Refine your query (more in Advanced-Search):
 Focus on the recent 5 years   Focus on the current year   Focus on the last 30 days   More choices ...
 Focus on articles with free fulltexts   More choices ...
 Do simple 'keyword' search (no query expansion)

[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 10 of about 726
1. Barbosa-Silva A, Satagopam VP, Schneider R, Ortega JM: Clustering of cognate proteins among distinct proteomes derived from multiple links to a single seed sequence. BMC Bioinformatics; 2008;9:141
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clustering of cognate proteins among distinct proteomes derived from multiple links to a single seed sequence.
  • BACKGROUND: Modern proteomes evolved by modification of pre-existing ones.
  • It is extremely important to comparative biology that related proteins be identified as members of the same cognate group, since a characterized putative homolog could be used to find clues about the function of uncharacterized proteins from the same group.
  • Typically, databases of related proteins focus on those from completely-sequenced genomes.
  • Unfortunately, relatively few organisms have had their genomes fully sequenced; accordingly, many proteins are ignored by the currently available databases of cognate proteins, despite the high amount of important genes that are functionally described only for these incomplete proteomes.
  • RESULTS: We have developed a method to cluster cognate proteins from multiple organisms beginning with only one sequence, through connectivity saturation with that Seed sequence.
  • We show that the generated clusters are in agreement with some other approaches based on full genome comparison.
  • CONCLUSION: The method produced results that are as reliable as those produced by conventional clustering approaches.
  • Generating clusters based only on individual proteins of interest is less time consuming than generating clusters for whole proteomes.
  • [MeSH-major] Algorithms. Cluster Analysis. Multigene Family. Pattern Recognition, Automated / methods. Proteome / chemistry. Sequence Alignment / methods. Sequence Analysis, Protein / methods
  • [MeSH-minor] Amino Acid Sequence. Molecular Sequence Data. Sequence Homology, Amino Acid

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genome Res. 2000 Nov;10(11):1679-89 [11076853.001]
  • [Cites] Genome Inform. 2005;16(2):32-44 [16901087.001]
  • [Cites] J Mol Biol. 2001 Dec 14;314(5):1041-52 [11743721.001]
  • [Cites] Genome Res. 2002 Mar;12(3):493-502 [11875039.001]
  • [Cites] Nucleic Acids Res. 2002 Oct 15;30(20):4339-50 [12384580.001]
  • [Cites] Trends Genet. 2002 Dec;18(12):619-20 [12446146.001]
  • [Cites] Genome Res. 2003 Sep;13(9):2178-89 [12952885.001]
  • [Cites] BMC Bioinformatics. 2003 Sep 11;4:41 [12969510.001]
  • [Cites] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D115-9 [14681372.001]
  • [Cites] In Silico Biol. 2004;4(1):5-6 [15089749.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D476-80 [15608241.001]
  • [Cites] Bioinformatics. 2005 Oct 1;21(19):3787-93 [15817693.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D363-8 [16381887.001]
  • [Cites] Bioinformatics. 2006 Jul 15;22(14):e9-15 [16873526.001]
  • [Cites] Nucleic Acids Res. 2001 Jan 1;29(1):22-8 [11125040.001]
  • (PMID = 18321373.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proteome
  • [Other-IDs] NLM/ PMC2277401
  •  go-up   go-down


2. Tiffin N, Adie E, Turner F, Brunner HG, van Driel MA, Oti M, Lopez-Bigas N, Ouzounis C, Perez-Iratxeta C, Andrade-Navarro MA, Adeyemo A, Patti ME, Semple CA, Hide W: Computational disease gene identification: a concert of methods prioritizes type 2 diabetes and obesity candidate genes. Nucleic Acids Res; 2006;34(10):3067-81
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Computational disease gene identification: a concert of methods prioritizes type 2 diabetes and obesity candidate genes.
  • Genome-wide experimental methods to identify disease genes, such as linkage analysis and association studies, generate increasingly large candidate gene sets for which comprehensive empirical analysis is impractical.
  • Computational methods employ data from a variety of sources to identify the most likely candidate disease genes from these gene sets.
  • Here, we review seven independent computational disease gene prioritization methods, and then apply them in concert to the analysis of 9556 positional candidate genes for type 2 diabetes (T2D) and the related trait obesity.
  • We generate and analyse a list of nine primary candidate genes for T2D genes and five for obesity.
  • Two genes, LPL and BCKDHA, are common to these two sets.
  • We also present a set of secondary candidates for T2D (94 genes) and for obesity (116 genes) with 58 genes in common to both diseases.

