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Gene Review

DNASE2  -  deoxyribonuclease II, lysosomal

Homo sapiens

Synonyms: Acid DNase, DNASE2A, DNL, DNL2, DNase II alpha, ...
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Disease relevance of DNASE2


Psychiatry related information on DNASE2

  • RESULTS: The fractional contribution from DNL to VLDL-triacylglycerol palmitate rose after alcohol consumption from 2 +/- 1% to 30 +/- 8%; nevertheless, the absolute rate of DNL (0.8 g/6 h) represented <5% of the ingested alcohol dose; 77 +/- 13% of the alcohol cleared from plasma was converted directly to acetate entering plasma [6].

High impact information on DNASE2


Chemical compound and disease context of DNASE2


Biological context of DNASE2

  • DNase II is ubiquitously expressed in human tissues, and the DNase II gene (DNASE2) was assigned to chromosome 19 [11].
  • Recently obtained information on the cDNA encoding human deoxyribonuclease II (DNase II) (T. Yasuda et al., 1998, J. Biol. Chem. 273, 2610-2616) has made it possible to demonstrate the precise position of the the human DNase II gene (DNASE2) on human chromosomes [12].
  • The distribution of the activities of both enzymes displayed clear-cut bimodality and the Japanese study population could be classified into two distinct types, namely low-activity (DNASE2 L) and high-activity (DNASE2 H), which indicates the existence of a genetic polymorphism in the activity levels of urinary and leukocytic DNase IIs [13].
  • The family study results were compatible with the model that the low activity type is due to an autosomal recessive gene, which indicates that DNASE2 L represents homozygosity for DNASE2*L and DNASE2 H corresponds to homozygosity for DNASE2*H and heterozygosity for DNASE2*L and DNASE2*H [13].
  • We also demonstrate that a mutant form of DNase II alpha that lacks the purported active-site His(295) can still bind DNA, indicating that this histidine residue is not simply involved in DNA binding, but may have a direct role in catalysis [1].

Anatomical context of DNASE2


Associations of DNASE2 with chemical compounds

  • DNase II alpha contains six evolutionarily conserved cysteine residues, and mutations in any one of these cysteines completely ablated enzymic activity, consistent with the importance of disulphide bridging in maintaining correct protein structure [1].
  • Following each condition, fasting fractional DNL and endogenous glucose production (EGP) were evaluated using [1-13C]sodium acetate and 6,6-2H2 glucose and a two-step hyperinsulinemic-euglycemic clamp was performed to assess insulin sensitivity [3].
  • Hepatic DNL was increased approximately 10-fold in ob/ob mice, whereas hepatic cholesterol synthesis was not affected [17].
  • However, after the low-fat, high-carbohydrate diet, triacylglycerols increased significantly and DNL was 5-6-fold higher than in normoinsulinemic subjects consuming a high-fat diet [18].
  • CONCLUSION: These data confirm the acute stimulation of DNL after meals in healthy subjects and validate the contribution of this pathway to elevations in triacylglycerol concentration [19].

Other interactions of DNASE2

  • Chromosomal localization of a human deoxyribonuclease II gene (DNASE2) to 19p13.2-p13.1 using both the polymerase chain reaction and fluorescence in situ hybridization analysis [12].
  • Although a recombinant protein for the putative human DLAD has a divalent cation-independent acid DNase activity, expression of the DLAD mRNA containing the entire open reading frame was not detected in any human tissues tested, except for lung, in which a short 1.1 kb transcript lacking the first two exons is expressed [20].
  • DNAS1L2, a member of the DNase I-like endonuclease family, is the only divalent cation-dependent acid DNase so far identified in mammals [21].

Analytical, diagnostic and therapeutic context of DNASE2

  • We suggest that a dyad-symmetric DNL IV.XRCC4 tetramer bridges the two ends of the broken DNA and catalyzes the coordinate ligation of the two DNA strands [22].
  • DESIGN: After 5 d of an isoenergetic high-fat, low-carbohydrate diet, fasting DNL was measured in normoinsulinemic (<or= 85 pmol/L) lean (n = 9) and obese (n = 6) and hyperinsulinemic (>or= 115 pmol/L) obese (n = 8) subjects [18].
  • Glucose metabolism and hepatic DNL were measured in the fasting state or after 3 d of continuous isoenergetic enteral feeding providing 28%, 53%, or 75% carbohydrate [5].
  • BACKGROUND: Conversion of glucose into lipid (de novo lipogenesis; DNL) is a possible fate of carbohydrate administered during nutritional support [5].
  • During the fasting and postprandial periods, serum insulin, glucose, triacylglycerol, and nonesterified fatty acid concentrations were measured, and rates of DNL were quantified via intravenous infusion of [1-(13)C] sodium acetate and mass isotopomer distribution analysis [19].


