R L Levine

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Methionine residues as endogenous antioxidants in proteins
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0320, USA
    Proc Natl Acad Sci U S A 93:15036-40. 1996
  2. ncbi request reprint Methionine residues may protect proteins from critical oxidative damage
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0320, USA
    Mech Ageing Dev 107:323-32. 1999
  3. ncbi request reprint Cyclic oxidation and reduction of protein methionine residues is an important antioxidant mechanism
    Earl R Stadtman
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 8012, USA
    Mol Cell Biochem 234:3-9. 2002
  4. ncbi request reprint Oxidation of methionine residues of proteins: biological consequences
    Earl R Stadtman
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 8012, USA
    Antioxid Redox Signal 5:577-82. 2003
  5. pmc Transcriptional profiling of MnSOD-mediated lifespan extension in Drosophila reveals a species-general network of aging and metabolic genes
    Christina Curtis
    Molecular and Computational Biology Program, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089 1340, USA
    Genome Biol 8:R262. 2007
  6. ncbi request reprint Carbonyl modified proteins in cellular regulation, aging, and disease
    Rodney L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0312, USA
    Free Radic Biol Med 32:790-6. 2002
  7. ncbi request reprint Fixation of nitrogen in an electrospray mass spectrometer
    Rodney L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD 20892 0812, USA
    Rapid Commun Mass Spectrom 20:1828-30. 2006
  8. ncbi request reprint Commentary on "Downregulation of the human Lon protease impairs mitochondrial structure and function and causes cell death" by D.A. Bota, J.K. Ngo, and K.J.A. Davies
    Rodney L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD, USA
    Free Radic Biol Med 38:1445-6. 2005
  9. ncbi request reprint Oxidation of methionine in proteins: roles in antioxidant defense and cellular regulation
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 0320, USA
    IUBMB Life 50:301-7. 2000
  10. ncbi request reprint Oxidative modification of proteins during aging
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Bethesda, MD 20892 0812, USA
    Exp Gerontol 36:1495-502. 2001

Collaborators

Detail Information

Publications53

  1. pmc Methionine residues as endogenous antioxidants in proteins
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0320, USA
    Proc Natl Acad Sci U S A 93:15036-40. 1996
    ..Furthermore, the susceptible residues were physically arranged in an array that guarded the entrance to the active site...
  2. ncbi request reprint Methionine residues may protect proteins from critical oxidative damage
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0320, USA
    Mech Ageing Dev 107:323-32. 1999
    ..Given the importance of oxidative stress during aging, the potential function of methionine residues as antioxidants during aging should be investigated experimentally...
  3. ncbi request reprint Cyclic oxidation and reduction of protein methionine residues is an important antioxidant mechanism
    Earl R Stadtman
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 8012, USA
    Mol Cell Biochem 234:3-9. 2002
    ..Deletion of the msrA gene in mice leads to increased sensitivity to oxidative stress and to a decrease (40%) in the maximum lifespan. This suggests that elimination of both Msr's would have more serious consequences...
  4. ncbi request reprint Oxidation of methionine residues of proteins: biological consequences
    Earl R Stadtman
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 8012, USA
    Antioxid Redox Signal 5:577-82. 2003
    ..In addition, a decrease in Msr activities in brain tissues is associated with the development of Alzheimer's disease...
  5. pmc Transcriptional profiling of MnSOD-mediated lifespan extension in Drosophila reveals a species-general network of aging and metabolic genes
    Christina Curtis
    Molecular and Computational Biology Program, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089 1340, USA
    Genome Biol 8:R262. 2007
    ..One question is whether these manipulations function through different mechanisms, or whether they intersect on common processes affecting aging...
  6. ncbi request reprint Carbonyl modified proteins in cellular regulation, aging, and disease
    Rodney L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0312, USA
    Free Radic Biol Med 32:790-6. 2002
    ..The molecular deficiencies that cause accumulation of oxidatively modified proteins are not identified, but regardless of cause, the accumulation is likely to disrupt normal cellular function...
