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Gene Review

Ache  -  acetylcholinesterase

Mus musculus

Synonyms: AChE, Acetylcholinesterase
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Disease relevance of Ache


Psychiatry related information on Ache


High impact information on Ache


Chemical compound and disease context of Ache


Biological context of Ache

  • The myogenic transcription factors do not accelerate transcription of the Ache gene in spite of the presence of E-boxes at -335 base pairs from the start of transcription and in the first intron, and they are not able to trigger stabilization of the Ache mRNA when constitutively expressed in 10T1/2 fibroblasts [18].
  • (ii) We analyze the Ache promoter region by deletion analysis, point mutagenesis, and gel mobility shift assays [18].
  • The strain distribution pattern for this polymorphism indicates that Ache is located on distal mouse chromosome 5 [19].
  • Thus, the lack of AChE catalytic activity in the mutants appears to be solely responsible for the observed phenotypes [20].
  • The down-regulation of HuR expression mediated through small interfering RNA further confirmed the role of HuR in the regulation of AChE mRNA levels [21].

Anatomical context of Ache


Associations of Ache with chemical compounds

  • Acetylcholinesterase (AChE) hydrolyses acetylcholine (ACh) ensuring the fast clearance of released neurotransmitter at cholinergic synapses [20].
  • The histaminergic H2 antagonist, ranitidine, has also been found to significantly inhibit acetylcholinesterase (AChE) in vitro [24].
  • 5 Muscarinic toxin-3 decreased evoked release in both AChE(-/-) and normal NMJs treated with low concentrations of neostigmine, galanthamine or fasciculin-1, but had no effect in normal NMJs pretreated with iso-OMPA, bambuterol, MTP and phospholine [25].
  • In vitro, the cholinergic agonists muscarine (50-100 microm) and nicotine (0.5-10 microm) induced tonic activity in respiratory motoneurons and increased the frequency of inspiratory bursts in AChE+/+ and +/- animals [2].
  • Therefore, the aims of this study were to explore the neurotrophic role of AChE by comparing the effects of mouse recombinant G1 and G4 AChE on the survival and development of mid-brain tyrosine hydroxylase immunoreactive neurons [26].

Physical interactions of Ache


Enzymatic interactions of Ache


Regulatory relationships of Ache

  • A monoclonal antibody against acetylcholinesterase inhibits the formation of amyloid fibrils induced by the enzyme [32].
  • Inhibition of amyloid formation was dependent on the molar ratio AChE:mAb 25B1, and at least 50% of the inhibition of the AChE promoting effect occurs at a molar ratio similar to that required for inhibition of the esterase activity [32].
  • In cultured neurons dissociated from the spinal cord of fetal mouse, high concentrations of KCl (47 mM) increased choline acetyltransferase (CAT) activity up to 5.5-fold but suppressed acetylcholinesterase (AChE) activity to less than half the level of control cells [33].
  • When added to rat myotubes devoid of membrane AChR, agrin-induced AChE clusters did not form [34].
  • Neuroblastoma x rodent nervous tissue hybrids express AChE and in a few instances have developed the ability to synthesize CAT [35].

Other interactions of Ache


Analytical, diagnostic and therapeutic context of Ache

  • Using several complementary approaches including supershift REMSA, mRNA-binding protein pull-down assays, and immunoprecipitation followed by reverse transcription-PCR, we found that the mRNA-stabilizing protein HuR interacts directly with AChE transcripts [21].
  • Active AChE molecular forms were characterized by sedimentation and non-denaturing electrophoresis, and AChE transcripts were quantified by real-time PCR [39].
  • To generalize this observation, we attempted to quantify AChE(R) and AChE(T) after organophosphate intoxication in the mouse brain and compared the observed effects with those of stress induced by swimming or immobilization; we also analyzed the effects of heat shock and AChE inhibition on neuroblastoma cells [39].
  • The readthrough variant of acetylcholinesterase remains very minor after heat shock, organophosphate inhibition and stress, in cell culture and in vivo [39].
  • RT-PCR assays revealed variable levels of R, H and T AChE mRNAs in thymus, bone marrow and spinal cord [1].


