Advanced Search
Display options
Filter resources
Text Availability
Article type
Publication date
Species
Language
Sex
Age
Showing 1 to 12 of 448 entries
Sorted by: Best Match Show Resources per page
Regulation of methionine biosynthesis in Escherichia coli: mapping of the metJ locus and properties of a metJ plus-metJ minus diploid.

Proceedings of the National Academy of Sciences of the United States of America

Su CH, Greene RC.
PMID: 5277087
Proc Natl Acad Sci U S A. 1971 Feb;68(2):367-71. doi: 10.1073/pnas.68.2.367.
Free PMC Article

MetJ(-) mutants of Escherichia coli have elevated nonrepressible levels of the enzymes of methionine biosynthesis and S-adenosylmethionine synthetase (ATP:L-methionine S-adenosyltransferase, EC 2.5.1.6). In E. coli, as in Salmonella typhimurium, the metJ locus is close to metB (95% cotransduction of...

Cite
Su CH, Greene RC. Regulation of methionine biosynthesis in Escherichia coli: mapping of the metJ locus and properties of a metJ plus-metJ minus diploid. Proc Natl Acad Sci U S A. 1971;68(2):367-71doi: 10.1073/pnas.68.2.367.
Su, C. H., & Greene, R. C. (1971). Regulation of methionine biosynthesis in Escherichia coli: mapping of the metJ locus and properties of a metJ plus-metJ minus diploid. Proceedings of the National Academy of Sciences of the United States of America, 68(2), 367-71. https://doi.org/10.1073/pnas.68.2.367
Su, C H, and Greene, R C. "Regulation of methionine biosynthesis in Escherichia coli: mapping of the metJ locus and properties of a metJ plus-metJ minus diploid." Proceedings of the National Academy of Sciences of the United States of America vol. 68,2 (1971): 367-71. doi: https://doi.org/10.1073/pnas.68.2.367
Su CH, Greene RC. Regulation of methionine biosynthesis in Escherichia coli: mapping of the metJ locus and properties of a metJ plus-metJ minus diploid. Proc Natl Acad Sci U S A. 1971 Feb;68(2):367-71. doi: 10.1073/pnas.68.2.367. PMID: 5277087; PMCID: PMC388939.
Copy Download .nbib Format: NLM
γ-Glutamyl hydrolase modulation significantly influences global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells.

Genes & nutrition

Kim SE, Hinoue T, Kim MS, Sohn KJ, Cho RC, Cole PD, Weisenberger DJ, Laird PW, Kim YI.
PMID: 25502219
Genes Nutr. 2015 Jan;10(1):444. doi: 10.1007/s12263-014-0444-0. Epub 2014 Dec 13.

γ-Glutamyl hydrolase (GGH) plays an important role in folate homeostasis by catalyzing hydrolysis of polyglutamylated folate into monoglutamates. Polyglutamylated folates are better substrates for several enzymes involved in the generation of S-adenosylmethionine, the primary methyl group donor, and hence,...

Cite
Kim SE, Hinoue T, Kim MS, et al. γ-Glutamyl hydrolase modulation significantly influences global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells. Genes Nutr. 2014;10(1):444doi: 10.1007/s12263-014-0444-0.
Kim, S. E., Hinoue, T., Kim, M. S., Sohn, K. J., Cho, R. C., Cole, P. D., Weisenberger, D. J., Laird, P. W., & Kim, Y. I. (2015). γ-Glutamyl hydrolase modulation significantly influences global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells. Genes & nutrition, 10(1), 444. https://doi.org/10.1007/s12263-014-0444-0
Kim, Sung-Eun, et al. "γ-Glutamyl hydrolase modulation significantly influences global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells." Genes & nutrition vol. 10,1 (2015): 444. doi: https://doi.org/10.1007/s12263-014-0444-0
Kim SE, Hinoue T, Kim MS, Sohn KJ, Cho RC, Cole PD, Weisenberger DJ, Laird PW, Kim YI. γ-Glutamyl hydrolase modulation significantly influences global and gene-specific DNA methylation and gene expression in human colon and breast cancer cells. Genes Nutr. 2015 Jan;10(1):444. doi: 10.1007/s12263-014-0444-0. Epub 2014 Dec 13. PMID: 25502219; PMCID: PMC4265218.
Copy Download .nbib Format: NLM
As(III) S-adenosylmethionine methyltransferases and other arsenic binding proteins.