  7. ncbi request reprint Fixation of nitrogen in an electrospray mass spectrometer
    Rodney L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD 20892 0812, USA
    Rapid Commun Mass Spectrom 20:1828-30. 2006
    ..The product is an iron nitride ion, [N(2)FeOH](1+), m/z 100.9438, and is capable of addition to peptides and proteins...
  8. ncbi request reprint Commentary on "Downregulation of the human Lon protease impairs mitochondrial structure and function and causes cell death" by D.A. Bota, J.K. Ngo, and K.J.A. Davies
    Rodney L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD, USA
    Free Radic Biol Med 38:1445-6. 2005
  9. ncbi request reprint Oxidation of methionine in proteins: roles in antioxidant defense and cellular regulation
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 0320, USA
    IUBMB Life 50:301-7. 2000
    ..Interconversion of methionine and methionine sulfoxide can function to regulate the biological activity of proteins, through alteration in catalytic efficiency and through modulation of the surface hydrophobicity of the protein...
  10. ncbi request reprint Oxidative modification of proteins during aging
    R L Levine
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Bethesda, MD 20892 0812, USA
    Exp Gerontol 36:1495-502. 2001
    ..Oxidized proteins bearing carbonyl groups are generally dysfunctional, and in the last third of lifespan the content of these oxidized proteins rises to a level likely to cause substantial disruption of cellular function...
  11. pmc Glutamic and aminoadipic semialdehydes are the main carbonyl products of metal-catalyzed oxidation of proteins
    J R Requena
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 3, Room 222, 3 Center Drive, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 98:69-74. 2001
    ....
  12. pmc Copper-catalyzed oxidation of the recombinant SHa(29-231) prion protein
    J R Requena
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, 50 South Drive, Room 2351 MSC 8012, Bethesda, MD 20892 8012, USA
    Proc Natl Acad Sci U S A 98:7170-5. 2001
    ..These findings indicate that PrP, a copper-binding protein, may be particularly susceptible to metal-catalyzed oxidation and that oxidation triggers an extensive structural transition leading to aggregation...
  13. pmc Antioxidant activity of Ferrozine-iron-amino acid complexes
    B S Berlett
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 3, Room 222, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 98:451-6. 2001
    ..p. These results suggest that identification of a physiological chelator that can replace Ferrozine in amino acid-iron complexes might have important physiological and pharmacological applications...
  14. ncbi request reprint Thiols mediate superoxide-dependent NADH modification of glyceraldehyde-3-phosphate dehydrogenase
    J Rivera-Nieves
    Pulmonary Critical Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 274:19525-31. 1999
    ..This thiol linkage was stable to HgCl2. Thus, linkage of GAPDH to NADH, in contrast to NAD, occurs in the presence of thiol, is independent of NO, and is mediated by superoxide...
  15. ncbi request reprint Carbonic anhydrase III: the phosphatase activity is extrinsic
    G Kim
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Arch Biochem Biophys 377:334-40. 2000
    ....
  16. ncbi request reprint Protein oxidation
    E R Stadtman
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 0320, USA
    Ann N Y Acad Sci 899:191-208. 2000
    ..Accumulation of modified proteins disrupts cellular function either by loss of catalytic and structural integrity or by interruption of regulatory pathways...
  17. ncbi request reprint MDP-1: A novel eukaryotic magnesium-dependent phosphatase
    J D Selengut
    Laboratory of Biochemistry, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 0320, USA
    Biochemistry 39:8315-24. 2000
    ..In recognition of these observations, the enzyme has been given the name magnesium-dependent phosphatase-1 (MDP-1)...
  18. ncbi request reprint Recent advances in the analysis of oxidized proteins
    J R Requena
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
    Amino Acids 25:221-6. 2003
    ....
  19. ncbi request reprint Thioredoxin converts the Syrian hamster (29-231) recombinant prion protein to an insoluble form
    J R Requena
    Laboratory of Biochemistry, NHLBI, National Institutes of Health, Bethesda, MD 20892, USA
    Free Radic Biol Med 30:141-7. 2001
    ..The thioredoxin/thioredoxin reductase system is approximately 7000 times more efficient than dithiothreitol...
