Ca2+ signal transduction. AU - Abe, T.. AU - Sugihara, H.. AU - Nawa, H.. AU - Shigemoto, R.. AU - Mizuno, N.. AU - Nakanishi, S.. N1 - Copyright: Copyright 2004 Elsevier B.V., All rights reserved.. PY - 1992. Y1 - 1992. N2 - A cDNA clone for a new metabotropic glutamate receptor, mGluR5, was isolated through polymerase chain reaction-mediated DNA amplification by using primer sequences conserved among the metabotropic glutamate receptor (mGluR) family and by the subsequent screening of a rat brain cDNA library. The cloned receptor consists of 1171 amino acid residues and exhibits a structural architecture common to the mGluR family, possessing a large extracellular domain preceding the seven putative membrane-spanning segments. mGluR5 shows the highest sequence similarity to mGluR1 among the mGluR members and is coupled to the stimulation of phosphatidylinositol ...
PLD-118, formerly BAY 10-8888, is a synthetic antifungal derivative of the naturally occurring beta-amino acid cispentacin. We studied the activity of PLD-118 in escalating dosages against experimental oropharyngeal and esophageal candidiasis (OPEC) caused by fluconazole (FLC)-resistant Candida albicans in immunocompromised rabbits. Infection was established by fluconazole-resistant (MIC | 64 microg/ml) clinical isolates from patients with refractory esophageal candidiasis. Antifungal therapy was administered for 7 days. Study groups consisted of untreated controls; animals receiving PLD-118 at 4, 10, 25, or 50 mg/kg of body weight/day via intravenous (i.v.) twice daily (BID) injections; animals receiving FLC at 2 mg/kg/day via i.v. BID injections; and animals receiving desoxycholate amphotericin B (DAMB) i.v. at 0.5 mg/kg/day. PLD-118- and DAMB-treated animals showed a significant dosage-dependent clearance of C. albicans from the tongue, oropharynx, and esophagus in comparison to untreated controls (P
Microglia are the immune cell of the central nervous system and become reactive in response to infection or trauma. In Multiple Sclerosis (MS) microglia show early reactivity which may contribute to subsequent neurotoxicity. Glutamate has been implicated in the neurodegeneration in MS. Microglia express subtypes of metabotropic glutamate receptors (mGluRs), the activation of which can lead to microglial evoked neurotoxicity (group II) or neuroprotection (group III). This suggests that release of glutamate from neurones or glial cells may activate microglia via these receptors. Increased microglial reactivity during disease is possibly due to an imbalance of mGluR expression with neurotoxic group II increased above neuroprotective group III mGluRs. Microglial expression of mGluR subtypes was therefore investigated on activated compared with untreated cells. It was found that microglia exposed to myelin expressed increased levels of group II and mGluRl and 8 subtypes compared with control cells. ...
This study tested the hypothesis that activation of group I mGluRs produces cardiovascular effects consistent with excitation of NTS neurons involved in inhibition of HR and sympathetic outflow. The primary findings of the study were that microinjection of DHPG into the NTS produced dose-dependent decreases in MAP, HR, and LSNA. These effects of DHPG were similar to those of general mGluR activation with ACPD. The effects of DHPG or ACPD were abolished by administration of the mGluR antagonist MCPG. Furthermore, blockade of ionotropic glutamate receptors with kynurenic acid did not attenuate the effects of DHPG or ACPD. These data suggest that DHPG and ACPD activate mGluRs in the NTS to produce depressor, bradycardic, and sympathoinhibitory responses that do not require ionotropic glutamate receptors. Thus the cardiovascular response to activation of group I mGluRs in the NTS mimics stimulation of the arterial baroreflex and appears to produce this effect by exciting neurons within the NTS that ...
The metabotropic glutamate receptors (mGluRs) are key receptors in the modulation of excitatory synaptic transmission in the central nervous system. Here we have determined three different crystal structures of the extracellular ligand-binding region of mGluR1--in a complex with glutamate and in two …
TY - JOUR. T1 - Functional partnership between mGlu3 and mGlu5 metabotropic glutamate receptors in the central nervous system. AU - Di Menna, Luisa. AU - Joffe, Max E.. AU - Iacovelli, Luisa. AU - Orlando, Rosamaria. AU - Lindsley, Craig W.. AU - Mairesse, Jèrome. AU - Gressèns, Pierre. AU - Cannella, Milena. AU - Caraci, Filippo. AU - Copani, Agata. AU - Bruno, Valeria. AU - Battaglia, Giuseppe. AU - Conn, P. Jeffrey. AU - Nicoletti, Ferdinando. PY - 2017/10/25. Y1 - 2017/10/25. N2 - mGlu5 receptors are involved in mechanisms of activity-dependent synaptic plasticity, and are targeted by drugs developed for the treatment of CNS disorders. We report that mGlu3 receptors, which are traditionally linked to the control of neurotransmitter release, support mGlu5 receptor signaling in neurons and largely contribute to the robust mGlu5 receptor-mediated polyphosphoinositide hydrolysis in the early postnatal life. In cortical pyramidal neurons, mGlu3 receptor activation potentiated mGlu5 ...
