The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

NAAA  -  N-acylethanolamine acid amidase

Homo sapiens

Synonyms: ASAH-like protein, ASAHL, Acid ceramidase-like protein, N-acylethanolamine-hydrolyzing acid amidase, N-acylsphingosine amidohydrolase-like, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of ASAHL

 

Psychiatry related information on ASAHL

  • Although majority of the coefficient of variations were acceptable, about 23 (12.6%) participants showed abnormality in at least one parameter after analysis by the 'Peer Group Mean and SDI'. Using CLIA'88, 5 WBC (6.5%), 6 RBC (7.6%), 8 HGB (9.7%), 15 HCT (19.0%), and 7 PLT (8.0%) results were unsatisfactory [5].
 

High impact information on ASAHL

  • Mean neutrophil and platelet nadirs were significantly improved and time to recovery for neutrophils (ANC to < 500/microL) and platelets (PLT < 20,000/microL) were significantly enhanced in the MPO-treated cohorts versus controls [6].
  • By the use of tunicamycin and endoglycosidase, NAAA was found to be a glycoprotein [7].
  • Most interestingly, a very low ceramide hydrolyzing activity was also detected with NAAA, and N-lauroylethanolamine hydrolyzing activity was observed with acid ceramidase [7].
  • The results show a high correlation (0.881 less than or equal to r less than or equal to 1.00) between the HLA-DRw specificity of the priming haplotype and the HLA-DRw specificity of unrelated panel cells that restimulate in PLT [8].
  • The genetics of PLT response. I. Methodology for optimal PLT discrimination [9].
 

Chemical compound and disease context of ASAHL

  • Blood samples, from healthy donors or from patients with congenital defects of PLT glycoprotein IIb-IIIa (GPIIb-IIIa), were anticoagulated with low-molecular-weight heparin [4].
  • For the nine patients who received 5-FU at the recommended dose level the median low counts were WBC 3.5 (2.2-4.0), HGB 10.3 (9.0-12.3), and PLT (x 1000) 167 (133-280), and the incidence of any grade greater than or equal to 3 toxicity was 22% diarrhea, 17% tenesmus, and 22% frequent bowel movements [10].
  • Clinical specimens from HIV-1 seronegative subjects containing various endogenous interferents were evaluated with and without an HIV-1 RNA spike to assess recovery and specificity, respectively, with a non-PCR NAAA (NASBA HIV-1 RNA QT, Organon Teknika) that incorporates Boom methodology for nucleic acid extraction [11].
 

Biological context of ASAHL

  • The 30-kb human ASAHL genomic sequence contained 11 exons, which ranged in size from 26 to 671 bp, and 10 introns, which ranged from 150 bp to 6.4 kb [12].
  • Sequence analysis of the 5'-flanking region of the human ASAHL gene revealed a putative promoter region that lacked a TATA box and was GC rich, typical features of a housekeeping gene promoter, as well as several tissue-specific and/or hormone-induced transcription regulatory sites [12].
  • The full-length human ASAHL cDNA was 1825 bp and contained an open-reading frame encoding a 359-amino-acid polypeptide that was 33% identical and 69% similar to the ASAH polypeptide over its entire length [12].
  • To investigate the structure of the non-LTR-associated PLT-related transcripts, additional clones were isolated from the placental cDNA library [13].
  • Southern analysis indicated that the corresponding gene, termed PLT, is most probably a single multi-exon locus and that related sequences are present in the mouse genome, suggesting that this gene has been evolutionarily conserved [13].
 

Anatomical context of ASAHL

  • Additional hybridization studies with RNAs from various cell lines suggested that the PLT locus is differentially expressed in different cell types [13].
  • When stimulating cells were absorbed with the corresponding DRw alloantisera or p29,34 heteroantiserum (against B cell specific antigens), PLT restimulation was significantly blocked [8].
  • Over all, 82% of the cultures tested were positive for donor PLT reactivity, suggesting that current culture conditions favor alloreactive lymphocyte proliferation [14].
  • STUDY DESIGN AND METHODS: We have measured microvesicles (MV) derived from red cells (RBC-MV), platelets (PLT-MV), and white blood cells (WBC-MV) and cellular prion protein (PrP(c)) in blood components produced by four whole-blood, five RBC, three PLT, and two plasma LD filters and three plateletpheresis techniques [15].
  • Collection of WBC-reduced single-donor PLT concentrates with a new blood cell separator: results of a multicenter study [16].
 