  20. ncbi request reprint Nucleotide sequence and structure of the mouse carbonic anhydrase III gene
    G Kim
    Laboratory of Biochemistry, National Heart Lung and Blood Institute, National Institutes of Health, 20892 0320, Bethesda, MD, USA
    Gene 265:37-44. 2001
    ..5 kb. The 5' flanking region of the genomic DNA is notable for a pyrimidine rich region consisting of two dinucleotide repeats containing 23 and 20 TC pairs separated by the same 15 bp spacer...
  21. pmc Iron-dependent oxidation, ubiquitination, and degradation of iron regulatory protein 2: implications for degradation of oxidized proteins
    K Iwai
    Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892 5430, USA
    Proc Natl Acad Sci U S A 95:4924-8. 1998
    ..Selective targeting and removal of oxidatively modified proteins may contribute to the turnover of many proteins that are degraded by the proteasome...
  22. ncbi request reprint Free radical-mediated oxidation of free amino acids and amino acid residues in proteins
    E R Stadtman
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 8012, USA
    Amino Acids 25:207-18. 2003
    ....
  23. pmc HIV-2 protease is inactivated after oxidation at the dimer interface and activity can be partly restored with methionine sulphoxide reductase
    D A Davis
    HIV and AIDS Malignancy Branch, National Cancer Institute, 9000 Rockville Pike, National Institutes of Health, Bethesda, MD 20892 1906, USA
    Biochem J 346:305-11. 2000
    ....
  24. pmc Loss of the ataxia-telangiectasia gene product causes oxidative damage in target organs
    C Barlow
    Laboratory of Genetic Disease Research, National Human Genome Research Institute, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 96:9915-9. 1999
    ..These observations provide a mechanistic basis for the A-T phenotype and lay a rational foundation for therapeutic intervention...
  25. ncbi request reprint Why have cells selected reactive oxygen species to regulate cell signaling events?
    E R Stadtman
    Laboratory of Biochemistry, NHLBI NIH, Bethesda, Maryland 20892 8012, USA
    Hum Exp Toxicol 21:83. 2002
    ..This raises the question: If ROS are so damaging to cells, why have cells selected ROS to trigger activation of so many cell signaling pathways?..
  26. ncbi request reprint Modulation of the hydrophobicity of glutamine synthetase by mixed-function oxidation
    J Cervera
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892
    FASEB J 2:2591-5. 1988
    ..Thus, oxidative modification modulates the surface hydrophobicity of glutamine synthetase, and this modulation can control susceptibility to proteolysis...
  27. ncbi request reprint Modification of the ADP-ribosyltransferase and NAD glycohydrolase activities of a mammalian transferase (ADP-ribosyltransferase 5) by auto-ADP-ribosylation
    B Weng
    Pulmonary Critical Care Medicine Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892 1434, USA
    J Biol Chem 274:31797-803. 1999
    ..These findings suggest that auto-ADP-ribosylation of ART5 was stoichiometric, resulted in at least two modifications and converted ART5 from an NADase to a transferase, and could be one mechanism for regulating enzyme activity...
  28. pmc The phosphatase activity of carbonic anhydrase III is reversibly regulated by glutathiolation
    E Cabiscol
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 0320, USA
    Proc Natl Acad Sci U S A 93:4170-4. 1996
    ..Thus, glutathiolation is a reversible covalent modification that can regulate CAIII, a phosphatase that may function in the cellular response to oxidative stress...
  29. pmc Group B Streptococcus, phospholipids and pulmonary hypertension
    J Curtis
    Office of Graduate Medical Education and Department of Pediatrics, Uniformed Services University of the Health Sciences, Bethesda, MD 20892, USA
    J Perinatol 31:S24-8. 2011
    ..Group B Streptococcus is the most common cause of bacterial infection in the newborn. Our aim was to purify and identify molecules produced by the bacterium, which cause pulmonary hypertension...
  30. ncbi request reprint Molecular cloning and characterization of a mitochondrial selenocysteine-containing thioredoxin reductase from rat liver
    S R Lee
    Laboratory of Cell Signaling, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 274:4722-34. 1999
    ....