Geomicrobiology journal

Ajees AA, Rosen BP.
PMID: 26366023
Geomicrobiol J. 2015;32(7):570-576. doi: 10.1080/01490451.2014.908983.

Efflux is by far the most common means of arsenic detoxification is by methylation catalyzed by a family of As(III) S-adenosylmethionine (SAM) methyltransferases (MTs) enzymes designated ArsM in microbes or AS3MT in higher eukaryotes. The protein sequence of more...

Cite
Ajees AA, Rosen BP. As(III) S-adenosylmethionine methyltransferases and other arsenic binding proteins. Geomicrobiol J. 2015;32(7):570-576doi: 10.1080/01490451.2014.908983.
Ajees, A. A., & Rosen, B. P. (2015). As(III) S-adenosylmethionine methyltransferases and other arsenic binding proteins. Geomicrobiology journal, 32(7), 570-576. https://doi.org/10.1080/01490451.2014.908983
Ajees, A Abdul, and Rosen, Barry P. "As(III) S-adenosylmethionine methyltransferases and other arsenic binding proteins." Geomicrobiology journal vol. 32,7 (2015): 570-576. doi: https://doi.org/10.1080/01490451.2014.908983
Ajees AA, Rosen BP. As(III) S-adenosylmethionine methyltransferases and other arsenic binding proteins. Geomicrobiol J. 2015;32(7):570-576. doi: 10.1080/01490451.2014.908983. PMID: 26366023; PMCID: PMC4564252.
Copy Download .nbib Format: NLM
Caspase-like activity during aging and cell death in the toxic dinoflagellate Karenia brevis.

Harmful algae

Johnson JG, Janech MG, Van Dolah FM.
PMID: 28040110
Harmful Algae. 2014 Jan;31:41-53. doi: 10.1016/j.hal.2013.08.005. Epub 2013 Oct 20.

The observation of caspase-like activity during cell death has provided a new framework for understanding the evolutionary and ecological contexts of programmed cell death in phytoplankton. However, additional roles for this caspase-like activity, the enzymes responsible, and the targets...

Cite
Johnson JG, Janech MG, Van Dolah FM. Caspase-like activity during aging and cell death in the toxic dinoflagellate Karenia brevis. Harmful Algae. 2013;31:41-53doi: 10.1016/j.hal.2013.08.005.
Johnson, J. G., Janech, M. G., & Van Dolah, F. M. (2014). Caspase-like activity during aging and cell death in the toxic dinoflagellate Karenia brevis. Harmful algae, 3141-53. https://doi.org/10.1016/j.hal.2013.08.005
Johnson, Jillian G, et al. "Caspase-like activity during aging and cell death in the toxic dinoflagellate Karenia brevis." Harmful algae vol. 31 (2014): 41-53. doi: https://doi.org/10.1016/j.hal.2013.08.005
Johnson JG, Janech MG, Van Dolah FM. Caspase-like activity during aging and cell death in the toxic dinoflagellate Karenia brevis. Harmful Algae. 2014 Jan;31:41-53. doi: 10.1016/j.hal.2013.08.005. Epub 2013 Oct 20. PMID: 28040110.
Copy Download .nbib Format: NLM
Clinical Trial of 24 Hours' Treatment with Glutathione Precursors in Acute Pancreatitis.

Clinical drug investigation

Sharer NM, Scott PD, Deardon DJ, Lee SH, Taylor PM, Braganza JM.
PMID: 27519198
Clin Drug Investig. 1995 Sep;10(3):147-57. doi: 10.2165/00044011-199510030-00003.

The depletion of thiols in pancreatic acinar cells, as a consequence of oxidative stress, seems to underlie acute pancreatitis. Therefore, immediate parenteral treatment with agents to refurbish tissue thiols should accelerate recovery. We tested this hypothesis in a randomised...