  1. Muscular dystrophy by merosin deficiency decreases acetylcholinesterase activity in thymus of Lama2dy mice. Nieto-Cerón, S., del Campo, L.F., Muñoz-Delgado, E., Vidal, C.J., Campoy, F.J. J. Neurochem. (2005) [Pubmed]
  2. Respiratory survival mechanisms in acetylcholinesterase knockout mouse. Chatonnet, F., Boudinot, E., Chatonnet, A., Taysse, L., Daulon, S., Champagnat, J., Foutz, A.S. Eur. J. Neurosci. (2003) [Pubmed]
  3. Regulation of muscarinic acetylcholine receptor function in acetylcholinesterase knockout mice. Li, B., Duysen, E.G., Volpicelli-Daley, L.A., Levey, A.I., Lockridge, O. Pharmacol. Biochem. Behav. (2003) [Pubmed]
  4. Evidence for nonacetylcholinesterase targets of organophosphorus nerve agent: supersensitivity of acetylcholinesterase knockout mouse to VX lethality. Duysen, E.G., Li, B., Xie, W., Schopfer, L.M., Anderson, R.S., Broomfield, C.A., Lockridge, O. J. Pharmacol. Exp. Ther. (2001) [Pubmed]
  5. Acetylcholinesterase is increased in the brains of transgenic mice expressing the C-terminal fragment (CT100) of the beta-amyloid protein precursor of Alzheimer's disease. Sberna, G., Sáez-Valero, J., Li, Q.X., Czech, C., Beyreuther, K., Masters, C.L., McLean, C.A., Small, D.H. J. Neurochem. (1998) [Pubmed]
  6. Acetylcholinesterase inhibitors ameliorate behavioral deficits in the Tg2576 mouse model of Alzheimer's disease. Dong, H., Csernansky, C.A., Martin, M.V., Bertchume, A., Vallera, D., Csernansky, J.G. Psychopharmacology (Berl.) (2005) [Pubmed]
  7. M2 muscarinic receptors in pontine reticular formation of C57BL/6J mouse contribute to rapid eye movement sleep generation. Coleman, C.G., Lydic, R., Baghdoyan, H.A. Neuroscience (2004) [Pubmed]
  8. Ganstigmine and donepezil improve neurodegeneration in AD11 antinerve growth factor transgenic mice. Capsoni, S., Giannotta, S., Stebel, M., Garcia, A.A., De Rosa, R., Villetti, G., Imbimbo, B.P., Pietra, C., Cattaneo, A. American journal of Alzheimer's disease and other dementias. (2004) [Pubmed]
  9. Acute stress facilitates long-lasting changes in cholinergic gene expression. Kaufer, D., Friedman, A., Seidman, S., Soreq, H. Nature (1998) [Pubmed]
  10. Association of the synaptic form of acetylcholinesterase with extracellular matrix in cultured mouse muscle cells. Inestrosa, N.C., Silberstein, L., Hall, Z.W. Cell (1982) [Pubmed]
  11. Creatine kinase, myokinase, and acetylcholinesterase activities in muscle-forming primary cultures of mouse teratocarcinoma cells. Gearhart, J.D., Mintz, B. Cell (1975) [Pubmed]
  12. Estrogen protects neuronal cells from the cytotoxicity induced by acetylcholinesterase-amyloid complexes. Bonnefont, A.B., Muñoz, F.J., Inestrosa, N.C. FEBS Lett. (1998) [Pubmed]
  13. Regulation of acetylcholine release by muscarinic receptors at the mouse neuromuscular junction depends on the activity of acetylcholinesterase. Minic, J., Molgó, J., Karlsson, E., Krejci, E. Eur. J. Neurosci. (2002) [Pubmed]
  14. Inhibition of acetylcholinesterase and butyrylcholinesterase by chlorpyrifos-oxon. Amitai, G., Moorad, D., Adani, R., Doctor, B.P. Biochem. Pharmacol. (1998) [Pubmed]
  15. Inhibitory effects of huperzine B on cholinesterase activity in mice. Liu, J., Zhang, H.Y., Wang, L.M., Tang, X.C. Zhongguo yao li xue bao = Acta pharmacologica Sinica. (1999) [Pubmed]
  16. Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer beta-amyloid peptide in rodent. Greig, N.H., Utsuki, T., Ingram, D.K., Wang, Y., Pepeu, G., Scali, C., Yu, Q.S., Mamczarz, J., Holloway, H.W., Giordano, T., Chen, D., Furukawa, K., Sambamurti, K., Brossi, A., Lahiri, D.K. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  17. CD41+/CD45+ cells without acetylcholinesterase activity are immature and a major megakaryocytic population in murine bone marrow. Matsumura-Takeda, K., Sogo, S., Isakari, Y., Harada, Y., Nishioka, K., Kawakami, T., Ono, T., Taki, T. Stem. Cells (2007) [Pubmed]
  18. Promoter elements of the mouse acetylcholinesterase gene. Transcriptional regulation during muscle differentiation. Mutero, A., Camp, S., Taylor, P. J. Biol. Chem. (1995) [Pubmed]
  19. Assignment of the gene for acetylcholinesterase to distal mouse chromosome 5. Rachinsky, T.L., Crenshaw, E.B., Taylor, P. Genomics (1992) [Pubmed]
  20. Are there non-catalytic functions of acetylcholinesterases? Lessons from mutant animal models. Cousin, X., Strähle, U., Chatonnet, A. Bioessays (2005) [Pubmed]
