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ACOT1  -  acyl-CoA thioesterase 1

Homo sapiens

Synonyms: ACH2, Acyl-CoA thioesterase 1, Acyl-coenzyme A thioesterase 1, CTE-1, CTE-I, ...
 
 
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Disease relevance of ACOT1

  • CD30 cross-linking does not alter proliferation of ACH-2 cells and the induction of HIV expression is not mediated by endogenous TNF alpha/beta [1].
  • In addition, Nef-dependent HIV-1 activation from latency was also observed in another independently derived, latently infected cell line, U1, though not in cell line ACH-2 [2].
  • In contrast to the responsiveness of ACH-2 cells, CpG ODNs failed to activate HIV provirus in the latently infected Jurkat clone J1 [3].
  • In contrast, superinfection of ACH-2 cells resulted in active expression of the secondarily introduced virus even in unstimulated cells and luciferase production higher than in the parental cell line A3.01 [4].
  • In order to elucidate the oligomerization-function relationship of the hot dog fold proteins, crystal structures of the phenylacetate degradation protein PaaI from Thermus thermophilus HB8 (TtPaaI), a tetrameric acyl-CoA thioesterase with the hot dog fold, have been determined and compared with those of other family members [5].
 

High impact information on ACOT1

 

Chemical compound and disease context of ACOT1

 

Biological context of ACOT1

 

Anatomical context of ACOT1

 

Associations of ACOT1 with chemical compounds

  • Finally, CD4-induced increases in the binding of antibodies to the V3 loop of ACH-2-cell-expressed envelope glycoproteins were reduced 25-fold when the glycoproteins were expressed in the presence of NB-DNJ [20].
  • However, treatment of ACH-2 cells with cycloheximide elicited production of the 3 kb transcript suggesting the possibility for a repressor protein(s) to act at the level of transcription and/or stability of the 3 kb mRNA [21].
  • RESULTS: Acyl-CoA thioesterase activity was found in human fibroblasts with all saturated acyl-CoAs from C4-CoA to C18-CoA, with highest activity detected with lauroyl-CoA and myristoyl-CoA (C12-CoA and C14-CoA) [19].
  • ACH-2 cultures, pretreated with various nontoxic concentrations of ascorbate or AZT were stimulated for 2 h with TNF-alpha, and incubated further with fresh supplements of ascorbate or AZT [22].
  • TPM also changed genes related with fatty acid beta-oxidation, increased 3-2-trans-enoyl-CoA isomerase and mitochondrial acyl-CoA thioesterase, and decreased fatty acid CoA ligase (long chain 2 and long chain 5) [23].
 

Regulatory relationships of ACOT1

  • In cells of lymphoid origin (ACH-2) chronic HIV infection inhibits the expression of CD95L, the phenomenon occurring at the transcriptional level [18].
  • This further suggests a new concept in the regulation of intracellular distribution of AA through a mechanism different from the classical PLA2-mediated pathway that involves a hormone-induced acyl-CoA synthetase and a hormone-regulated acyl-CoA thioesterase [24].
  • CD4-induced exposure of cryptic gp41 epitopes on the surfaces of HIV-expressing ACH-2 cells was also greatly impaired, and the exposure of virion-associated gp41 epitopes was reduced 4.0-fold [20].
 

Other interactions of ACOT1

  • We therefore set out to characterize the human genes, and we show here that the human ACOT4 protein catalyzes the activities of three mouse peroxisomal ACOTs (ACOT3, 4, and 5), being active on succinyl-CoA and medium to long chain acyl-CoAs, while ACOT1 and ACOT2 carry out similar functions to the corresponding mouse genes [12].
  • The stimulatory effect of the HMGB1 was not present when latently infected T-cells (ACH-2) were used as target cells [25].
  • By using a retroviral vector delivery system, mutant forms of p53 genes were expressed in two HIV-1 latently infected cell lines, ACH-2 and U1 [26].
  • This pattern of NF-kappa B-related moieties differs from the latently infected T lymphocytic cell line ACH-2, and from the U937 monocytic line, the parental cell line of the U1 cellular clone [27].
  • Here, we describe a cytosolic long-chain acyl-CoA hydrolase (referred to as BACH) that is constitutively expressed in the brain, comparing it with other acyl-CoA hydrolases found in peripheral organs that have a role in fatty acid oxidation [28].
 

