A chelating agent relatively more specific for calcium and less toxic than EDETIC ACID.

Plasticity of first-order sensory synapses: interactions between homosynaptic long-term potentiation and heterosynaptically evoked dopaminergic potentiation. (1/3731)

Persistent potentiations of the chemical and electrotonic components of the eighth nerve (NVIII) EPSP recorded in vivo in the goldfish reticulospinal neuron, the Mauthner cell, can be evoked by afferent tetanization or local dendritic application of an endogenous transmitter, dopamine (3-hydroxytyramine). These modifications are attributable to the activation of distinct intracellular kinase cascades. Although dopamine-evoked potentiation (DEP) is mediated by the cAMP-dependent protein kinase (PKA), tetanization most likely activates a Ca2+-dependent protein kinase via an increased intracellular Ca2+ concentration. We present evidence that the eighth nerve tetanus that induces LTP does not act by triggering dopamine release, because it is evoked in the presence of a broad spectrum of dopamine antagonists. To test for interactions between these pathways, we applied the potentiating paradigms sequentially. When dopamine was applied first, tetanization produced additional potentiation of the mixed synaptic response, but when the sequence was reversed, DEP was occluded, indicating that the synapses potentiated by the two procedures belong to the same or overlapping populations. Experiments were conducted to determine interactions between the underlying regulatory mechanisms and the level of their convergence. Inhibiting PKA does not impede tetanus-induced LTP, and chelating postsynaptic Ca2+ with BAPTA does not block DEP, indicating that the initial steps of the induction processes are independent. Pharmacological and voltage-clamp analyses indicate that the two pathways converge on functional AMPA/kainate receptors for the chemically mediated EPSP and gap junctions for the electrotonic component or at intermediaries common to both pathways. A cellular model incorporating these interactions is proposed on the basis of differential modulation of synaptic responses via receptor-protein phosphorylation.  (+info)

Augmentation is a potentiation of the exocytotic process. (2/3731)

Short-term synaptic enhancement is caused by an increase in the probability with which synaptic terminals release transmitter in response to presynaptic action potentials. Since exocytosed vesicles are drawn from a readily releasable pool of packaged transmitter, enhancement must result either from an increase in the size of the pool or an elevation in the fraction of releasable vesicles that undergoes exocytosis with each action potential. We show here that at least one major component of enhancement, augmentation, is not caused by an increase in the size of the readily releasable pool but is instead associated with an increase in the efficiency with which action potentials induce the exocytosis of readily releasable vesicles.  (+info)

Selective induction of LTP and LTD by postsynaptic [Ca2+]i elevation. (3/3731)

Long-term potentiation (LTP) and long-term depression (LTD), two prominent forms of synaptic plasticity at glutamatergic afferents to CA1 hippocampal pyramidal cells, are both triggered by the elevation of postsynaptic intracellular calcium concentration ([Ca2+]i). To understand how one signaling molecule can be responsible for triggering two opposing forms of synaptic modulation, different postsynaptic [Ca2+]i elevation patterns were generated by a new caged calcium compound nitrophenyl-ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid in CA1 pyramidal cells. We found that specific patterns of [Ca2+]i elevation selectively activate LTP or LTD. In particular, only LTP was triggered by a brief increase of [Ca2+]i with relatively high magnitude, which mimics the [Ca2+]i rise during electrical stimulation typically used to induce LTP. In contrast, a prolonged modest rise of [Ca2+]i reliably induced LTD. An important implication of the results is that both the amplitude and the duration of an intracellular chemical signal can carry significant biological information.  (+info)

Diffusion barriers limit the effect of mobile calcium buffers on exocytosis of large dense cored vesicles. (4/3731)

Fast exocytosis in melanotropic cells, activated by calcium entry through voltage-gated calcium channels, is very sensitive to mobile calcium buffers (complete block at 800 microM ethylene glycol bis(beta-aminoethyl ether)-N,N,N'N'-tetraacetic acid (EGTA)). This indicates that calcium diffuses a substantial distance from the channel to the vesicle. Surprisingly, 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), having a similar KD for calcium as EGTA but a approximately 100 times faster binding rate, blocked exocytosis only twice as effectively as EGTA. Using computer simulations, we demonstrate that this result cannot be explained by free diffusion and buffer binding rates. We hypothesized that local saturation of calcium buffers is involved. A diffusion barrier for both calcium and buffer molecules, located 50-300 nm from the membrane and reducing diffusion 1000 to 10,000 times, generated similar calcium concentrations for specific concentrations of EGTA and BAPTA. With such barriers, calcium rise phase kinetics upon short step depolarizations (2-20 ms) were faster for EGTA than for BAPTA, implying that short depolarizations should allow exocytosis with 50 microM EGTA but not with 25 microM BAPTA. This prediction was confirmed experimentally with capacitance measurements. Coupling exocytosis to calcium dynamics in the model, we found that a barrier with a approximately 3000 times reduced diffusion at approximately 130 nm beneath the membrane best explains the experimentally observed effects of EGTA and BAPTA on block and kinetics of release.  (+info)