4OO9: Structure of the human class C GPCR metabotropic glutamate receptor 5 transmembrane domain in complex with the negative allosteric modulator mavoglurant
Attwell PJ, Singh Kent N, Jane DE, Croucher MJ, Bradford HF (1998). „Anticonvulsant and glutamate release-inhibiting properties of the highly potent metabotropic glutamate receptor agonist (2S,2R, 3R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV). Brain Research. 805 (1-2): 138-43. PMID 9733953. doi:10.1016/S0006-8993(98)00698-2 ...
Name: Naphthalene-1,4-dicarboxylic acid CA Name: 1,4-Naphthalenedicarboxylic acid Molecular Structure: Naphthalene-1,4-dicarboxylic acid,1,4-Naphthalenedicarboxylic acid,CAS 605-70-9,216.19,C12H8O4 Naphthalene-1,4-dicarboxylic acid,1,4-Naphthalenedicarboxylic acid,CAS 605-70-9,216.19,C12H8O4 Molecular Formula:C12H8O4 Molecular Weight: 216.19 CAS Registry Number: 605-70-9
To gain insight into melanoma pathogenesis, we characterized an insertional mouse mutant, TG3, that is predisposed to develop multiple melanomas. Physical mapping identified multiple tandem insertions of the transgene into intron 3 of Grm1 (encoding metabotropic glutamate receptor 1) with concomitan …
Capot chimico CAS# 81303-65-3, 2-Methyl-2H-pyrazole-3,4-dicarboxylic acid 4-ethyl ester. 81303-65-3 MSDS,ROS,81303-65-3 MOA,COA,SPECS,pecifications,1H-NMR,GHS,CAT #32047;1-Methyl-1H-pyrazole-4,5-dicarboxylic acid 4-ethyl ester;4-ethoxycarbonyl-2-methylpyrazole-3-carboxylic acid
Relatively unreactive organic reagents should be collected in container A. If halogenated, they should be collected in container B. For solid residues use container C ...
The present invention relates to a novel 2-hydroxy-naphthalene-3,6-dicarboxylic acid derivative. The compound is useful as a raw material for dyes, pigments, photosensitive materials and the like.
Vilskersts Reinis; Vigante Brigita; Neidere Zaiga; Krauze Aivars; Domracheva Ilona; Shestakova Irina; Duburs Gunars; Dambrova Maija; Bisenieks Egils; Velena Astrida. 2,6-dimethyl-4-(2,3-dichlorophenyl)-1,4-dihydropyridine-3,5-dicarboxylic acid propyloxyalkyl esters. LV14662, 20.06.2013 ...
TY - JOUR. T1 - Activation of metabotropic glutamate receptors induces an inward current in rat dopamine mesencephalic neurons. AU - Mercuri, N. B.. AU - Stratta, F.. AU - Calabresi, P.. AU - Bonci, A.. AU - Bernardi, G.. PY - 1993. Y1 - 1993. N2 - To investigate the electrophysiological effects of the stimulation of the metabotropic excitatory amino acid receptors, we applied trans-1-amino-cyclopentane-1,3-dicarboxylate, an agonist of this type of receptors, on presumed rat dopamine cells intracellularly recorded in vitro. Trans-1-amino-cyclopentane-1,3-dicarboxylate (3-30 μM, t-ACPD) caused a sustained increase of the spontaneous firing rate and a depolarization. When the membrane potential was held at about the resting level (-50, -60 mV), by the single-electrode voltage-clamp technique, t-ACPD induced an inward current. In 57% of the tested cells the inward current was associated with a decrease of the apparent input conductance. In the remaining cells no obvious changes in membrane ...
