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CELA2A  -  chymotrypsin-like elastase family, member 2A

Homo sapiens

Synonyms: Chymotrypsin-like elastase family member 2A, ELA2A, Elastase-2A, PE-1
 
 
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Disease relevance of ELA2A

  • METHODS: Recombinant ELA2A and ELA2B were expressed in Escherichia coli, and their activity was tested on Glt-Ala-Ala-Pro-Leu-p-nitroanilide, DQ elastin and bovine milk protein [1].
  • This surgical procedure resulted in an irreversible state of shock (splanchnic artery occlusion shock) characterized by high mortality rate (0% survival, 120 min following the release of clamps), a profound hypotension and vascular dysfunction consisting of a marked hyporeactivity to phenylephrine (PE 1 nM-10 microM) of aortic rings [2].
 

High impact information on ELA2A

  • In vitro footprinting and quantitative gel shift analyses showed that PF1 binds preferentially to the PE1 element but also at lower affinity to two other AT-rich regions upstream of PE1 [3].
  • We have isolated a rice cDNA clone (pR4) encoding a DNA binding protein that binds to the AT-rich PE1 element [3].
  • Functional analysis of the oat PHYA3 promoter in a transfection assay has revealed two positive elements, PE1 and PE3, that function synergistically to support high levels of transcription in the absence of light [3].
  • In contrast, chymotrypsin B, elastase 2A, or elastase 3A (proteinase E) are ineffective [4].
  • The 100-base pair ELA1 transcriptional enhancer drives high level transcription to pancreatic acinar cells of transgenic mice and in transfected pancreatic acinar cells in culture [5].
 

Biological context of ELA2A

  • Finally, chimeras and point mutations engineered between ELA2A and ELA2B revealed that multiple evolutionary mutations inactivated ELA2B [1].
  • The binding domains of PE-1 and PE-2 have been broadly located, with respect to the primary translation product, within the amino acid sequences 152-207 and 84-131, respectively [6].
  • USF recognition of the PE1/PE2 region E box sites required phosphorylation with several potential involved residues, including T153, maping to the USF-specific region (USR) [7].
 

Anatomical context of ELA2A

  • CONCLUSIONS: The results indicate that ELA2B is not an elastase enzyme and confirm that ELA2A is the major elastase in the human pancreas [1].
  • Immunoblot analysis of total bovine adrenomedullary chromaffin granule lysate reveals PE-1 and PE-2 immunoreactive forms of observed molecular mass 35, 33, 29, 24, 22, and 15 kDa, and an 18-kDa PE-1 immunoreactive form [6].
 

Associations of ELA2A with chemical compounds

  • There is preliminary evidence that PE-1 may be detecting a subset of polypeptides where shortening from the NH2 terminus has occurred [6].
  • Incorporation of vitamin E in PE1- to PE7-treated cells were significantly (P < 0.05) increased compared to controls and were comparable to each other [8].
  • Mafosfamide-lysine, a stable cyclophosphamide congener, strongly inhibited primary colony formation (PE1) with a D10 value of 14.46 +/- 1.76 micrograms/ml, but was much less efficient in the PE2 assay [9].
  • Moreover, melphalan was equally effective in inhibiting CFU-L growth in both PE1 and PE2 assays, with D10 values of 1.53 +/- 0.17 micrograms/ml and 1.59 +/- 0.21 micrograms/ml for PE1 and PE2, respectively (p = 0.48) [9].
  • Vesnarinone suppressed the primary (PE1) and secondary (PE2) colony-formation of leukemic blast progenitors in six AML patients tested [10].
 

Other interactions of ELA2A

  • RESULTS: Surprisingly, recombinant ELA2B was completely devoid of proteolytic activity, while ELA2A readily hydrolyzed all three test substrates [1].
  • MCP-1 protein (ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1 [11].
  • The NH2-terminal 20-amino acid sequence shares 50-55% identity with human alpha-tryptase, elastase 2A and 2B, chymotrypsin, acrosin, and the catalytic chains of hepsin, plasma kallikrein, and coagulation factor XI [12].

References

  1. Inactivity of recombinant ELA2B provides a new example of evolutionary elastase silencing in humans. Szepessy, E., Sahin-Tóth, M. Pancreatology (2006) [Pubmed]
  2. Recombinant human granulocyte colony-stimulating factor reverts vascular dysfunction. Squadrito, F., Altavilla, D., Squadrito, G., Campo, G.M., Ioculano, M., Serranò, M., Minutoli, L., Arlotta, M., Musolino, C., Saitta, A., Caputi, A.P. International journal of microcirculation, clinical and experimental / sponsored by the European Society for Microcirculation. (1997) [Pubmed]
  3. PF1: an A-T hook-containing DNA binding protein from rice that interacts with a functionally defined d(AT)-rich element in the oat phytochrome A3 gene promoter. Nieto-Sotelo, J., Ichida, A., Quail, P.H. Plant Cell (1994) [Pubmed]
  4. Chymotrypsin C (caldecrin) stimulates autoactivation of human cationic trypsinogen. Nemoda, Z., Sahin-Tóth, M. J. Biol. Chem. (2006) [Pubmed]
  5. The role of PTF1-P48 in pancreatic acinar gene expression. Rose, S.D., Swift, G.H., Peyton, M.J., Hammer, R.E., MacDonald, R.J. J. Biol. Chem. (2001) [Pubmed]
  6. Monoclonal antibodies to a proenkephalin A fusion peptide synthesized in Escherichia coli recognize novel proenkephalin A precursor forms. Spruce, B.A., Jackson, S., Lowry, P.J., Lane, D.P., Glover, D.M. J. Biol. Chem. (1988) [Pubmed]
  7. PAI-1 transcriptional regulation during the G(0) --> G(1) transition in human epidermal keratinocytes. Qi, L., Allen, R.R., Lu, Q., Higgins, C.E., Garone, R., Staiano-Coico, L., Higgins, P.J. J. Cell. Biochem. (2006) [Pubmed]
  8. Effect of phospholipid acyl chain modulation on vitamin E incorporation into pulmonary artery endothelial cell membranes. Patel, J.M., Abeles, A.J., Block, E.R. J. Cell. Physiol. (1993) [Pubmed]
  9. Effect of melphalan against self-renewal capacity of leukemic progenitors in acute myeloblastic leukemia. Demur, C., Chiron, M., Saivin, S., Attal, M., Dastugue, N., Bousquet, C., Galinier, J.L., Colombies, P., Laurent, G. Leukemia (1992) [Pubmed]
  10. Effect of vesnarinone, a quinolinone derivative, on the growth of leukemic blasts in acute myelogenous leukemia. Nara, N., Kurokawa, H., Tohda, S., Tomiyama, J., Nagata, K., Tanikawa, S. Exp. Hematol. (1997) [Pubmed]
  11. Cardiac inflammation contributes to right ventricular dysfunction following experimental pulmonary embolism in rats. Watts, J.A., Zagorski, J., Gellar, M.A., Stevinson, B.G., Kline, J.A. J. Mol. Cell. Cardiol. (2006) [Pubmed]
  12. Prostasin is a novel human serine proteinase from seminal fluid. Purification, tissue distribution, and localization in prostate gland. Yu, J.X., Chao, L., Chao, J. J. Biol. Chem. (1994) [Pubmed]
 
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