  • Genetic Alliance. consumer health - Diabetes.
  • Genetic Alliance. consumer health - Diabetes, Type 2.
  • Genetic Alliance. consumer health - Obesity.
  • MedlinePlus Health Information. consumer health - Diabetes Type 2.
  • MedlinePlus Health Information. consumer health - Obesity.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] Nature. 1997 Oct 9;389(6651):610-4 [9335502.001]
  • [Cites] Am J Hum Genet. 1998 Oct;63(4):1130-8 [9758619.001]
  • [Cites] Am J Hum Genet. 1999 Apr;64(4):1127-40 [10090898.001]
  • [Cites] Diabetes. 1999 May;48(5):1175-82 [10331426.001]
  • [Cites] Eur J Endocrinol. 2004 Nov;151 Suppl 3:U131-9 [15554898.001]
  • [Cites] J Hum Genet. 2004;49(11):629-34 [15490285.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D39-45 [15608222.001]
  • [Cites] Science. 2005 Jan 21;307(5708):370-3 [15662000.001]
  • [Cites] Science. 2005 Jan 21;307(5708):373-5 [15662001.001]
  • [Cites] Science. 2005 Jan 21;307(5708):384-7 [15662004.001]
  • [Cites] Nat Med. 2005 Feb;11(2):183-90 [15685173.001]
  • [Cites] Diabetes. 2005 Mar;54(3):664-71 [15734841.001]
  • [Cites] Nat Rev Genet. 2005 Mar;6(3):221-34 [15703762.001]
  • [Cites] J Biol Chem. 2005 Mar 11;280(10):9023-9 [15637076.001]
  • [Cites] Nucleic Acids Res. 2005;33(5):1423-34 [15755745.001]
  • [Cites] Nucleic Acids Res. 2005;33(5):1544-52 [15767279.001]
  • [Cites] BMC Bioinformatics. 2005;6:55 [15766383.001]
  • [Cites] Lancet. 2005 Apr 9-15;365(9467):1333-46 [15823385.001]
  • [Cites] J Clin Invest. 2005 May;115(5):1323-32 [15841215.001]
  • [Cites] J Clin Invest. 2005 May;115(5):1111-9 [15864338.001]
  • [Cites] Diabetologia. 2005 Jun;48(6):1038-50 [15864529.001]
  • [Cites] Diabetologia. 2005 Jun;48(6):1207-15 [15864534.001]
  • [Cites] Diabetes. 2003 Feb;52(2):550-7 [12540634.001]
  • [Cites] Nat Genet. 2003 Feb;33(2):177-82 [12524541.001]
  • [Cites] Am J Hum Genet. 2003 Mar;72(3):636-49 [12592605.001]
  • [Cites] Nat Genet. 2003 Mar;33 Suppl:305-10 [12610540.001]
  • [Cites] Kidney Int. 2003 May;63(5):1831-5 [12675860.001]
  • [Cites] Nat Rev Genet. 2003 May;4(5):337-45 [12728276.001]
  • [Cites] Curr Opin Clin Nutr Metab Care. 2003 Jul;6(4):369-75 [12806208.001]
  • [Cites] Nat Genet. 2003 Jul;34(3):267-73 [12808457.001]
  • [Cites] Nucleic Acids Res. 2005 Jul 1;33(Web Server issue):W758-61 [15980578.001]
  • [Cites] BMC Genet. 2005;6:45 [16115313.001]
  • [Cites] Bioinformatics. 2006 Feb 1;22(3):269-77 [16287936.001]
  • [Cites] Diabetes. 2006 Mar;55(3):839-42 [16505252.001]
  • [Cites] Diabetes. 2006 Mar;55(3):849-55 [16505254.001]
  • [Cites] Bioinformatics. 2006 Mar 15;22(6):773-4 [16423925.001]
  • [Cites] Cytokine. 2006 Feb 7;33(3):129-37 [16503147.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7522-7 [11390966.001]
  • [Cites] Am J Hum Genet. 2001 Sep;69(3):553-69 [11484155.001]
  • [Cites] J Med Genet. 2001 Sep;38(9):569-78 [11546824.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2001 Sep;15(3):293-308 [11554772.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2001 Sep;21(9):1488-93 [11557677.001]
  • [Cites] Nature. 2001 Dec 13;414(6865):807-12 [11742413.001]
  • [Cites] Am J Hum Genet. 2002 Feb;70(2):349-57 [11742441.001]
  • [Cites] Am J Hum Genet. 2002 Feb;70(2):509-16 [11791216.001]
  • [Cites] Atherosclerosis. 2002 Mar;161(1):133-41 [11882325.001]
  • [Cites] Diabetes. 2002 Apr;51(4):1247-55 [11916952.001]
  • [Cites] Nat Rev Genet. 2002 May;3(5):391-7 [11988764.001]
  • [Cites] Diabetes. 2002 Jun;51(6):1913-20 [12031981.001]
  • [Cites] Nat Genet. 2002 Jul;31(3):316-9 [12006977.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2002 Aug;283(2):E217-25 [12110525.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10587-92 [12149437.001]