TY - JOUR. T1 - Activation of interneurons at the stratum oriens/alveus border suppresses excitatory transmission to apical dendrites in the CA1 area of the mouse hippocampus. AU - Yanovsky, Y.. AU - Sergeeva, O. A.. AU - Freund, T.. AU - Haas, H. L.. PY - 1997/1/6. Y1 - 1997/1/6. N2 - The consequences of activation or inactivation of interneurons at the CA1 stratum oriens/alveus border for signal transmission at the apical dendritic region of pyramidal cells were investigated in slices from mice submerged in a perfusion chamber. A characteristic subpopulation of interneurons with a horizontal dendritic tree in this region, which sends a GABAergic projection to the apical dendrites of CA1 pyramidal cells is strongly excited by metabotropic glutamate receptor activation and receives GABAergic input from vasoactive intestinal polypeptide-containing interneurons. Pressure ejection of glutamate or the metabotropic agonist 1s,3r-aminocyclopentane dicarboxylic acid from micropipettes onto the stratum ...
Metabotropic glutamate receptors (mGluRs) are G protein-coupled receptors (GPCRs) that contribute to the regulation of integrative brain functions such as cognition, motor control, and neural development. Metabotropic glutamate receptors are members of a unique class of GPCRs (class III) that include the calcium sensing and γ-aminobutyric acid type B receptors. Although mGluRs bear little sequence homology to well-characterized members of the GPCR superfamily, both second messenger-dependent protein kinases and G protein-coupled receptor kinases (GRKs) contribute to mGluR desensitization. Therefore, in the present study, we examined whether β-arrestins, regulators of GPCR desensitization and endocytosis, are required for mGluR1a desensitization and internalization in human embryonic kidney (HEK) 293 cells. Unlike what has been reported for other GPCRs, we find that in response to agonist stimulation, mGluR1a internalization is selectively mediated by β-arrestin1 in HEK 293 cells. However, ...
TY - JOUR. T1 - Homer1a-Dependent Crosstalk Between NMDA and Metabotropic Glutamate Receptors in Mouse Neurons. AU - Bertaso, Federica. AU - Roussignol, Gautier. AU - Worley, Paul. AU - Bockaert, Joël. AU - Fagni, Laurent. AU - Ango, Fabrice. N1 - Copyright: Copyright 2013 Elsevier B.V., All rights reserved.. PY - 2010. Y1 - 2010. N2 - Background: A large number of evidences suggest that group-I metabotropic glutamate receptors (mGluR1a, 1b, 1c, 5a, 5b) can modulate NMDA receptor activity. Interestingly, a physical link exists between these receptors through a Homer-Shank multi-protein scaffold that can be disrupted by the immediate early gene, Homer1a. Whether such a versatile link supports functional crosstalk between the receptors is unknown. Methodology/Principal Findings: Here we used biochemical, electrophysiological and molecular biological approaches in cultured mouse cerebellar neurons to investigate this issue. We found that Homer1a or dominant negative Shank3 mutants that disrupt the ...
Metabotropic glutamate receptor (mGluR)-dependent calcium ion (Ca2+) signaling in astrocytic processes regulates synaptic transmission and local blood flow essential for brain function. However, because of difficulties in imaging astrocytic processes, the subcellular spatial organization of mGluR-dependent Ca2+ signaling is not well characterized and its regulatory mechanism remains unclear. Using genetically encoded Ca2+ indicators, we showed that despite global stimulation by an mGluR agonist, astrocyte processes intrinsically exhibited a marked enrichment of Ca2+ responses. Immunocytochemistry indicated that these polarized Ca2+ responses could be attributed to increased density of surface mGluR5 on processes relative to the soma. Single-particle tracking of surface mGluR5 dynamics revealed a membrane barrier that blocked the movement of mGluR5 between the processes and the soma. Overexpression of mGluR or expression of its carboxyl terminus enabled diffusion of mGluR5 between the soma and ...
Engers DW, Blobaum AL, Gogliotti RD, Cheung YY, Salovich JM, Garcia-Barrantes PM, Daniels JS, Morrison R, Jones CK, Soars MG, Zhuo X, Hurley J, Macor JE, Bronson JJ, Conn PJ, Lindsley CW, Niswender CM, Hopkins CR (2016). Discovery, Synthesis, and Preclinical Characterization of N-(3-Chloro-4-fluorophenyl)-1H-pyrazolo[4,3-b]pyridin-3-amine (VU0418506), a Novel Positive Allosteric Modulator of the Metabotropic Glutamate Receptor 4 (mGlu4). ACS Chem Neurosci. 7: 1192-200. doi:10.1021/acschemneuro.6b00035. PMID 27075300 ...