Cite
Sharer NM, Scott PD, Deardon DJ, et al. Clinical Trial of 24 Hours' Treatment with Glutathione Precursors in Acute Pancreatitis. Clin Drug Investig. 1995;10(3):147-57doi: 10.2165/00044011-199510030-00003.
Sharer, N. M., Scott, P. D., Deardon, D. J., Lee, S. H., Taylor, P. M., & Braganza, J. M. (1995). Clinical Trial of 24 Hours' Treatment with Glutathione Precursors in Acute Pancreatitis. Clinical drug investigation, 10(3), 147-57. https://doi.org/10.2165/00044011-199510030-00003
Sharer, N M, et al. "Clinical Trial of 24 Hours' Treatment with Glutathione Precursors in Acute Pancreatitis." Clinical drug investigation vol. 10,3 (1995): 147-57. doi: https://doi.org/10.2165/00044011-199510030-00003
Sharer NM, Scott PD, Deardon DJ, Lee SH, Taylor PM, Braganza JM. Clinical Trial of 24 Hours' Treatment with Glutathione Precursors in Acute Pancreatitis. Clin Drug Investig. 1995 Sep;10(3):147-57. doi: 10.2165/00044011-199510030-00003. PMID: 27519198.
Copy Download .nbib Format: NLM
Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach.

Nutrition & metabolism

Ahmed AA, Balogun KA, Bykova NV, Cheema SK.
PMID: 24438320
Nutr Metab (Lond). 2014 Jan 17;11(1):6. doi: 10.1186/1743-7075-11-6.

BACKGROUND: Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been shown to alleviate the symptoms of metabolic disorders, such as heart disease, diabetes, obesity and insulin resistance. Several putative mechanisms by which n-3 PUFA elicit beneficial health effects have been...

Cite
Ahmed AA, Balogun KA, Bykova NV, et al. Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach. Nutr Metab (Lond). 2014;11(1):6doi: 10.1186/1743-7075-11-6.
Ahmed, A. A., Balogun, K. A., Bykova, N. V., & Cheema, S. K. (2014). Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach. Nutrition & metabolism, 11(1), 6. https://doi.org/10.1186/1743-7075-11-6
Ahmed, Abeer A, et al. "Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach." Nutrition & metabolism vol. 11,1 (2014): 6. doi: https://doi.org/10.1186/1743-7075-11-6
Ahmed AA, Balogun KA, Bykova NV, Cheema SK. Novel regulatory roles of omega-3 fatty acids in metabolic pathways: a proteomics approach. Nutr Metab (Lond). 2014 Jan 17;11(1):6. doi: 10.1186/1743-7075-11-6. PMID: 24438320; PMCID: PMC3898484.
Copy Download .nbib Format: NLM
Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain.

Toxicology reports

Allan AM, Hafez AK, Labrecque MT, Solomon ER, Shaikh MN, Zheng X, Ali A.
PMID: 26855884
Toxicol Rep. 2015 Oct;2:1376-1390. doi: 10.1016/j.toxrep.2015.10.003.

Previously we have shown that prenatal moderate arsenic exposure (50 ppb) disrupts glucocorticoid receptor (GR) programming and that these changes continue into adolescence in males. However, it was not clear what the molecular mechanisms were promoting these GR programming...

Cite
Allan AM, Hafez AK, Labrecque MT, et al. Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain. Toxicol Rep. 2015;2:1376-1390doi: 10.1016/j.toxrep.2015.10.003.
Allan, A. M., Hafez, A. K., Labrecque, M. T., Solomon, E. R., Shaikh, M. N., Zheng, X., & Ali, A. (2015). Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain. Toxicology reports, 21376-1390. https://doi.org/10.1016/j.toxrep.2015.10.003
Allan, Andrea M, et al. "Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain." Toxicology reports vol. 2 (2015): 1376-1390. doi: https://doi.org/10.1016/j.toxrep.2015.10.003
Allan AM, Hafez AK, Labrecque MT, Solomon ER, Shaikh MN, Zheng X, Ali A. Sex-Dependent effects of developmental arsenic exposure on methylation capacity and methylation regulation of the glucocorticoid receptor system in the embryonic mouse brain. Toxicol Rep. 2015 Oct;2:1376-1390. doi: 10.1016/j.toxrep.2015.10.003. PMID: 26855884; PMCID: PMC4741109.
Copy Download .nbib Format: NLM
Potential Misdiagnosis of Hyperhomocysteinemia due to Cystathionine Beta-Synthase Deficiency During Pregnancy.

JIMD reports

Stabler SP, Freehauf C, Allen RH, Thomas J, Gallagher R.
PMID: 28275971
JIMD Rep. 2017;37:55-61. doi: 10.1007/8904_2017_15. Epub 2017 Mar 09.