  • [Cites] Diabetes. 2002 Oct;51(10):2944-50 [12351431.001]
  • [Cites] Science. 2002 Dec 20;298(5602):2345-9 [12493905.001]
  • [Cites] JAMA. 2003 Jan 1;289(1):76-9 [12503980.001]
  • [Cites] Eur J Hum Genet. 2003 Jan;11(1):57-63 [12529706.001]
  • [Cites] Diabetes. 2003 Feb;52(2):291-9 [12540599.001]
  • [Cites] Bioinformatics. 2003 Jul 1;19(10):1275-83 [12835272.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8466-71 [12832613.001]
  • [Cites] Hum Mol Genet. 2003 Aug 1;12(15):1865-73 [12874106.001]
  • [Cites] Endocrinology. 2003 Sep;144(9):3757-64 [12933645.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2003;4:257-91 [14527304.001]
  • [Cites] Proteins. 2003;53 Suppl 6:395-409 [14579328.001]
  • [Cites] Genome Biol. 2003;4(11):R75 [14611661.001]
  • [Cites] Diabetes. 2003 Dec;52(12):3001-4 [14633863.001]
  • [Cites] Eur J Clin Invest. 2003 Dec;33(12):1070-4 [14636289.001]
  • [Cites] Metabolism. 2003 Dec;52(12):1547-50 [14669153.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52298-306 [14530283.001]
  • [Cites] Diabetes. 2004 Jan;53(1):228-34 [14693720.001]
  • [Cites] Diabetes. 2004 Feb;53(2):492-9 [14747303.001]
  • [Cites] N Engl J Med. 2004 Feb 12;350(7):664-71 [14960743.001]
  • [Cites] Diabetes. 2004 Mar;53(3):821-9 [14988269.001]
  • [Cites] Diabetes. 2004 Mar;53(3):830-7 [14988270.001]
  • [Cites] Diabetes. 2004 Mar;53(3):838-41 [14988271.001]
  • [Cites] Diabetes. 2004 Jun;53(6):1609-13 [15161769.001]
  • [Cites] Curr Opin Genet Dev. 2004 Jun;14(3):229-32 [15172663.001]
  • [Cites] Nucleic Acids Res. 2004;32(10):3108-14 [15181176.001]
  • [Cites] Diabetes. 1999 Nov;48(11):2246-51 [10535461.001]
  • [Cites] FASEB J. 1999 Nov;13(14):2051-60 [10544188.001]
  • [Cites] Nature. 2000 Jun 15;405(6788):847-56 [10866211.001]
  • [Cites] J Clin Invest. 2000 Jul;106(2):171-6 [10903330.001]
  • [Cites] Am J Hum Genet. 2000 Nov;67(5):1174-85 [11032783.001]
  • [Cites] Am J Hum Genet. 2000 Dec;67(6):1470-80 [11067779.001]
  • [Cites] Diabetes. 2000 Dec;49(12):2212-6 [11118028.001]
  • [Cites] Am J Med. 2000 Feb;108(2):143-52 [11126308.001]
  • [Cites] Am J Hum Genet. 2000 Jun;66(6):1871-81 [10793009.001]
  • [Cites] Diabetes. 2001 Mar;50(3):681-5 [11246891.001]
  • [Cites] Diabetologia. 2001 Apr;44(4):501-6 [11357482.001]
  • [Cites] Diabetes. 2004 Sep;53(9):2487-91 [15331565.001]
  • [Cites] Med Sci Sports Exerc. 2004 Sep;36(9):1451-69 [15354024.001]
  • [Cites] J Atheroscler Thromb. 2004;11(4):200-8 [15356379.001]
  • [Cites] Diabetes. 2004 Oct;53(10):2676-83 [15448100.001]
  • [Cites] Mol Cell Biol. 1991 Feb;11(2):920-7 [1990292.001]
  • [Cites] Comp Biochem Physiol A Comp Physiol. 1991;100(2):473-6 [1685963.001]
  • [Cites] Biochim Biophys Acta. 1995 Jan 20;1254(2):140-6 [7827118.001]
  • [Cites] J Clin Invest. 1995 Mar;95(3):1383-8 [7533791.001]
  • [Cites] Nat Genet. 1996 Jun;13(2):161-6 [8640221.001]
  • [Cites] Circulation. 1996 Apr 1;93(7):1339-45 [8641022.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):90-4 [8782826.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5336-48 [8895578.001]
  • [Cites] J Appl Physiol (1985). 1997 Jul;83(1):166-71 [9216960.001]
  • (PMID = 16757574.001).
  • [ISSN] 1362-4962
  • [Journal-full-title] Nucleic acids research
  • [ISO-abbreviation] Nucleic Acids Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK060837; United States / NIDDK NIH HHS / DK / R01 DK062948; United States / NIDDK NIH HHS / DK / DK060837; United States / NIDDK NIH HHS / DK / DK062948
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1475747
  •  go-up   go-down