Isolation and partial characterization of Drosophila myoblasts from primary cultures of embryonic cells. (5/3731)

We describe a method for preparing highly enriched cultures of Drosophila myoblasts from a heterogeneous cell population derived from gastrulating embryos. Enriched cultures are prepared by plating this heterogeneous population of cells in medium from which much of the free calcium is chelated by ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N'-tetraacetate (EGTA). Adhesion of myoblasts to tissue culture plastic is better than that of other cell types when plated in this medium. Data concerning cell identity, timing of S phase, and fusion kinetics document the degree of enrichment for myogenic cells and illustrate their synchronous differentiation in vitro.  (+info)

Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve. (6/3731)

1. Using a microelectrode technique, acetylcholine (ACh)-induced membrane potential changes were characterized using various types of inhibitors of K+ and Cl- channels in rabbit aortic valve endothelial cells (RAVEC). 2. ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization. 3. High K+ blocked and low K+ potentiated the two ACh-induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh-induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization. 4. In Ca2+-free solution or in the presence of Co2+ or Ni2+, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA-AM-treated cells, ACh produced only a depolarization. 5. A low concentration of A23187 attenuated the ACh-induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co2+. 6. Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization. 7. It is concluded that in RAVEC, ACh produces a two-component hyperpolarization followed by a depolarization. It is suggested that ACh-induced Ca2+ release from the storage sites causes a transient hyperpolarization due to activation of ChTX-sensitive K+ channels and that ACh-activated Ca2+ influx causes a sustained hyperpolarization by activating both ChTX- and apamin-sensitive K+ channels. Both volume-sensitive Cl- channels and the Na+-K+-Cl- cotransporter probably contribute to the ACh-induced depolarization.  (+info)

Mechanisms involved in the metabotropic glutamate receptor-enhancement of NMDA-mediated motoneurone responses in frog spinal cord. (7/3731)

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)

Cross-coupling between voltage-dependent Ca2+ channels and ryanodine receptors in developing ascidian muscle blastomeres. (8/3731)

1. Ascidian blastomeres of muscle lineage express voltage-dependent calcium channels (VDCCs) despite isolation and cleavage arrest. Taking advantage of these large developing cells, developmental changes in functional relations between VDCC currents and intracellular Ca2+ stores were studied. 2. Inactivation of ascidian VDCCs is Ca2+ dependent, as demonstrated by two pieces of evidence: (1) a bell-shaped relationship between prepulse voltage and amplitude during the test pulse in Ca2+, but not in Ba2+, and (2) the decay kinetics of Ca2+ currents (ICa) obtained as the size of tail currents. 3. During replacement in the external solution of Ca2+ with Ba2+, the inward current appeared biphasic: it showed rapid decay followed by recovery and slow decay. This current profile was most evident in the mixed bath solution (2 % Ca2+ and 98 % Ba2+, abbreviated to '2Ca/98Ba'). 4. The biphasic profile of I2Ca/98Ba was significantly attenuated in caffeine and in ryanodine, indicating that Ca2+ release is involved in shaping the current kinetics of VDCCs. After washing out the caffeine, the biphasic pattern was reproducibly restored by depolarizing the membrane in calcium-rich solution, which is expected to refill the internal Ca2+ stores. 5. The inhibitors of endoplasmic reticulum (ER) Ca2+-ATPase (SERCAs) cyclopiazonic acid (CPA) and thapsigargin facilitated elimination of the biphasic profile with repetitive depolarization. 6. At a stage earlier than 36 h after fertilization, the biphasic profile of I2Ca/98Ba was not observed. However, caffeine induced a remarkable decrease in the amplitude of I2Ca/98Ba and this suppression was blocked by microinjection of the Ca2+ chelator BAPTA, showing the presence of caffeine-sensitive Ca2+ stores at this stage. 7. Electron microscopic observation shows that sarcoplasmic membranes (SR) arrange closer to the sarcolemma with maturation, suggesting that the formation of the ultrastructural machinery underlies development of the cross-coupling between VDCCs and Ca2+ stores.  (+info)

I apologize, but I am not able to provide a medical definition for "Egtazic Acid" because it is not a term that is recognized in the field of medicine or pharmacology. It is possible that you may have meant "Egтарic Acid," which also does not have a specific medical meaning, or "Ethylene Glycol Tetraacetic Acid (EGTA)," which is a chemical compound used in research and medicine for its ability to bind calcium ions. If you have any other questions, I would be happy to try to help answer them.