  31. pmc Myristoylated methionine sulfoxide reductase A protects the heart from ischemia-reperfusion injury
    Hang Zhao
    Laboratory of Biochemistry, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 8012, USA
    Am J Physiol Heart Circ Physiol 301:H1513-8. 2011
    ..We conclude that cytosolic MsrA protects the heart from ischemia-reperfusion damage. The requirement for myristoylation suggests that MsrA must interact with a hydrophobic domain to provide protection...
  32. ncbi request reprint Reversible oxidation of HIV-2 protease
    David A Davis
    HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Methods Enzymol 348:249-59. 2002
  33. ncbi request reprint Detection and affinity purification of oxidant-sensitive proteins using biotinylated glutathione ethyl ester
    Daniel M Sullivan
    Laboratory of Molecular Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Methods Enzymol 353:101-13. 2002
  34. ncbi request reprint Metal-catalyzed oxidation of the Werner syndrome protein causes loss of catalytic activities and impaired protein-protein interactions
    Jeanine A Harrigan
    Laboratory of Molecular Gerontology, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA
    J Biol Chem 282:36403-11. 2007
    ....
  35. ncbi request reprint Iron regulatory protein 2 as iron sensor. Iron-dependent oxidative modification of cysteine
    Dae Kyung Kang
    Laboratory of Biochemistry, NHLBI, National Institutes of Health and the Cell Biology and Metabolism Branch, NICHD, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 278:14857-64. 2003
    ..One cysteine residue is oxidized to dehydrocysteine and other products. This covalent modification may thus mark the protein molecule for degradation by the proteasome system...
  36. ncbi request reprint Metal-catalyzed oxidation of alpha-synuclein: helping to define the relationship between oligomers, protofibrils, and filaments
    Nelson B Cole
    Genetic Diseases Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 280:9678-90. 2005
    ....
  37. ncbi request reprint Oxidation of methionine residues in the prion protein by hydrogen peroxide
    Jesús R Requena
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Arch Biochem Biophys 432:188-95. 2004
    ..The high number of solvent exposed methionine residues in PrP suggests their possible role as protective endogenous antioxidants...
  38. ncbi request reprint Methionine oxidation and aging
    Earl R Stadtman
    Laboratory of Biochemistry, National Heart, Lung and Blood Institute, Bethesda, MD 20892, USA
    Biochim Biophys Acta 1703:135-40. 2005
    ....
  39. pmc High urea and NaCl carbonylate proteins in renal cells in culture and in vivo, and high urea causes 8-oxoguanine lesions in their DNA
    Zheng Zhang
    Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 101:9491-6. 2004
    ..iii) In mIMCD3 cells a normal plasma concentration of urea causes carbonylation, and carbonylation increases over the uremic range of urea concentration, indicating that urea can contribute directly to the carbonylation found in uremia...
  40. ncbi request reprint Numerous proteins in Mammalian cells are prone to iron-dependent oxidation and proteasomal degradation
    Steven K Drake
    National Institute of Child Health and Human Development, Bethesda, MD, USA
    Dev Neurosci 24:114-24. 2002
    ..As iron overload is a feature of many human neurological diseases, further characterization of the process of degradation of iron-dependently oxidized proteins may yield insights into mechanisms of human disease...
  41. ncbi request reprint The role of endogenous heme synthesis and degradation domain cysteines in cellular iron-dependent degradation of IRP2
    Emmanuel Bourdon
    Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892, USA
    Blood Cells Mol Dis 31:247-55. 2003
    ..Thus, we could not discern a role for the recently defined in vitro cysteine-dependent iron-binding site of IRP2 in cellular physiology. The early molecular events in iron-dependent degradation of IRP2 remain to be elucidated...
  42. pmc Lon protease promotes survival of Escherichia coli during anaerobic glucose starvation
    Shen Luo
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, 20892 8012, USA
    Arch Microbiol 189:181-5. 2008
    ..We conclude that the Lon protease supports survival during anaerobic carbon starvation by a mechanism which does not depend on Clp...