3. Orlian AI, Schaefer M, Golub J: Multiple bilateral sialoliths of the submandibular ducts. N Y State Dent J; 1998 Aug-Sep;64(7):42-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Multiple bilateral sialoliths of the submandibular ducts.
  • A patient with a history of 20 years of intermittent pain and swelling of the floor of the mouth was diagnosed with bilateral multiple sialoliths of the submandibular ducts.
  • Subsequent to the excision of all the sialoliths, the patient was asymptomatic.
  • She will be observed periodically.
  • [MeSH-major] Salivary Duct Calculi / diagnosis. Submandibular Gland Diseases / diagnosis
  • [MeSH-minor] Female. Humans. Middle Aged. Mouth Floor / pathology. Pain / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 9785838.001).
  • [ISSN] 0028-7571
  • [Journal-full-title] The New York state dental journal
  • [ISO-abbreviation] N Y State Dent J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
  •  go-up   go-down


Advertisement
4. Fiß T, Schaefer M, van den Berg N, Hoffmann W: [Time required and associated costs for implementation of home medication review with associated pharmaceutical and medical evaluation in the ambulatory health care sector]. Gesundheitswesen; 2012 May;74(5):322-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Time required and associated costs for implementation of home medication review with associated pharmaceutical and medical evaluation in the ambulatory health care sector].
  • [Transliterated title] Zeitbedarf und Kosten für die Umsetzung eines Medikamentenreviews und assoziierter pharmazeutischer und medizinischer Evaluation im ambulanten Versorgungssektor.
  • INTRODUCTION: We aimed to estimate the time which is needed to conduct a home medication review (HMR) in the context of the AGnES implementation studies (AGnES=GP-supporting, community-based, e-health-assisted, systemic intervention).
  • In a subsequent step associated costs were calculated.
  • METHODS: IT-supported HMR were conducted by specially qualified AGnES-practice assistants to detect selected drug-related problems (DRP).
  • The patient received pharmaceutical care by their local pharmacist and medical evaluation by their GP, respectively.
  • RESULTS: The data from 471 patients (w: 339; m: 132) were evaluated (median age: w=81; m=78).
  • The interview to detect selected DRP was 6 min (median) long.
  • The subsequent drug record took 14.4 min.
  • There was an additional effort for documentation of 5 min.
  • The local pharmacist needed a median time of 15 min for pharmaceutical evaluation, whereas the GP needed 8 min.
  • The estimated costs accounted for: AGnES-practice assistant: 9.12 €; pharmacist: 11.05 €; GP: 6.30 €.
  • The overall estimated costs were 26.47 €.
  • CONCLUSION: For the first time we present objective costs which were associated with the implementation of HMR.
  • Due to high DRP-induced costs the HMR should be mandatory for groups with a high risk like for the occurrence of DRP.
  • [MeSH-major] Health Care Costs / statistics & numerical data. Home Care Services / economics. Workload / economics
  • [MeSH-minor] Ambulatory Care Facilities. Germany. Telemedicine

  • MedlinePlus Health Information. consumer health - Home Care Services.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © Georg Thieme Verlag KG Stuttgart · New York.
  • (PMID = 21563050.001).
  • [ISSN] 1439-4421
  • [Journal-full-title] Gesundheitswesen (Bundesverband der Ärzte des Öffentlichen Gesundheitsdienstes (Germany))
  • [ISO-abbreviation] Gesundheitswesen
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


5. Hofmann T, Schaefer M, Schultz G, Gudermann T: Cloning, expression and subcellular localization of two novel splice variants of mouse transient receptor potential channel 2. Biochem J; 2000 Oct 1;351(Pt 1):115-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cloning, expression and subcellular localization of two novel splice variants of mouse transient receptor potential channel 2.
  • Transient receptor potential channels (TRPCs) are known as candidate molecular correlates of receptor-activated or store-operated calcium entry.
  • While functional roles for most TRPCs have been suggested, the physiological relevance of TRPC2 remains obscure.
  • Whereas human and bovine TRPC2 are candidate pseudogenes, full-length rodent TRPC2 transcripts have been reported.
  • There is, however, considerable controversy concerning mRNA splicing, tissue distribution and the function of these proteins.
  • We report the molecular cloning of two novel murine TRPC2 splice variants, mTRPC2alpha and mTRPC2beta. mTRPC2alpha RNA is expressed at low levels in many tissues and cell systems, while mTRPC2beta is exclusively and abundantly expressed in the vomeronasal organ (VNO).
  • When expressed in human embryonic kidney (HEK)-293 cells, mTRPC2 did not enhance receptor- or store-activated calcium entry.
  • In order to investigate the basis of such a functional defect, mTRPC2-green fluorescent protein fusion proteins were examined by confocal microscopy.
  • Fusion proteins were retained in endomembranes when expressed in HEK-293 or other cells of epithelial or neuronal origin.
  • Co-expression of TRPC2 with other TRPCs did not restore plasma-membrane trafficking.
  • We conclude that TRPC2 may form functional channels in the cellular context of the VNO, but is unlikely to have a physiological function in other tissues.
  • [MeSH-major] Alternative Splicing / genetics. Calcium Channels. Ion Channels / analysis. Ion Channels / genetics. Membrane Proteins
  • [MeSH-minor] Amino Acid Sequence. Animals. Brain / metabolism. Calcium / metabolism. Cell Line. Cell Membrane / metabolism. Cloning, Molecular. Gene Expression Profiling. Humans. Male. Manganese / metabolism. Mice. Molecular Sequence Data. Myocardium / metabolism. Organ Specificity. Protein Transport. RNA, Messenger / analysis. RNA, Messenger / genetics. Recombinant Fusion Proteins / metabolism. Sequence Alignment. TRPC Cation Channels. TRPM Cation Channels. Testis / metabolism. Transfection