Associations of ASAHL with chemical compounds

  • In a parallel model of active infection with free virus, human PLT in 35 percent autologous plasma and 65 percent PAS were dosed with 1 x 10(5) and 1 x 10(6) PFUs of MCMV [17].
  • However, it has not been clarified whether DDAVP is effective in correcting the bleeding time (BT) in this PLT disorder [18].
  • CONCLUSIONS: PCT of PLT preparations with the specified doses of amotosalen hydrochloride and UVA light prevents transfusion transmission of free and latent MCMV in a murine model [17].
  • After 30 minutes, 2- to 3-mL aliquots were processed through a PLT-reducing filter into a sample pouch containing sodium polyanethol sulfonate and entrained air [19].
  • ADP, collagen, and U46619 (a thromboxane-A2 analog)-induced PLT aggregation was investigated in basal (donor) and final (plateletpheresis unit) samples [20].
 

Analytical, diagnostic and therapeutic context of ASAHL

  • Northern blotting experiments revealed a major 2.0-kb ASAHL transcript that was expressed at high levels in the liver and kidney, but at relatively low levels in other tissues such as the lung, heart, and brain [12].
  • Molecular cloning and characterization of a human cDNA and gene encoding a novel acid ceramidase-like protein [12].
  • A comparison of PLT collections from two apheresis devices [21].
  • We investigated whether this collection modality could induce more PLT activation compared to standard plateletpheresis [20].
  • STUDY DESIGN AND METHODS: PLT-reactive antibodies were characterized by three different solid-phase assays and by flow cytometry [22].