Extreme hyperhomocysteinemia with low cystathionine and cysteine is virtually diagnostic of cystathionine beta-synthase (CBS) deficiency since remethylation defects and hypermethioninemia due to other inborn errors cause elevated serum cystathionine. However, a pregnant CBS deficient patient was found to have...

Cite
Stabler SP, Freehauf C, Allen RH, et al. Potential Misdiagnosis of Hyperhomocysteinemia due to Cystathionine Beta-Synthase Deficiency During Pregnancy. JIMD Rep. 2017;37:55-61doi: 10.1007/8904_2017_15.
Stabler, S. P., Freehauf, C., Allen, R. H., Thomas, J., & Gallagher, R. (2017). Potential Misdiagnosis of Hyperhomocysteinemia due to Cystathionine Beta-Synthase Deficiency During Pregnancy. JIMD reports, 3755-61. https://doi.org/10.1007/8904_2017_15
Stabler, Sally P, et al. "Potential Misdiagnosis of Hyperhomocysteinemia due to Cystathionine Beta-Synthase Deficiency During Pregnancy." JIMD reports vol. 37 (2017): 55-61. doi: https://doi.org/10.1007/8904_2017_15
Stabler SP, Freehauf C, Allen RH, Thomas J, Gallagher R. Potential Misdiagnosis of Hyperhomocysteinemia due to Cystathionine Beta-Synthase Deficiency During Pregnancy. JIMD Rep. 2017;37:55-61. doi: 10.1007/8904_2017_15. Epub 2017 Mar 09. PMID: 28275971; PMCID: PMC5740052.
Copy Download .nbib Format: NLM
The Effect of S-Adenosylmethionine on Self-Mutilation in a Patient with Lesch-Nyhan Disease.

JIMD reports

Lauber M, Plecko B, Pfiffner M, Nuoffer JM, Häberle J.
PMID: 27295197
JIMD Rep. 2017;32:51-57. doi: 10.1007/8904_2016_571. Epub 2016 Jun 14.

BACKGROUND: Lesch-Nyhan disease (LND) is an X-chromosomal disorder of purine metabolism characterized by hyperuricemia, dystonia, and self-mutilation, leading to an extremely high burden of disease in affected patients and families. Although allopurinol therapy can control hyperuricemia, it has no...

Cite
Lauber M, Plecko B, Pfiffner M, et al. The Effect of S-Adenosylmethionine on Self-Mutilation in a Patient with Lesch-Nyhan Disease. JIMD Rep. 2016;32:51-57doi: 10.1007/8904_2016_571.
Lauber, M., Plecko, B., Pfiffner, M., Nuoffer, J. M., & Häberle, J. (2017). The Effect of S-Adenosylmethionine on Self-Mutilation in a Patient with Lesch-Nyhan Disease. JIMD reports, 3251-57. https://doi.org/10.1007/8904_2016_571
Lauber, Matthias, et al. "The Effect of S-Adenosylmethionine on Self-Mutilation in a Patient with Lesch-Nyhan Disease." JIMD reports vol. 32 (2017): 51-57. doi: https://doi.org/10.1007/8904_2016_571
Lauber M, Plecko B, Pfiffner M, Nuoffer JM, Häberle J. The Effect of S-Adenosylmethionine on Self-Mutilation in a Patient with Lesch-Nyhan Disease. JIMD Rep. 2017;32:51-57. doi: 10.1007/8904_2016_571. Epub 2016 Jun 14. PMID: 27295197; PMCID: PMC5362561.
Copy Download .nbib Format: NLM
Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome.

Korean circulation journal

Yeter D, Deth R, Kuo HC.
PMID: 24174958
Korean Circ J. 2013 Sep;43(9):581-91. doi: 10.4070/kcj.2013.43.9.581.

Previously, we reviewed biological evidence that mercury could induce autoimmunity and coronary arterial wall relaxation as observed in Kawasaki syndrome (KS) through its effects on calcium signaling, and that inositol 1,4,5-triphosphate 3-kinase C (ITPKC) susceptibility in KS would predispose...