EGTA (ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid), also known as egtazic acid (INN, USAN), is an ... aminopolycarboxylic acid, a chelating agent. It is a white solid that is related to the better known EDTA. Compared to EDTA, it ...
... edetic acid MeSH D02.241.081.038.455 - egtazic acid MeSH D02.241.081.038.581 - iodoacetic acid MeSH D02.241.081.038.581.400 - ... quinic acid MeSH D02.241.511.852 - shikimic acid MeSH D02.241.511.902 - sugar acids MeSH D02.241.511.902.107 - ascorbic acid ... edetic acid MeSH D02.092.782.258.368.257 - egtazic acid MeSH D02.092.782.258.368.265 - ethambutol MeSH D02.092.782.258.368.500 ... hexuronic acids MeSH D02.241.081.844.915.400.500 - iduronic acid MeSH D02.241.081.901.177 - aconitic acid MeSH D02.241.081.901. ...
... egtazic acid (INN) egualen (INN) elacridar (INN) elacytarabine (USAN, INN) elagolix (USAN, INN) elantrine (INN) elanzepine (INN ... edetic acid (INN) edetol (INN) Edex. Redirects to Prostaglandin E1. edifoligide (USAN) edifolone (INN) edobacomab (INN) ... redirects to rasburicase Elixicon Elixomin Elixophyllin ellagic acid (INN) Ellence Ellence (Pharmacia & Upjohn Company) ...
Egtazic Acid * Cyclic AMP * Cyclic AMP-Dependent Protein Kinases * Milrinone * 1,2-bis(2-aminophenoxy)ethane-N,N,N,N- ...
Egtazic Acid Disodium Salt Egtazic Acid Potassium Salt Egtazic Acid Sodium Salt Ethylene Glycol Bis(2-aminoethyl ether) ... Egtazic Acid Disodium Salt Narrower Concept UI. M0330429. Registry Number. 0. Terms. Egtazic Acid Disodium Salt Preferred Term ... Egtazic Acid Sodium Salt Narrower Concept UI. M0330428. Registry Number. 31571-71-8. Terms. Egtazic Acid Sodium Salt Preferred ... Egtazic Acid Potassium Salt Narrower Concept UI. M0330430. Registry Number. 64492-97-3. Terms. Egtazic Acid Potassium Salt ...
EGTA (ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid), also known as egtazic acid (INN, USAN), is an ... aminopolycarboxylic acid, a chelating agent. It is a white solid that is related to the better known EDTA. Compared to EDTA, it ...
Egtazic Acid (MeSH) * Endothelins (MeSH) * Indoles (MeSH) * Isotonic Solutions (MeSH) * Male (MeSH) ... In the presence of sarcoplasmic reticulum Ca(2+)-pump inhibitor, cyclopiazonic acid, the above biphasic contraction brought ...
1 mM egtazic acid (EGTA), 50 mM β-glycerophosphate, 25 mM NaF, 1 mM Na3VO4, 100 mg/mL phenylmethylsulfonyl fluoride, and ... formic acid and 3% acetonitrile in deionized water and the mobile phase B was 0.1% formic acid in acetonitrile. The ... Ursodeoxycholic acid ameliorates cell migration retarded by the SARS-CoV-2 spike protein in BEAS-2B human bronchial epithelial ... The bound peptides were eluted with 5 μL of 70% ACN with 5% (v/v) formic acid. ...
Egtazic Acid. 1. 1995. 44. 0.030. Why? Point Mutation. 1. 1996. 243 ...
Egtazic Acid 44% * Patch-Clamp Techniques 20% * Muscle Cells 17% 32 Scopus citations ...
Egtazic Acid 19% * Methylene Blue 19% * NG-Nitroarginine Methyl Ester 18% * Phenylephrine 17% ...
Investigation into the spontaneous dissolution of tungsten using acid media. Smith, K. A. & Dean, J., 1993, In: The Analyst. ... Determination of the growth promoter, 4-hydroxy-3-nitrophenyl-arsonic acid in chicken tissue by coupled high-performance liquid ... The recovery of added malondialdehyde from rancid chicken by the distillation method for thiobarbituric acid-reactive ...
Egtazic Acid Medicine & Life Sciences 12% * Nerve Growth Factors Medicine & Life Sciences 11% ...
Egtazic Acid Medicine & Life Sciences 100% * Transforming Growth Factors Medicine & Life Sciences 87% ... tetraacetic acid (EGTA) leads to withdrawal from the cell cycle and high level expression of muscle-specific mRNAs and proteins ... tetraacetic acid (EGTA) leads to withdrawal from the cell cycle and high level expression of muscle-specific mRNAs and proteins ... tetraacetic acid (EGTA) leads to withdrawal from the cell cycle and high level expression of muscle-specific mRNAs and proteins ...
