Disease relevance of Phenyltrimethylammonium

• We have previously shown that phenyltrimethylammonium (TMA)-specific, first-order suppressor T cells (Ts1) and soluble factors extracted from these cells (TsF1) can suppress delayed-type hypersensitivity (DTH) responses [1].

High impact information on Phenyltrimethylammonium

• We had previously demonstrated that expression of the cross-reactive idiotypes (CRI) in the phenyltrimethylammonium (TMA) system depends on the presence of a second-order T helper (Th2) cell [2].
• No specific alkylation of the AChR alpha-subunit was detected in the absence of agonist, or in the presence of the partial agonist phenyltrimethylammonium or the competitive antagonists, d-tubocurarine, gallamine triethiodide, or decamethonium [3].
• We have previously demonstrated the requirement of two T helper (Th) populations for the expression of plaque-forming cells (PFC) that bear the dominant cross-reactive idiotype (CRI) associated with the phenyltrimethylammonium (TMA) response (1) [4].
• The reaction sequence involved treatment of CD with phenyltrimethylammonium perbromide to give 6,12-dibromo-CD (2), dehydrohalogenation of 2 to 12-bromo-CC (3), and the subsequent conversions of 3 to 12-azido- (4), 12-iodo- (5), and 12-cyano-CC (6) [5].
• 5. The specific ACh antagonist phenyltrimethylammonium (10(-4) M) blocked both excitatory, biphasic (inhibitory-excitatory) and inhibitory monosynaptic connections from the SO to feeding CPG interneurons and motor neurons [6].

Biological context of Phenyltrimethylammonium

• Different spin labelled fluorophosphates and fluorophosphonates with different chain length were investigated with respect to their sensitivity to the allosteric changes of acetylcholinesterase active site produced by phenyltrimethylammonium (Pta) or d-tubocurarine (TC); only fluorophosphates were found to be sensitive to these changes [7].

Anatomical context of Phenyltrimethylammonium

• Experiments described in this report will characterize a monoclonal phenyltrimethylammonium (TMA) specific, first-order T-suppressor factor (TsF1) produced by a T-cell hybridoma, 8A [8].
• With substituted trimethylanilinium, the concentrations in the blood, skeletal and cardiac muscles, diaphragm and salivary gland after i.v. injection to mice increased in the order: m-NO2 less than Cl less than OCH3 less than H less than CH3 [9].

Associations of Phenyltrimethylammonium with other chemical compounds

• PTMA (phenyltrimethylammonium) is less potent than TMA and is ineffective at the slow inhibitory receptor, which is the only receptor sensitive to arecoline [10].
• To prove the validity of this kinetic method, the model experiments were carried out with acetylcholinesterase and its inhibitors, phenyltrimethylammonium and trimethylammonium [11].

Gene context of Phenyltrimethylammonium

• The effect of the cholinergic activator, phenyltrimethylammonium, on the ESR spectra of spin-labeled membrane bound acetylcholinesterase was studied; a reduction of maximal hyperfine splitting of the anisotropic ESR spectrum by 2 G was observed [12].

Analytical, diagnostic and therapeutic context of Phenyltrimethylammonium

• Potentiometric titrations of rabbit antibody to the hapten trimethylphenylammonium ion demonstrate the speed and convenience of the new method for the determination of binding equilibria [13].
• In order to determine the relationship between structure and distribution in mono-quaternary ammonium ions, the distribution of a series of 14C-labeled tetraalkylammonium and substituted trimethylanilinium ions in mice were comparatively studied by means of whole-body autoradiography and radioassay [9].

References