References

  1. Platelet size and mass as an indicator for platelet transfusion after cardiopulmonary bypass. Mohr, R., Martinowitz, U., Golan, M., Ayala, L., Goor, D.A., Ramot, B. Circulation (1986) [Pubmed]
  2. Elevated vascular endothelial growth factor (VEGF) serum levels in idiopathic myelofibrosis. Di Raimondo, F., Azzaro, M.P., Palumbo, G.A., Bagnato, S., Stagno, F., Giustolisi, G.M., Cacciola, E., Sortino, G., Guglielmo, P., Giustolisi, R. Leukemia (2001) [Pubmed]
  3. Peritonitis after liver transplantation: Incidence, risk factors, microbiology profiles, and outcome. Pungpapong, S., Alvarez, S., Hellinger, W.C., Kramer, D.J., Willingham, D.L., Mendez, J.C., Nguyen, J.H., Hewitt, W.R., Aranda-Michel, J., Harnois, D.M., Rosser, B.G., Hughes, C.B., Grewal, H.P., Satyanarayana, R., Dickson, R.C., Steers, J.L., Keaveny, A.P. Liver Transpl. (2006) [Pubmed]
  4. Increased local procoagulant action: a mechanism contributing to the favorable hemostatic effect of recombinant FVIIa in PLT disorders. Galán, A.M., Tonda, R., Pino, M., Reverter, J.C., Ordinas, A., Escolar, G. Transfusion (2003) [Pubmed]
  5. Second national external quality assessment scheme in hematology: the Philippine experience. Veloso, D.J., Saavedra, M.A., Mendoza, R.D., Mauhay, S.M., Tulio, R.P., Shirakami, A., Fujimoto, K., Maramba, T.P. Southeast Asian J. Trop. Med. Public Health (2002) [Pubmed]
  6. Myelopoietin, an engineered chimeric IL-3 and G-CSF receptor agonist, stimulates multilineage hematopoietic recovery in a nonhuman primate model of radiation-induced myelosuppression. MacVittie, T.J., Farese, A.M., Smith, W.G., Baum, C.M., Burton, E., McKearn, J.P. Blood (2000) [Pubmed]
  7. Molecular characterization of N-acylethanolamine-hydrolyzing acid amidase, a novel member of the choloylglycine hydrolase family with structural and functional similarity to acid ceramidase. Tsuboi, K., Sun, Y.X., Okamoto, Y., Araki, N., Tonai, T., Ueda, N. J. Biol. Chem. (2005) [Pubmed]
  8. The genetics of PLT response. II. HLA-DRw is a major PLT-stimulating determinant. DeWolf, W.C., Carroll, P.G., Mehta, C.R., Martin, S.L., Yunis, E.J. J. Immunol. (1979) [Pubmed]
  9. The genetics of PLT response. I. Methodology for optimal PLT discrimination. DeWolf, W.C., Carroll, P.G., Yunis, E.J. J. Immunol. (1979) [Pubmed]
  10. Phase I trial of postoperative 5-FU, radiation therapy, and high dose leucovorin for resectable rectal cancer. Minsky, B.D., Cohen, A.M., Enker, W.E., Kelsen, D.P., Kemeny, N., Riechman, B., Saltz, L., Sigurdson, E.R., Frankel, J. Int. J. Radiat. Oncol. Biol. Phys. (1992) [Pubmed]
  11. Techniques for the evaluation of nucleic acid amplification technology performance with specimens containing interfering substances: efficacy of boom methodology for extraction of HIV-1 RNA. Witt, D.J., Kemper, M. J. Virol. Methods (1999) [Pubmed]
  12. Molecular cloning and characterization of a human cDNA and gene encoding a novel acid ceramidase-like protein. Hong, S.B., Li, C.M., Rhee, H.J., Park, J.H., He, X., Levy, B., Yoo, O.J., Schuchman, E.H. Genomics (1999) [Pubmed]
  13. A human endogenous long terminal repeat provides a polyadenylation signal to a novel, alternatively spliced transcript in normal placenta. Goodchild, N.L., Wilkinson, D.A., Mager, D.L. Gene (1992) [Pubmed]
  14. Propagation of lymphocytes infiltrating human liver allografts. Correlation with histologic diagnosis of rejection. Saidman, S.L., Demetris, A.J., Zeevi, A., Duquesnoy, R.J. Transplantation (1990) [Pubmed]
  15. The effects of leukodepletion on the generation and removal of microvesicles and prion protein in blood components. Krailadsiri, P., Seghatchian, J., Macgregor, I., Drummond, O., Perrin, R., Spring, F., Prescott, R., Williamson, L., Prowse, C., Anstee, D., Turner, M. Transfusion (2006) [Pubmed]
  16. Collection of WBC-reduced single-donor PLT concentrates with a new blood cell separator: results of a multicenter study. Moog, R., Zeiler, T., Heuft, H.G., Stephan, B., Fischer, E.G., Kretschmer, V., Rödel-Spieker, R., Strasser, E., Zingsem, J., Moog, R., Stephan, B., Strasser, S. Transfusion (2003) [Pubmed]
  17. Photochemical treatment of platelet concentrates with amotosalen hydrochloride and ultraviolet A light inactivates free and latent cytomegalovirus in a murine transfusion model. Jordan, C.T., Saakadze, N., Newman, J.L., Lezhava, L.J., Maiers, T.T., Hillyer, W.M., Roback, J.D., Hillyer, C.D. Transfusion (2004) [Pubmed]
  18. DDAVP normalized the bleeding time in patients with congenital platelet TxA2 receptor abnormality. Fuse, I., Higuchi, W., Mito, M., Aizawa, Y. Transfusion (2003) [Pubmed]
  19. Detection of bacteria in WBC-reduced PLT concentrates using percent oxygen as a marker for bacteria growth. Ortolano, G.A., Freundlich, L.F., Holme, S., Russell, R.L., Cortus, M.A., Wilkins, K., Nomura, H., Chong, C., Carmen, R., Capetandes, A., Wenz, B. Transfusion (2003) [Pubmed]
  20. Platelet activation during plasma-reduced multicomponent PLT collection: a comparison between COBE Trima and Spectra LRS turbo cell separators. Perseghin, P., Mascaretti, L., Speranza, T., Belotti, D., Baldini, V., Dassi, M., Riva, M., Pogliani, E.M., Sciorelli, G. Transfusion (2004) [Pubmed]
  21. A comparison of PLT collections from two apheresis devices. Bueno, J.L., Barea, L., García, F., Castro, E. Transfusion (2004) [Pubmed]
  22. Severe neonatal alloimmune thrombocytopenia caused by antibodies to human platelet antigen 3a (Baka) detectable only in whole platelet assays. Harrison, C.R., Curtis, B.R., McFarland, J.G., Huff, R.W., Aster, R.H. Transfusion (2003) [Pubmed]
 
WikiGenes - Universities