  21. The RNA-binding protein HuR binds to acetylcholinesterase transcripts and regulates their expression in differentiating skeletal muscle cells. Deschênes-Furry, J., Bélanger, G., Mwanjewe, J., Lunde, J.A., Parks, R.J., Perrone-Bizzozero, N., Jasmin, B.J. J. Biol. Chem. (2005) [Pubmed]
  22. PRiMA: the membrane anchor of acetylcholinesterase in the brain. Perrier, A.L., Massoulié, J., Krejci, E. Neuron (2002) [Pubmed]
  23. Reduced acetylcholinesterase (AChE) activity in adrenal medulla and loss of sympathetic preganglionic neurons in TrkA-deficient, but not TrkB-deficient, mice. Schober, A., Minichiello, L., Keller, M., Huber, K., Layer, P.G., Roig-López, J.L., García-Arrarás, J.E., Klein, R., Unsicker, K. J. Neurosci. (1997) [Pubmed]
  24. Synthesis and cholinergic properties of bis[[(dimethylamino)methyl]furanyl] analogues of ranitidine. Sowell, J.W., Tang, Y., Valli, M.J., Chapman, J.M., Usher, L.A., Vaughan, C.M., Kosh, J.W. J. Med. Chem. (1992) [Pubmed]
  25. Butyrylcholinesterase and acetylcholinesterase activity and quantal transmitter release at normal and acetylcholinesterase knockout mouse neuromuscular junctions. Minic, J., Chatonnet, A., Krejci, E., Molgó, J. Br. J. Pharmacol. (2003) [Pubmed]
  26. Non-cholinergic, trophic action of recombinant acetylcholinesterase on mid-brain dopaminergic neurons. Holmes, C., Jones, S.A., Budd, T.C., Greenfield, S.A. J. Neurosci. Res. (1997) [Pubmed]
  27. The dystroglycan complex is necessary for stabilization of acetylcholine receptor clusters at neuromuscular junctions and formation of the synaptic basement membrane. Jacobson, C., Côté, P.D., Rossi, S.G., Rotundo, R.L., Carbonetto, S. J. Cell Biol. (2001) [Pubmed]
  28. Postnatal maturation of brain cholinergic systems in the precocial murid Acomys cahirinus: comparison with the altricial rat. Pintor, A., Alleva, E., Michalek, H. Int. J. Dev. Neurosci. (1986) [Pubmed]
  29. Effects of inhibitors of ornithine decarboxylase on the differentiation of mouse neuroblastoma cells. Chen, K.Y., Nau, D., Liu, A.Y. Cancer Res. (1983) [Pubmed]
  30. The anticancer prodrug CPT-11 is a potent inhibitor of acetylcholinesterase but is rapidly catalyzed to SN-38 by butyrylcholinesterase. Morton, C.L., Wadkins, R.M., Danks, M.K., Potter, P.M. Cancer Res. (1999) [Pubmed]
  31. Oxidation of pesticides by purified cytochrome P-450 isozymes from mouse liver. Levi, P.E., Hodgson, E. Toxicol. Lett. (1985) [Pubmed]
  32. A monoclonal antibody against acetylcholinesterase inhibits the formation of amyloid fibrils induced by the enzyme. Reyes, A.E., Perez, D.R., Alvarez, A., Garrido, J., Gentry, M.K., Doctor, B.P., Inestrosa, N.C. Biochem. Biophys. Res. Commun. (1997) [Pubmed]
  33. Effect of depolarizing agents on choline acetyltransferase and acetylcholinesterase activities in primary cell cultures of spinal cord. Ishida, I., Deguchi, T. J. Neurosci. (1983) [Pubmed]
  34. Accumulation of acetylcholine receptors is a necessary condition for normal accumulation of acetylcholinesterase during in vitro neuromuscular synaptogenesis. De La Porte, S., Chaubourt, E., Fabre, F., Poulas, K., Chapron, J., Eymard, B., Tzartos, S., Koenig, J. Eur. J. Neurosci. (1998) [Pubmed]
  35. Expression of phenotypes in hybrid somatic cells derived from the nervous system. Minna, J.D., Yavelow, J., Coon, H.G. Genetics (1975) [Pubmed]
  36. Interaction of "readthrough" acetylcholinesterase with RACK1 and PKCbeta II correlates with intensified fear-induced conflict behavior. Birikh, K.R., Sklan, E.H., Shoham, S., Soreq, H. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  37. Amyloid precursor protein fragment and acetylcholinesterase increase with cell confluence and differentiation in a neuronal cell line. Bronfman, F.C., Fernandez, H.L., Inestrosa, N.C. Exp. Cell Res. (1996) [Pubmed]
  38. Acetylcholinesterase and nicotinic acetylcholine receptor expression diverge in muscular dysgenic mice lacking the L-type calcium channel. Luo, Z.D., Pincon-Raymond, M., Taylor, P. J. Neurochem. (1996) [Pubmed]
  39. The readthrough variant of acetylcholinesterase remains very minor after heat shock, organophosphate inhibition and stress, in cell culture and in vivo. Perrier, N.A., Salani, M., Falasca, C., Bon, S., Augusti-Tocco, G., Massoulié, J. J. Neurochem. (2005) [Pubmed]
  40. Postnatal developmental delay and supersensitivity to organophosphate in gene-targeted mice lacking acetylcholinesterase. Xie, W., Stribley, J.A., Chatonnet, A., Wilder, P.J., Rizzino, A., McComb, R.D., Taylor, P., Hinrichs, S.H., Lockridge, O. J. Pharmacol. Exp. Ther. (2000) [Pubmed]
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