  1. Structural requirements of human DNase II alpha for formation of the active enzyme: the role of the signal peptide, N-glycosylation, and disulphide bridging. MacLea, K.S., Krieser, R.J., Eastman, A. Biochem. J. (2003) [Pubmed]
  2. Effect of human polymorphonuclear and mononuclear leukocytes on chromosomal and plasmid DNA of Escherichia coli. Role of acid DNase. Rozenberg-Arska, M., van Strijp, J.A., Hoekstra, W.P., Verhoef, J. J. Clin. Invest. (1984) [Pubmed]
  3. Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men. Faeh, D., Minehira, K., Schwarz, J.M., Periasamy, R., Periasami, R., Park, S., Seongsu, P., Tappy, L. Diabetes (2005) [Pubmed]
  4. Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men. Marques-Lopes, I., Ansorena, D., Astiasaran, I., Forga, L., Martínez, J.A. Am. J. Clin. Nutr. (2001) [Pubmed]
  5. Effects of enteral carbohydrates on de novo lipogenesis in critically ill patients. Schwarz, J.M., Chioléro, R., Revelly, J.P., Cayeux, C., Schneiter, P., Jéquier, E., Chen, T., Tappy, L. Am. J. Clin. Nutr. (2000) [Pubmed]
  6. De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption. Siler, S.Q., Neese, R.A., Hellerstein, M.K. Am. J. Clin. Nutr. (1999) [Pubmed]
  7. Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection. Schwarz, J.M., Neese, R.A., Turner, S., Dare, D., Hellerstein, M.K. J. Clin. Invest. (1995) [Pubmed]
  8. Development, characterization, and subcellular location of DNAse activity in HL-60 cells and monocytes. Roberts, P.J. Blood (1990) [Pubmed]
  9. A broad-based metabolic approach to study VLDL apoB100 metabolism in patients with ESRD and patients treated with peritoneal dialysis. Prinsen, B.H., Rabelink, T.J., Romijn, J.A., Bisschop, P.H., de Barse, M.M., de Boer, J., van Haeften, T.W., Barrett, P.H., Berger, R., de Sain-van der Velden, M.G. Kidney Int. (2004) [Pubmed]
  10. Gas chromatography/mass spectrometry method to quantify blood hydroxycitrate concentration. Loe , Y.C., Bergeron, N., Rodriguez, N., Schwarz, J.M. Anal. Biochem. (2001) [Pubmed]
  11. Molecular cloning of the cDNA encoding human deoxyribonuclease II. Yasuda, T., Takeshita, H., Iida, R., Nakajima, T., Hosomi, O., Nakashima, Y., Kishi, K. J. Biol. Chem. (1998) [Pubmed]
  12. Chromosomal localization of a human deoxyribonuclease II gene (DNASE2) to 19p13.2-p13.1 using both the polymerase chain reaction and fluorescence in situ hybridization analysis. Yasuda, T., Takeshita, H., Iida, R., Nakajima, T., Hosomi, O., Nakashima, Y., Mogi, K., Kishi, K. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
  13. Genetic polymorphism of human deoxyribonuclease II (DNase II): low activity levels in urine and leukocytes are due to an autosomal recessive allele. Yasuda, T., Nadano, D., Sawazaki, K., Kishi, K. Ann. Hum. Genet. (1992) [Pubmed]
  14. Regulation of hepatic de novo lipogenesis in humans. Hellerstein, M.K., Schwarz, J.M., Neese, R.A. Annu. Rev. Nutr. (1996) [Pubmed]
  15. Concept of fat balance in human obesity revisited with particular reference to de novo lipogenesis. Schutz, Y. Int. J. Obes. Relat. Metab. Disord. (2004) [Pubmed]
  16. Hepatic de novo lipogenesis in stable low-birth-weight infants during exclusive breast milk feedings and during parenteral nutrition. Garg, M., Bassilian, S., Bell, C., Lee, S., Lee, W.N. JPEN. Journal of parenteral and enteral nutrition. (2005) [Pubmed]
  17. Hepatic VLDL production in ob/ob mice is not stimulated by massive de novo lipogenesis but is less sensitive to the suppressive effects of insulin. Wiegman, C.H., Bandsma, R.H., Ouwens, M., van der Sluijs, F.H., Havinga, R., Boer, T., Reijngoud, D.J., Romijn, J.A., Kuipers, F. Diabetes (2003) [Pubmed]
  18. Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets. Schwarz, J.M., Linfoot, P., Dare, D., Aghajanian, K. Am. J. Clin. Nutr. (2003) [Pubmed]
  19. Temporal pattern of de novo lipogenesis in the postprandial state in healthy men. Timlin, M.T., Parks, E.J. Am. J. Clin. Nutr. (2005) [Pubmed]
  20. Isolation and characterization of the DLAD/Dlad genes, which lie head-to-head with the genes for urate oxidase. Shiokawa, D., Tanuma, S.I. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
  21. Characterization of the human DNAS1L2 gene and the molecular mechanism for its transcriptional activation induced by inflammatory cytokines. Shiokawa, D., Matsushita, T., Kobayashi, T., Matsumoto, Y., Tanuma, S. Genomics (2004) [Pubmed]
  22. DNA ligase IV and XRCC4 form a stable mixed tetramer that functions synergistically with other repair factors in a cell-free end-joining system. Lee, K.J., Huang, J., Takeda, Y., Dynan, W.S. J. Biol. Chem. (2000) [Pubmed]
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