Analytical, diagnostic and therapeutic context of ACOT1

References

  1. Cross-linking of CD30 induces HIV expression in chronically infected T cells. Biswas, P., Smith, C.A., Goletti, D., Hardy, E.C., Jackson, R.W., Fauci, A.S. Immunity (1995) [Pubmed]
  2. Extracellular Nef protein regulates productive HIV-1 infection from latency. Fujinaga, K., Zhong, Q., Nakaya, T., Kameoka, M., Meguro, T., Yamada, K., Ikuta, K. J. Immunol. (1995) [Pubmed]
  3. CpG oligodeoxynucleotides activate HIV replication in latently infected human T cells. Scheller, C., Ullrich, A., McPherson, K., Hefele, B., Knöferle, J., Lamla, S., Olbrich, A.R., Stocker, H., Arasteh, K., ter Meulen, V., Rethwilm, A., Koutsilieri, E., Dittmer, U. J. Biol. Chem. (2004) [Pubmed]
  4. Distinct modes of human immunodeficiency virus type 1 proviral latency revealed by superinfection of nonproductively infected cell lines with recombinant luciferase-encoding viruses. Chen, B.K., Saksela, K., Andino, R., Baltimore, D. J. Virol. (1994) [Pubmed]
  5. A novel induced-fit reaction mechanism of asymmetric hot dog thioesterase PAAI. Kunishima, N., Asada, Y., Sugahara, M., Ishijima, J., Nodake, Y., Sugahara, M., Miyano, M., Kuramitsu, S., Yokoyama, S., Sugahara, M. J. Mol. Biol. (2005) [Pubmed]
  6. Transforming growth factor beta suppresses human immunodeficiency virus expression and replication in infected cells of the monocyte/macrophage lineage. Poli, G., Kinter, A.L., Justement, J.S., Bressler, P., Kehrl, J.H., Fauci, A.S. J. Exp. Med. (1991) [Pubmed]
  7. Activated B lymphocytes from human immunodeficiency virus-infected individuals induce virus expression in infected T cells and a promonocytic cell line, U1. Rieckmann, P., Poli, G., Kehrl, J.H., Fauci, A.S. J. Exp. Med. (1991) [Pubmed]
  8. Tumor necrosis factor alpha induces expression of human immunodeficiency virus in a chronically infected T-cell clone. Folks, T.M., Clouse, K.A., Justement, J., Rabson, A., Duh, E., Kehrl, J.H., Fauci, A.S. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  9. Caspase inhibition activates HIV in latently infected cells. Role of tumor necrosis factor receptor 1 and CD95. Scheller, C., Sopper, S., Chen, P., Flory, E., Koutsilieri, E., Racek, T., Ludwig, S., ter Meulen, V., Jassoy, C. J. Biol. Chem. (2002) [Pubmed]
  10. Cystamine inhibits HIV type 1 replication in cells of monocyte/macrophage and T cell lineages. Ho, W.Z., Zhu, X.H., Song, L., Lee, H.R., Cutilli, J.R., Douglas, S.D. AIDS Res. Hum. Retroviruses (1995) [Pubmed]
  11. Activation of the HIV type 1 long terminal repeat and viral replication by dimethylsulfoxide and related solvents. Klebanoff, S.J., Mehlin, C., Headley, C.M. AIDS Res. Hum. Retroviruses (1997) [Pubmed]
  12. Analysis of the mouse and human acyl-CoA thioesterase (ACOT) gene clusters shows that convergent, functional evolution results in a reduced number of human peroxisomal ACOTs. Hunt, M.C., Rautanen, A., Westin, M.A., Svensson, L.T., Alexson, S.E. FASEB J. (2006) [Pubmed]
  13. Thalidomide inhibits the replication of human immunodeficiency virus type 1. Makonkawkeyoon, S., Limson-Pobre, R.N., Moreira, A.L., Schauf, V., Kaplan, G. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  14. Biochemical and molecular characterization of ACH2, an acyl-CoA thioesterase from Arabidopsis thaliana. Tilton, G.B., Shockey, J.M., Browse, J. J. Biol. Chem. (2004) [Pubmed]
  15. Overexpression of human acyl-CoA thioesterase upregulates peroxisome biogenesis. Ishizuka, M., Toyama, Y., Watanabe, H., Fujiki, Y., Takeuchi, A., Yamasaki, S., Yuasa, S., Miyazaki, M., Nakajima, N., Taki, S., Saito, T. Exp. Cell Res. (2004) [Pubmed]
  16. A novel method for detecting HIV-1 by non-radioactive in situ hybridization: application of a peptide nucleic acid probe and catalysed signal amplification. Murakami, T., Hagiwara, T., Yamamoto, K., Hattori, J., Kasami, M., Utsumi, M., Kaneda, T. J. Pathol. (2001) [Pubmed]