Définitions de Metabotropic_glutamate_receptor_5, synonymes, antonymes, dérivés de Metabotropic_glutamate_receptor_5, dictionnaire analogique de Metabotropic_glutamate_receptor_5 (anglais)
Molbase Encyclopedia provides furan-2,5-dicarboxylic acid (3238-40-2) basic information, physical and chemical properties, safety information, toxicity, customs data, synthetic routes, maps, MSDS, generation methods and uses, and its upstream and downstream products, find furan-2,5-dicarboxylic acid introduction, on the Molbase Encyclopedia!
1ISS: Structural views of the ligand-binding cores of a metabotropic glutamate receptor complexed with an antagonist and both glutamate and Gd3+.
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PRF readers can get free access to a selected Journal of Pain paper each month, thanks to the American Pain Society. Get the free full text of the selection from the November 2017 issue here.. ...
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Clinical Trials - clinicaltrials.gov This noninterventional study will assess genomic changes in the metabotropic glutamate receptor (mGluR) network in children...
C. Millán, R. Luján, R. Shigemoto, and J. Sánchez Prieto, The inhibition of glutamate release by metabotropic glutamate receptor 7 affects both [Ca2+]c and cAMP. Evidence for a strong reduction of Ca2+ entry in single nerve terminals, Journal of Biological Chemistry, vol. 277, no. 16, pp. 14092-14101, 2002 ...
Buy LY 379268 (CAS 191471-52-0), a water soluble systemically active group II mGluR agonist. Join researchers using high quality LY 379268 from Abcam and…
Disclosed is an optimized process and apparatus for more efficiently and economically producing aromatic discarboxylic acids. The process reduces costs associated with hydrogenation by forming a final composite product containing unhydrogenated acid particles.
Comprehensive VHDL ist das 5-tägige Training für den Industriestandard, in dem die Anwendung von VHDL für PLD- und ASIC-Design trainiert wird.
Cycloleucine is a non-proteinogenic amino acid. It could be classified as a cyclic derivate of norleucine, having two hydrogen ... Cycloleucine is a non-metabolisable amino acid and is a specific and reversible inhibitor of nucleic acid methylation, and as ... Cycloleucine treatment in conjunction with higher levels of cytochrome P450 2E1 (CYP2E1) and lower SAM levels in pyrazole ... Cycloleucine at Sigma-Aldrich Caboche M, Bachellerie JP (March 1977). "RNA methylation and control of eukaryotic RNA ...
Evidence that cycloleucine affects the high-affinity systems of amino acid uptake in cultured human fibroblasts M Feneant; M ... The influence of cycloleucine on the amino acid uptake was not specific either to the amino acid concerned or to a particular ... The influence of cycloleucine on kinetic parameters of uptake of L-alanine, L-proline and L-leucine into cultured human ... M Feneant, N Moatti, J Maccario, M Gautier, S Guerroui, A Lemonnier; Evidence that cycloleucine affects the high-affinity ...
Cycloleucine could be classified as a cyclic derivative of norleucine. With a cyclopentane-ring, it has two hydrogen atoms ...
The effect of cycloleucine on SFV A7(74) infection in mice. International Journal of Experimental Pathology. 1987 Apr;68(2):225 ... Amor, S ; Webb, H E. / The effect of cycloleucine on SFV A7(74) infection in mice. In: International Journal of Experimental ... The effect of cycloleucine on SFV A7(74) infection in mice. / Amor, S; Webb, H E. ... Cycloleucine (CL), a non-metabolizable amino acid analogue, was found to reduce thymus and spleen weights in Semliki Forest ...
Cycloleucine / analogs & derivatives * Cycloleucine / pharmacology * Egtazic Acid / pharmacology * Glycine / analogs & ...
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The S-adenosylmethionine synthesis inhibitor cycloleucine blocks methionine-dependent autoinducer synthesis. Thus, it appears ...
Cycloleucine. Purity: 98%. [52-52-8], MFCD00001381. SS-1051. Cyclo(-leu-phe). Purity: 95%. [7280-77-5], MFCD00672388. ...
Fmoc-cycloleucine. Purity: 98%. [117322-30-2], MFCD01074696. SS-2576. Fmoc-cyclopentyl-Gly-OH. Purity: 98%. [220497-61-0], ...