6. Hofmann T, Schaefer M, Schultz G, Gudermann T: Transient receptor potential channels as molecular substrates of receptor-mediated cation entry. J Mol Med (Berl); 2000;78(1):14-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transient receptor potential channels as molecular substrates of receptor-mediated cation entry.
  • Calcium is a versatile multitarget intracellular second messenger in eukaryotic cells.
  • In addition to calcium release from intracellular stores and influx via voltage- or ligand-operated channels, agonist-induced calcium entry constitutes one of the main pathways by which cytosolic calcium is elevated.
  • Receptor-stimulated currents are initiated in response to agonist binding to G-protein-coupled receptors and to receptor tyrosine kinases.
  • Within the past few years our knowledge about the molecular identity of receptor-stimulated channels has expanded substantially.
  • Drosophila melanogaster visual transduction channels associated with the transient receptor potential (trp) and the trp-like (trpl) mutant visual phenotypes were the first members of this category of channels to be identified at the molecular level.
  • Since then an entire mammalian gene family of TRP homologues has been discovered by homology cloning.
  • Only now are we beginning to fully understand the functional roles of TRP channels in mammalian cells.
  • We review recent findings in TRP channel research and discuss the role of these proteins for receptor-activated cation entry.
  • [MeSH-major] Calcium Channels / metabolism. Calmodulin-Binding Proteins / metabolism. Drosophila Proteins. Insect Proteins / metabolism. Ion Pumps / metabolism. Membrane Proteins / metabolism
  • [MeSH-minor] Animals. Cations / metabolism. Humans. Phylogeny. Sequence Homology, Amino Acid. Transient Receptor Potential Channels

  • FlyBase. FlyBase .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10759026.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Calcium Channels; 0 / Calmodulin-Binding Proteins; 0 / Cations; 0 / Drosophila Proteins; 0 / Insect Proteins; 0 / Ion Pumps; 0 / Membrane Proteins; 0 / Transient Receptor Potential Channels; 0 / trp protein, Drosophila; 0 / trpl protein, Drosophila
  • [Number-of-references] 113
  •  go-up   go-down


7. Shih J, Hodge R, Andrade-Navarro MA: Comparison of inter- and intraspecies variation in humans and fruit flies. Genom Data; 2015 Mar;3:49-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of inter- and intraspecies variation in humans and fruit flies.
  • Variation is essential to species survival and adaptation during evolution.
  • This variation is conferred by the imperfection of biochemical processes, such as mutations and alterations in DNA sequences, and can also be seen within genomes through processes such as the generation of antibodies.
  • Recent sequencing projects have produced multiple versions of the genomes of humans and fruit flies (Drosophila melanogaster).
  • These give us a chance to study how individual gene sequences vary within and between species.
  • Here we arranged human and fly genes in orthologous pairs and compared such within-species variability with their degree of conservation between flies and humans.
  • We observed that a significant number of proteins associated with mRNA translation are highly conserved between species and yet are highly variable within each species.
  • The fact that we observe this in two species whose lineages separated more than 700 million years ago suggests that this is the result of a very ancient process.
  • We hypothesize that this effect might be attributed to a positive selection for variability of virus-interacting proteins that confers a general resistance to viral hijacking of the mRNA translation machinery within populations.
  • Our analysis points to this and to other processes resulting in positive selection for gene variation.

  • FlyBase. FlyBase .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 26484147.001).
  • [ISSN] 2213-5960
  • [Journal-full-title] Genomics data
  • [ISO-abbreviation] Genom Data
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4536057
  • [Keywords] NOTNLM ; Drosophila / Evolution / Human genome / Population / Variation
  •  go-up   go-down


8. Schaefer M, Hofmann T, Schultz G, Gudermann T: A new prostaglandin E receptor mediates calcium influx and acrosome reaction in human spermatozoa. Proc Natl Acad Sci U S A; 1998 Mar 17;95(6):3008-13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new prostaglandin E receptor mediates calcium influx and acrosome reaction in human spermatozoa.
  • Zona pellucida protein 3, a protein of the egg's extracellular matrix, and progesterone secreted by granulosa cells surrounding the oocyte are regarded as physiological stimuli of sperm acrosome reaction.
  • Signal transduction steps initiated by both stimuli result in influx of Ca2+ from the extracellular space.
  • Herein, we propose a role for prostaglandin (PG) E as a physiological inducer of Ca2+ influx and acrosome reaction in human spermatozoa.
  • PGE1 specifically binds to human sperm membranes (Kd = 20.4 nM; Bmax = 88 fmol/mg protein) and induces a pertussis toxin-insensitive, transient increase in intracellular Ca2+ concentrations, which can be blocked by microM concentrations of La3+, Gd3+, and Zn2+.
  • The kinetic profile was similar to that observed after progesterone challenge.
  • Sequential application of both agonists did not lead to cross-desensitization.
  • E prostaglandins were found to be the only prostanoids with agonistic properties (EC50 values for PGE1 and PGE2: <10 nM and 300 nM, respectively).
  • Pharmacological characteristics were not compatible with those of cloned prostanoid receptors indicating the expression of a distinct membrane receptor.
  • Activation of the sperm E prostanoid receptor stimulates incorporation of [alpha-32P]GTP azidoanilide into immunoprecipitated Galphaq/11 subunits.
  • Thus, in human sperm, PG induces Ca2+ influx and acrosome reaction via a Gq/11-coupled E prostanoid receptor.
  • The block of PGE1-induced Ca2+ transients and acrosome reaction by physiological Zn2+ concentrations highlights a role of Zn2+ as an endogenous Ca2+ channel blocker present in seminal plasma protecting sperm from premature PGE1-evoked increases in intracellular Ca2+ concentrations.
  • [MeSH-major] Acrosome / physiology. Calcium / metabolism. Prostaglandins E / metabolism. Receptors, Prostaglandin E / metabolism
  • [MeSH-minor] Alprostadil / metabolism. Calcium Channel Blockers / pharmacology. Cyclic AMP / metabolism. Dinoprostone / metabolism. GTP-Binding Proteins / metabolism. Humans. Male. Signal Transduction. Spermatozoa. Zinc / pharmacology