  17. Activation of human immunodeficiency virus type 1 provirus in T-cells and macrophages is associated with induction of inducer-specific NF-kappa B binding proteins. Vlach, J., Pitha, P.M. Virology (1992) [Pubmed]
  18. Differential down-regulation of CD95 or CD95L in chronically HIV-infected cells of monocytic or lymphocytic origin: cellular studies and molecular analysis by quantitative competitive RT-PCR. Pinti, M., Pedrazzi, J., Benatti, F., Sorrentino, V., Nuzzo, C., Cavazzuti, V., Biswas, P., Petrusca, D.N., Mussini, C., De Rienzo, B., Cossarizza, A. FEBS Lett. (1999) [Pubmed]
  19. Identification of fatty acid oxidation disorder patients with lowered acyl-CoA thioesterase activity in human skin fibroblasts. Hunt, M.C., Ruiter, J., Mooyer, P., van Roermond, C.W., Ofman, R., Ijlst, L., Wanders, R.J. Eur. J. Clin. Invest. (2005) [Pubmed]
  20. N-butyldeoxynojirimycin-mediated inhibition of human immunodeficiency virus entry correlates with impaired gp120 shedding and gp41 exposure. Fischer, P.B., Karlsson, G.B., Dwek, R.A., Platt, F.M. J. Virol. (1996) [Pubmed]
  21. Transcriptional and post-transcriptional mechanisms are involved in the absence of CD4 surface expression in two HIV-1 chronically infected T cell lines. Serpente, N., Hemar, A., Cefai, D., Dautry-Varsat, A., Fagard, R., Fischer, S., Vaquero, C. Int. Immunol. (1993) [Pubmed]
  22. Ascorbate effect on cytokine stimulation of HIV production. Harakeh, S., Jariwalla, R.J. Nutrition (Burbank, Los Angeles County, Calif.) (1995) [Pubmed]
  23. The messenger RNA profiles in liver, hypothalamus, white adipose tissue, and skeletal muscle of female Zucker diabetic fatty rats after topiramate treatment. Liang, Y., She, P., Wang, X., Demarest, K. Metab. Clin. Exp. (2006) [Pubmed]
  24. Arachidonic acid regulation of steroid synthesis: new partners in the signaling pathway of steroidogenic hormones. Castilla, R., Maloberti, P., Castillo, F., Duarte, A., Cano, F., Maciel, F.C., Neuman, I., Mendez, C.F., Paz, C., Podestá, E.J. Endocr. Res. (2004) [Pubmed]
  25. HMGB1 activates replication of latent HIV-1 in a monocytic cell-line, but inhibits HIV-1 replication in primary macrophages. Nowak, P., Barqasho, B., Treutiger, C.J., Harris, H.E., Tracey, K.J., Andersson, J., Sönnerborg, A. Cytokine (2006) [Pubmed]
  26. The tumor suppressor protein p53 strongly alters human immunodeficiency virus type 1 replication. Duan, L., Ozaki, I., Oakes, J.W., Taylor, J.P., Khalili, K., Pomerantz, R.J. J. Virol. (1994) [Pubmed]
  27. Association of alterations in NF-kappa B moieties with HIV type 1 proviral latency in certain monocytic cells. Oakes, J.W., Bagasra, O., Duan, L., Pomerantz, R.J. AIDS Res. Hum. Retroviruses (1994) [Pubmed]
  28. Long-chain acyl-CoA hydrolase in the brain. Yamada, J. Amino Acids (2005) [Pubmed]
  29. Recombinant gp120 specifically enhances tumor necrosis factor-alpha production and Ig secretion in B lymphocytes from HIV-infected individuals but not from seronegative donors. Rieckmann, P., Poli, G., Fox, C.H., Kehrl, J.H., Fauci, A.S. J. Immunol. (1991) [Pubmed]
  30. Consequences of human immunodeficiency virus type 1 superinfection of chronically infected cells. Kim, J.H., Mosca, J.D., Vahey, M.T., McLinden, R.J., Burke, D.S., Redfield, R.R. AIDS Res. Hum. Retroviruses (1993) [Pubmed]
  31. Iron chelation decreases NF-kappa B and HIV type 1 activation due to oxidative stress. Sappey, C., Boelaert, J.R., Legrand-Poels, S., Forceille, C., Favier, A., Piette, J. AIDS Res. Hum. Retroviruses (1995) [Pubmed]
  32. Purification, molecular cloning, and genomic organization of human brain long-chain acyl-CoA hydrolase. Yamada, J., Kurata, A., Hirata, M., Taniguchi, T., Takama, H., Furihata, T., Shiratori, K., Iida, N., Takagi-Sakuma, M., Watanabe, T., Kurosaki, K., Endo, T., Suga, T. J. Biochem. (1999) [Pubmed]
 
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