Cite
Yeter D, Deth R, Kuo HC. Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome. Korean Circ J. 2013;43(9):581-91doi: 10.4070/kcj.2013.43.9.581.
Yeter, D., Deth, R., & Kuo, H. C. (2013). Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome. Korean circulation journal, 43(9), 581-91. https://doi.org/10.4070/kcj.2013.43.9.581
Yeter, Deniz, et al. "Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome." Korean circulation journal vol. 43,9 (2013): 581-91. doi: https://doi.org/10.4070/kcj.2013.43.9.581
Yeter D, Deth R, Kuo HC. Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome. Korean Circ J. 2013 Sep;43(9):581-91. doi: 10.4070/kcj.2013.43.9.581. PMID: 24174958; PMCID: PMC3808853.
Copy Download .nbib Format: NLM
Travels with carbon-centered radicals. 5'-deoxyadenosine and 5'-deoxyadenosine-5'-yl in radical enzymology.

Accounts of chemical research

Frey PA.
PMID: 24308628
Acc Chem Res. 2014 Feb 18;47(2):540-9. doi: 10.1021/ar400194k. Epub 2013 Dec 05.

As a graduate student under Professor R. H. Abeles, I began my journey with 5'-deoxyadenosine, studying the coenzyme B12 (adenosylcobalamin)-dependent dioldehydrase (DDH). I proved that suicide inactivation of dioldehydrase by glycolaldehyde proceeded with irreversible cleavage of adenosylcobalamin to 5'-deoxyadenosine....

Cite
Frey PA. Travels with carbon-centered radicals. 5'-deoxyadenosine and 5'-deoxyadenosine-5'-yl in radical enzymology. Acc Chem Res. 2013;47(2):540-9doi: 10.1021/ar400194k.
Frey, P. A. (2014). Travels with carbon-centered radicals. 5'-deoxyadenosine and 5'-deoxyadenosine-5'-yl in radical enzymology. Accounts of chemical research, 47(2), 540-9. https://doi.org/10.1021/ar400194k
Frey, Perry A. "Travels with carbon-centered radicals. 5'-deoxyadenosine and 5'-deoxyadenosine-5'-yl in radical enzymology." Accounts of chemical research vol. 47,2 (2014): 540-9. doi: https://doi.org/10.1021/ar400194k
Frey PA. Travels with carbon-centered radicals. 5'-deoxyadenosine and 5'-deoxyadenosine-5'-yl in radical enzymology. Acc Chem Res. 2014 Feb 18;47(2):540-9. doi: 10.1021/ar400194k. Epub 2013 Dec 05. PMID: 24308628.
Copy Download .nbib Format: NLM
Oxidative stress modulation in hepatitis C virus infected cells.

World journal of hepatology

Lozano-Sepulveda SA, Bryan-Marrugo OL, Cordova-Fletes C, Gutierrez-Ruiz MC, Rivas-Estilla AM.
PMID: 26692473
World J Hepatol. 2015 Dec 18;7(29):2880-9. doi: 10.4254/wjh.v7.i29.2880.

Hepatitis C virus (HCV) replication is associated with the endoplasmic reticulum, where the virus can induce cellular stress. Oxidative cell damage plays an important role in HCV physiopathology. Oxidative stress is triggered when the concentration of oxygen species in...

Cite
Lozano-Sepulveda SA, Bryan-Marrugo OL, Cordova-Fletes C, et al. Oxidative stress modulation in hepatitis C virus infected cells. World J Hepatol. 2015;7(29):2880-9doi: 10.4254/wjh.v7.i29.2880.
Lozano-Sepulveda, S. A., Bryan-Marrugo, O. L., Cordova-Fletes, C., Gutierrez-Ruiz, M. C., & Rivas-Estilla, A. M. (2015). Oxidative stress modulation in hepatitis C virus infected cells. World journal of hepatology, 7(29), 2880-9. https://doi.org/10.4254/wjh.v7.i29.2880
Lozano-Sepulveda, Sonia A, et al. "Oxidative stress modulation in hepatitis C virus infected cells." World journal of hepatology vol. 7,29 (2015): 2880-9. doi: https://doi.org/10.4254/wjh.v7.i29.2880
Lozano-Sepulveda SA, Bryan-Marrugo OL, Cordova-Fletes C, Gutierrez-Ruiz MC, Rivas-Estilla AM. Oxidative stress modulation in hepatitis C virus infected cells. World J Hepatol. 2015 Dec 18;7(29):2880-9. doi: 10.4254/wjh.v7.i29.2880. PMID: 26692473; PMCID: PMC4678374.
Copy Download .nbib Format: NLM
Showing 1 to 12 of 448 entries