  • Hazardous Substances Data Bank. ZINC, ELEMENTAL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neuron. 1993 Feb;10(2):233-42 [8382499.001]
  • [Cites] Int J Androl. 1992 Jun;15(3):229-37 [1399086.001]
  • [Cites] Biochem J. 1993 Aug 15;294 ( Pt 1):279-83 [7689832.001]
  • [Cites] J Biol Chem. 1993 Dec 15;268(35):26767-72 [8253813.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):504-8 [8290554.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):529-33 [8290559.001]
  • [Cites] J Biol Chem. 1994 Jan 28;269(4):2632-6 [8300593.001]
  • [Cites] Biochem J. 1994 Mar 1;298 ( Pt 2):263-7 [8135729.001]
  • [Cites] Nature. 1994 Apr 28;368(6474):859-63 [7512693.001]
  • [Cites] J Biol Chem. 1994 May 6;269(18):13254-8 [8175755.001]
  • [Cites] J Biol Chem. 1994 May 13;269(19):13733-5 [8188646.001]
  • [Cites] J Biol Chem. 1994 Jul 22;269(29):19000-4 [8034657.001]
  • [Cites] Methods Enzymol. 1994;237:283-94 [7935004.001]
  • [Cites] Pharmacol Rev. 1994 Jun;46(2):205-29 [7938166.001]
  • [Cites] Science. 1994 Dec 2;266(5190):1578-81 [7985030.001]
  • [Cites] Hum Reprod. 1994 Oct;9(10):1897-902 [7844223.001]
  • [Cites] Biol Reprod. 1994 Dec;51(6):1238-47 [7888501.001]
  • [Cites] Prep Biochem. 1995 Feb-May;25(1-2):69-80 [7603973.001]
  • [Cites] J Cell Biol. 1995 Aug;130(4):857-69 [7642703.001]
  • [Cites] Curr Top Dev Biol. 1995;30:1-19 [7555043.001]
  • [Cites] J Biol Chem. 1995 Nov 3;270(44):26025-8 [7592795.001]
  • [Cites] J Lipid Mediat Cell Signal. 1995 Oct;12(2-3):343-59 [8777578.001]
  • [Cites] J Biol Chem. 1996 Jul 12;271(28):16764-72 [8663226.001]
  • [Cites] Endocrinology. 1996 Sep;137(9):3999-4009 [8756577.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):13004-9 [8917534.001]
  • [Cites] J Biol Chem. 1997 Apr 11;272(15):10188-95 [9092566.001]
  • [Cites] J Exp Zool. 1984 Aug;231(2):283-8 [6434693.001]
  • [Cites] J Reprod Fertil. 1986 Jul;77(2):451-62 [3016256.001]
  • [Cites] J Androl. 1987 Mar-Apr;8(2):74-82 [3108222.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Apr 28;160(2):828-33 [2719699.001]
  • [Cites] J Biol Chem. 1989 May 15;264(14):8171-8 [2498308.001]
  • [Cites] Gamete Res. 1989 Jun;23(2):159-70 [2731901.001]
  • [Cites] J Biol Chem. 1990 Jan 25;265(3):1376-80 [2104840.001]
  • [Cites] Dev Biol. 1991 Aug;146(2):438-50 [1907582.001]
  • [Cites] Nature. 1992 Jan 30;355(6359):453-5 [1370859.001]
  • [Cites] Mol Reprod Dev. 1992 Jan;31(1):78-86 [1562331.001]
  • [Cites] J Biol Chem. 1992 Jul 15;267(20):14061-7 [1629205.001]
  • [Cites] Dev Biol. 1993 Jul;158(1):9-34 [8392473.001]
  • (PMID = 9501206.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Prostaglandins E; 0 / Receptors, Prostaglandin E; E0399OZS9N / Cyclic AMP; EC 3.6.1.- / GTP-Binding Proteins; F5TD010360 / Alprostadil; J41CSQ7QDS / Zinc; K7Q1JQR04M / Dinoprostone; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC19685
  •  go-up   go-down


9. Perez-Iratxeta C, Andrade-Navarro MA: K2D2: estimation of protein secondary structure from circular dichroism spectra. BMC Struct Biol; 2008;8:25
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] K2D2: estimation of protein secondary structure from circular dichroism spectra.
  • BACKGROUND: Circular dichroism spectroscopy is a widely used technique to analyze the secondary structure of proteins in solution.
  • Predictive methods use the circular dichroism spectra from proteins of known tertiary structure to assess the secondary structure contents of a protein with unknown structure given its circular dichroism spectrum.
  • RESULTS: We developed K2D2, a method with an associated web server to estimate protein secondary structure from circular dichroism spectra.
  • The method uses a self-organized map of spectra from proteins with known structure to deduce a map of protein secondary structure that is used to do the predictions.
  • CONCLUSION: The K2D2 server is publicly accessible at http://www.ogic.ca/projects/k2d2/.
  • It accepts as input a circular dichroism spectrum and outputs the estimated secondary structure content (alpha-helix and beta-strand) of the corresponding protein, as well as an estimated measure of error.
  • [MeSH-major] Circular Dichroism / statistics & numerical data. Protein Structure, Secondary
  • [MeSH-minor] Algorithms. Computational Biology. Internet. Software