CH$NAME: Cycloleucine. CH$NAME: Cycloleucin. CH$NAME: 1-Amino-1-cyclopentanecarboxylic acid. CH$NAME: acpc. CH$COMPOUND_CLASS: ...
Effect of 5-Bromo-2-deoxyuridine on Transport of Deoxyglucose and Cycloleucine in 3T6 Fibroblasts ...
Administration of cycloleucine, an inhibitor of MAT, causes decreases of proteolipid protein and dimmer-20, major components of ... Distal motor axonopathy and central nervous system myelin vacuolation caused by cycloleucine, an inhibitor of methionine ... myelin in CNS of rats (8). Light and electron microscopic examination after administration of cycloleucine reveals that ...
Crystal structure of the NR1 ligand binding core in complex with cycloleucine. ...
... cycloleucine, in HeLa cells indicated that reduced methylation did not alter the pattern of pre-rRNA processing but rather ...
Chemical-registry-number] 0 / Sulfides; 0TQU7668EI / Cycloleucine; 2425D15SYM / lead sulfide; 2P299V784P / Lead; 3814-46-8 / ...
... d-fructose-cyclo-leucine). Acta Crystallogr E Crystallogr Commun. 75(Pt 8):1096-1101. doi: 10.1107/S2056989019009253. ...
... or cycloleucine. This effect is specific for ADMA but not symmetrical dimethylarginine. The upregulation of ADMA release by ...
... cycloleucine) and, ββ-cyclopentamethylene-β-mercaptopropionic acid (see Hruby et al. (1990), supra). ...
However, cycloleucine, an upstream inhibitor of Sam-S, also increases life span, suggesting that life span extension is most ...
... cycloleucine, cyclomenol, cyclomethicone, cyclomethycaine, cyclopentamine, cyclopenthiazide, cyclopentolate, cyclopenazine, ...
Alguard, M. J., Ash, W. W., Baum, G., Clendenin, J. E., Cooper, P. S., Coward, D. H., Ehrlich, R. D., Etkin, A., Hughes, V. W., Kobayakawa, H., Kondo, K., Lubell, M. S., Miller, R. H., Palmer, D. A., Raith, W., Sasao, N., Schüler, K. P., Sherden, D. J., Sinclair, C. K. & Souder, P. A., Jan 1 1976, In : Physical Review Letters. 37, 19, p. 1261-1265 5 p.. Research output: Contribution to journal › Article ...
Cycloleucine/analogs & derivatives. *Cycloleucine/pharmacology. *Dendrites/chemistry. *Dendrites/physiology*. * ...
Cycloleucine - Preferred Concept UI. M0005476. Scope note. An amino acid formed by cyclization of leucine. It has cytostatic, ... Cycloleucine Entry term(s). 1 Aminocyclopentanecarboxylic Acid 1-Aminocyclopentanecarboxylic Acid Acid, 1- ... Cycloleucine Entry term(s):. 1 Aminocyclopentanecarboxylic Acid. 1-Aminocyclopentanecarboxylic Acid. Acid, 1- ...
cycloleucine. 52-52-8. 5-fluoro-2-iodobenzoic acid. 52548-63-7. ...
Chopra, V., Quinti, L., Kim, J., Vollor, L., Narayanan, K. L., Edgerly, C., Cipicchio, P. M., Lauver, M. A., Choi, S. H., Silverman, R. B., Ferrante, R. J., Hersch, S. & Kazantsev, A. G., 2012 Dec 27, In : Cell Reports. 2, 6, p. 1492-1497 6 p.. Research output: Contribution to journal › Article ...
Cycloleucine / analogs & derivatives * Cycloleucine / pharmacology * Electric Conductivity * Electrophysiology * Hippocampus / ...
For example, cycloleucine, which is often treated as a classic inhibitor of MAT activity, only has a Ki of 10 mM against human ... cycloleucine, is treated in the literature as a classic inhibitor of MAT activity, but typically acts weakly [23]. Of the ...
3. Correction of influx data for the extracellular compartment revealed influx of 14C-cycloleucine and 14C-glycine to be ... 3. Correction of influx data for the extracellular compartment revealed influx of 14C-cycloleucine and 14C-glycine to be ... 3. Correction of influx data for the extracellular compartment revealed influx of 14C-cycloleucine and 14C-glycine to be ... 3. Correction of influx data for the extracellular compartment revealed influx of 14C-cycloleucine and 14C-glycine to be ...

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