Egtazic Acid Medicine & Life Sciences 71% * Neurons Medicine & Life Sciences 36% View full fingerprint ...
Egtazic Acid. *Endometrial Neoplasms. *Endoscopy, Digestive System. *Endoscopy, Gastrointestinal. *Endosonography. *Enterocytes ...
Verapamil and egtazic acid were used to testify whether the insulinreleasing. effect of reishi was mediated by its ability to ... The insulin-releasing effect of reishi was inhibited by verapamil/egtazic acid. Reishi possesses the hypoglycemic effect on ... and triterpenoids called ganoderic acids. Ganoderic acids may lower blood pressure as well as decrease LDL (bad) cholesterol. ... It is the only known source of a group of triterpenes known as ganoderic acids, which have a molecular structure similar to ...
Animals, Calcium, Cell Line, Egtazic Acid, Image Processing, Computer-Assisted, Inositol 1,4,5-Trisphosphate, Lithium, ...
Egtazic Acid, Exocytosis, GTP-Binding Proteins, Guanosine 5-O-(3-Thiotriphosphate), Guanylyl Imidodiphosphate, Kinetics, ...
... dependent enzyme that acts on membrane phospholipids to release arachidonic acid, which in platelets is converted to ... Annexin A5, Biological Transport, Blood Platelets, Calcium Chloride, Cell Membrane, Cytochalasins, Cytosol, Egtazic Acid, ... Cytosolic phospholipase A(2) is a Ca(2+)-dependent enzyme that acts on membrane phospholipids to release arachidonic acid, ...
Edetic Acid. *Egtazic Acid. *Fluoroacetates. *Glycolates. *Iodoacetates. *Nitrilotriacetic Acid. *Pentetic Acid. *Peracetic ...
EGTA (ethylene glycol-bis(β-aminoethyl ether)-N,N,N,N-tetraacetic acid), also known as egtazic acid (INN, USAN),[1] is an ... Aminocaproic acid (also known as ε-aminocaproic acid, ε-Ahx, or 6-aminohexanoic acid) is a derivative and analogue of the amino ... It is a hexa-peptide containing the unusual amino acid statine (Sta, (3S,4S)-4-amino-3-hydroxy-6-methylheptanoic acid), having ... By splitting the peptide bonds that link amino acid residues, the proteases are involved in digesting long protein chains into ...
Browse a full range of Carboxylic acids and derivatives products from leading suppliers. Shop now at Fisher Scientific for all ... egta,egtazic acid,gedta,ethylenebis oxyethylenenitrilo tetraacetic acid,ebonta,6,9-dioxa-3,12-diazatetradecanedioic acid, 3,12- ... egtazic acid,gedta,ethylenebis oxyethylenenitrilo tetraacetic acid,ebonta,6,9-dioxa-3,12-diazatetradecanedioic acid, 3,12-bis ... sodium formate,formic acid, sodium salt,salachlor,formic acid sodium salt,formic acid, na salt,sodium formate, refined,sodium ...
In calcium-free Krebs remedy comprising 0.01 mmol/L egtazic acid (EGTA), genistein and resveratrol inhibited the 1st phasic ... stimulates phosphatidylinositol turnover and arachidonic acid launch via activation of the mitogen-activated protein kinases ...
Egtazic Acid, Hematopoietic Cell Growth Factors, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypothermia, Induced, ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
D2.886.300.692.240 Edetic Acid D2.241.81.38.440 D2.241.81.18.253 Egtazic Acid D2.241.81.38.455 D2.241.81.18.269 Elephantiasis ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... D2.705.675 Phosphoric Acid Esters D2.705.673 D2.705.400 (Replaced for 2012 by Organophosphates) Phosphorous Acids D2.705.676 ...
  • Exposure of C2 myoblasts to growth factor-deficient medium containing 1.4 mM [ethylenebis(oxyethylenenitrilo)]tetraacetic acid (EGTA) leads to withdrawal from the cell cycle and high level expression of muscle-specific mRNAs and proteins. (elsevierpure.com)
  • Hu, JS & Olson, EN 1990, ' Functional receptors for transforming growth factor-β are retained by biochemically differentiated G2 myocytes in growth factor-deficient medium containing EGTA but down-regulated during terminal differentiation ', Journal of Biological Chemistry , vol. 265, no. 14, pp. 7914-7919. (elsevierpure.com)
  • A chelating agent relatively more specific for calcium and less toxic than EDETIC ACID . (nih.gov)
  • Includes compounds that are derived from carboxylic acids. (fishersci.com)