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anal Biochem. 2000 Dec 15;287(2):252-60 [11112271.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D301-3 [17142228.001]
  • [Cites] Anal Biochem. 2001 Dec 15;299(2):271-4 [11730356.001]
  • [Cites] Protein Sci. 2003 Apr;12(4):875-84 [12649445.001]
  • [Cites] Biochem Biophys Res Commun. 1971 Sep 17;44(6):1285-91 [5168596.001]
  • [Cites] J Mol Biol. 1980 Apr;138(2):149-78 [7411608.001]
  • [Cites] Biochemistry. 1981 Jan 6;20(1):33-7 [7470476.001]
  • [Cites] Biochemistry. 1981 Mar 3;20(5):1085-94 [7225319.001]
  • [Cites] Biopolymers. 1983 Dec;22(12):2577-637 [6667333.001]
  • [Cites] Methods Enzymol. 1986;130:208-69 [3773734.001]
  • [Cites] Anal Biochem. 1987 Nov 15;167(1):76-85 [3434802.001]
  • [Cites] Protein Eng. 1991 Aug;4(6):669-79 [1946324.001]
  • [Cites] Protein Eng. 1992 Apr;5(3):191-5 [1409538.001]
  • [Cites] Anal Biochem. 1993 Feb 15;209(1):32-44 [8465960.001]
  • [Cites] Protein Eng. 1993 Jun;6(4):383-90 [8332596.001]
  • [Cites] Protein Sci. 1995 Jul;4(7):1384-401 [7670380.001]
  • [Cites] Anal Biochem. 1978 Nov;91(1):13-31 [9762080.001]
  • [Cites] Proteins. 1999 May 15;35(3):307-12 [10328265.001]
  • [Cites] Bioinformatics. 2006 Aug 15;22(16):1955-62 [16787970.001]
  • [Cites] BMC Bioinformatics. 2006;7:507 [17112372.001]
  • [Cites] Proteins. 2001 Mar 1;42(4):460-70 [11170201.001]
  • (PMID = 18477405.001).
  • [ISSN] 1472-6807
  • [Journal-full-title] BMC structural biology
  • [ISO-abbreviation] BMC Struct. Biol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2397409
  •  go-up   go-down


10. Shih J, May LD, Gonzalez HE, Lee EW, Alvi RS, Sall JW, Rau V, Bickler PE, Lalchandani GR, Yusupova M, Woodward E, Kang H, Wilk AJ, Carlston CM, Mendoza MV, Guggenheim JN, Schaefer M, Rowe AM, Stratmann G: Delayed environmental enrichment reverses sevoflurane-induced memory impairment in rats. Anesthesiology; 2012 Mar;116(3):586-602
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Delayed environmental enrichment reverses sevoflurane-induced memory impairment in rats.
  • BACKGROUND: Anesthesia given to immature rodents causes cognitive decline, raising the possibility that the same might be true for millions of children undergoing surgical procedures under general anesthesia each year.
  • We tested the hypothesis that anesthesia-induced cognitive decline in rats is treatable.
  • We also tested if anesthesia-induced cognitive decline is aggravated by tissue injury.
  • METHODS: Seven-day old rats underwent sevoflurane anesthesia (1 minimum alveolar concentration, 4 h) with or without tail clamping.
  • At 4 weeks, rats were randomized to environmental enrichment or normal housing.
  • At 8 weeks rats underwent neurocognitive testing, which consisted of fear conditioning, spatial reference memory, and water maze-based memory consolidation tests, and interrogated working memory, short-term memory, and early long-term memory.
  • RESULTS: Sevoflurane-treated rats had a greater escape latency when the delay between memory acquisition and memory retrieval was increased from 1 min to 1 h, indicating that short-term memory was impaired.
  • Delayed environmental enrichment reversed the effects of sevoflurane on short-term memory and generally improved many tested aspects of cognitive function, both in sevoflurane-treated and control animals.
  • The performance of tail-clamped rats did not differ from those rats receiving anesthesia alone.
  • CONCLUSION: Sevoflurane-induced cognitive decline in rats is treatable.
  • Delayed environmental enrichment rescued the sevoflurane-induced impairment in short-term memory.
  • Tissue injury did not worsen the anesthesia-induced memory impairment.
  • These findings may have relevance to neonatal and pediatric anesthesia.
  • [MeSH-major] Housing, Animal. Memory Disorders / chemically induced. Memory Disorders / therapy. Methyl Ethers / toxicity
  • [MeSH-minor] Age Factors. Animals. Animals, Newborn. Male. Maze Learning / drug effects. Maze Learning / physiology. Random Allocation. Rats. Rats, Sprague-Dawley. Time Factors