  43. pmc Phosphorylation of actin Tyr-53 inhibits filament nucleation and elongation and destabilizes filaments
    Xiong Liu
    Laboratory of Cell Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 103:13694-9. 2006
    ..Tyr-53 phosphorylation does not affect the ability of filamentous actin to activate myosin ATPase...
  44. ncbi request reprint Assessment of skin carbonyl content as a noninvasive measure of biological age
    Susann Richert
    Laboratory of Biochemistry, National Institutes of Health, Bethesda, Maryland 20892 0812, USA
    Arch Biochem Biophys 397:430-2. 2002
    ..This was not the case, as we found no age-dependent relationship in the protein carbonyl content of skin cells from volunteers aged 20 to 79 years...
  45. ncbi request reprint Quantitation of protein on gels and blots by infrared fluorescence of Coomassie blue and Fast Green
    Shen Luo
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
    Anal Biochem 350:233-8. 2006
    ..The fluorescence response is quantitative for protein content between 10 ng and 20 microg per band or spot. Staining and destaining require only 30 min, and the method is compatible with subsequent immunodetection...
  46. ncbi request reprint Proteasomal degradation of mutant superoxide dismutases linked to amyotrophic lateral sclerosis
    Luca Di Noto
    Laboratory of Biochemistry, NHLBI, National Institutes of Health, Bethesda, Maryland 20892 0812, USA
    J Biol Chem 280:39907-13. 2005
    ..Exposure of hydrophobic regions as a consequence of decreased thermal stability may allow the proteasome to recognize these molecules as non-native...
  47. ncbi request reprint Mutation of the adenylylated tyrosine of glutamine synthetase alters its catalytic properties
    Shen Luo
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892, USA
    Biochemistry 44:9441-6. 2005
    ..Thus, subtle modifications in the environment of residue 397 are sufficient to induce changes previously thought to require adenylylation...
  48. pmc Direct detection of potential selenium delivery proteins by using an Escherichia coli strain unable to incorporate selenium from selenite into proteins
    Gerard M Lacourciere
    Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 99:9150-3. 2002
    ..A 28-kDa protein identified as deoxyribose phosphate aldolase also contained bound selenium. These (75)Se-labeled proteins may have alternate roles as selenium delivery proteins...
  49. pmc Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence
    Hongtao Zhao
    Department of Biophysics and Free Radical Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA
    Proc Natl Acad Sci U S A 102:5727-32. 2005
    ..We conclude that the HPLC/fluorescence assay using HE as a probe is more suitable [corrected] for detecting intracellular O(2)(.-)...
  50. ncbi request reprint Treatment with a catalytic antioxidant corrects the neurobehavioral defect in ataxia-telangiectasia mice
    Susan E Browne
    Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, NY, USA
    Free Radic Biol Med 36:938-42. 2004
    ..We show that treatment with a catalytic antioxidant corrects the neurobehavioral deficit in these mice...
  51. ncbi request reprint Identification of a heme-sensing domain in iron regulatory protein 2
    Jinsook Jeong
    Laboratory of Biochemistry, NHLBI, National Institutes of Health, Bethesda, MD 20892, USA
    J Biol Chem 279:45450-4. 2004
    ..This covalent modification may thus mark the protein molecule for degradation by the proteasome system, providing another mechanism by which heme can regulate the level of iron regulatory protein 2...
  52. pmc Carbonic anhydrase III is not required in the mouse for normal growth, development, and life span
    Geumsoo Kim
    Laboratories of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 0812, USA
    Mol Cell Biol 24:9942-7. 2004
    ..We conclude that carbonic anhydrase III is dispensable for mice living under standard laboratory husbandry conditions...
  53. ncbi request reprint Mass spectrometry analysis of recombinant human ZP3 expressed in glycosylation-deficient CHO cells
    Ming Zhao
    Laboratory of Cellular and Developmental Biology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biochemistry 43:12090-104. 2004
    ..Taken together, these data indicate that human and mouse ZP3 proteins are quite similar, and alternative explanations of taxon-specific sperm binding warrant exploration...