  • MedlinePlus Health Information. consumer health - Memory.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • Hazardous Substances Data Bank. Sevoflurane .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Behav Pharmacol. 1998 Sep;9(5-6):421-7 [9832927.001]
  • [Cites] Nature. 1998 Jun 18;393(6686):635-6 [9641675.001]
  • [Cites] Anesthesiology. 1963 May-Jun;24:346-57 [13935000.001]
  • [Cites] Brain Res. 2005 Mar 10;1037(1-2):139-47 [15777762.001]
  • [Cites] Nat Rev Neurosci. 2006 Sep;7(9):697-709 [16924259.001]
  • [Cites] Anesthesiology. 2007 Mar;106(3):436-43 [17325501.001]
  • [Cites] Anesthesiology. 2007 Apr;106(4):746-53 [17413912.001]
  • [Cites] Pediatr Res. 2007 Sep;62(3):283-90 [17551412.001]
  • [Cites] J Neurosurg Anesthesiol. 2008 Jan;20(1):21-8 [18157021.001]
  • [Cites] Chin Med J (Engl). 2008 Feb 20;121(4):341-6 [18304468.001]
  • [Cites] Anesth Analg. 2008 Jun;106(6):1681-707 [18499597.001]
  • [Cites] Anesthesiology. 2008 Aug;109(2):243-50 [18648233.001]
  • [Cites] Anesthesiology. 2008 Nov;109(5):757-61 [18946281.001]
  • [Cites] Ann Neurol. 2008 Oct;64(4):434-45 [18991352.001]
  • [Cites] Anesth Analg. 2009 Jan;108(1):90-104 [19095836.001]
  • [Cites] Anesthesiology. 2009 Mar;110(3):628-37 [19212262.001]
  • [Cites] Anesthesiology. 2009 Apr;110(4):849-61 [19293696.001]
  • [Cites] Anesthesiology. 2009 Apr;110(4):813-25 [19293698.001]
  • [Cites] Anesthesiology. 2009 Apr;110(4):805-12 [19293699.001]
  • [Cites] Anesthesiology. 2009 Apr;110(4):796-804 [19293700.001]
  • [Cites] Anesthesiology. 2009 Apr;110(4):834-48 [19293705.001]
  • [Cites] Anesthesiology. 2009 May;110(5):1077-85 [19352168.001]
  • [Cites] Neurotox Res. 2009 Aug;16(2):140-7 [19526290.001]
  • [Cites] Anesth Analg. 2009 Sep;109(3):801-6 [19690249.001]
  • [Cites] PLoS One. 2009;4(9):e7043 [19756154.001]
  • [Cites] Neurotox Res. 2010 Feb;17(2):179-88 [19626389.001]
  • [Cites] Anesthesiology. 2010 Mar;112(3):567-75 [20124973.001]
  • [Cites] J Comp Neurol. 2010 May 15;518(10):1711-23 [20235164.001]
  • [Cites] Anesthesiology. 2010 Jun;112(6):1325-34 [20460994.001]
  • [Cites] Cell Death Differ. 2010 Jul;17(7):1092-103 [20019745.001]
  • [Cites] Eur J Neurosci. 2010 Jun;31(12):2292-307 [20550571.001]
  • [Cites] J Neurosci. 2010 Sep 22;30(38):12653-63 [20861371.001]
  • [Cites] Anesthesiology. 2011 Mar;114(3):578-87 [21293251.001]
  • [Cites] Anesthesiology. 2011 Nov;115(5):1132-3; author's reply 1133-5 [22027626.001]
  • [Cites] Anesthesiology. 2011 Nov;115(5):979-91 [21956042.001]
  • [Cites] Nature. 1999 Aug 12;400(6745):671-5 [10458162.001]
  • [Cites] Science. 2000 Jan 14;287(5451):248-51 [10634773.001]
  • [Cites] Nat Rev Neurosci. 2000 Dec;1(3):191-8 [11257907.001]
  • [Cites] Behav Brain Sci. 1999 Jun;22(3):425-44; discussion 444-89 [11301518.001]
  • [Cites] Ann Neurol. 2002 Aug;52(2):135-43 [12210782.001]
  • [Cites] Nat Rev Neurosci. 2002 Sep;3(9):728-39 [12209121.001]
  • [Cites] J Neurosci. 2003 Feb 1;23(3):876-82 [12574416.001]
  • [Cites] Anesthesiology. 1965 Nov-Dec;26(6):756-63 [5844267.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5568-72 [1695380.001]
  • [Cites] Science. 1992 May 1;256(5057):675-7 [1585183.001]
  • [Cites] Nature. 1997 Apr 3;386(6624):493-5 [9087407.001]
  • [Cites] Brain Res Cogn Brain Res. 1997 Jun;5(4):329-33 [9197520.001]
  • [Cites] Neurobiol Learn Mem. 1997 Nov;68(3):285-316 [9398590.001]
  • [Cites] Neurobiol Learn Mem. 1998 Mar;69(2):163-203 [9619995.001]
  • [CommentIn] Anesthesiology. 2012 Mar;116(3):507-9 [22258021.001]
  • (PMID = 22354242.001).
  • [ISSN] 1528-1175
  • [Journal-full-title] Anesthesiology
  • [ISO-abbreviation] Anesthesiology
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / K08 GM086511; United States / NIGMS NIH HHS / GM / K08 GM086511-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Methyl Ethers; 38LVP0K73A / sevoflurane
  • [Other-IDs] NLM/ NIHMS351573; NLM/ PMC4146425
  •  go-up   go-down






Advertisement