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  1. AU="Boorman, James P"
  2. AU="Duan, Jiasong"
  3. AU="He, Ruiying"
  4. AU="Auricchio, Salvatore"
  5. AU="Farnesini, L"
  6. AU="Gerald Berger"
  7. AU="Lenning, Ole Bernt"
  8. AU="Voetsch, Barbara"
  9. AU="Jakielska, Ewelina"
  10. AU="Sholl, Lynette"
  11. AU="Izquierdo, Inmaculada"
  12. AU="Miller, Andrew S"
  13. AU="Vincent-Levy-Frebault, V"
  14. AU="Willis, Zachary I"
  15. AU="Kruger, Eric S"
  16. AU="Ge, Shiyu"
  17. AU="Srivastava, Rajat"
  18. AU="Nemanja Vuksanovic"

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  1. Artikel: Voltage-gated sodium channels and pain pathways.

    Wood, John N / Boorman, James P / Okuse, Kenji / Baker, Mark D

    Journal of neurobiology

    2004  Band 61, Heft 1, Seite(n) 55–71

    Abstract: Acute, inflammatory, and neuropathic pain can all be attenuated or abolished by local treatment with sodium channel blockers such as lidocaine. The peripheral input that drives pain perception thus depends on the presence of functional voltage-gated ... ...

    Abstract Acute, inflammatory, and neuropathic pain can all be attenuated or abolished by local treatment with sodium channel blockers such as lidocaine. The peripheral input that drives pain perception thus depends on the presence of functional voltage-gated sodium channels. Remarkably, two voltage-gated sodium channel genes (Nav1.8 and Nav1.9) are expressed selectively in damage-sensing peripheral neurons, while a third channel (Nav1.7) is found predominantly in sensory and sympathetic neurons. An embryonic channel (Nav1.3) is also upregulated in damaged peripheral nerves and associated with increased electrical excitability in neuropathic pain states. A combination of antisense and knock-out studies support a specialized role for these sodium channels in pain pathways, and pharmacological studies with conotoxins suggest that isotype-specific antagonists should be feasible. Taken together, these data suggest that isotype-specific sodium channel blockers could be useful analgesics.
    Mesh-Begriff(e) Amino Acid Sequence ; Animals ; Humans ; Molecular Sequence Data ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Neuropeptides/physiology ; Pain/drug therapy ; Pain/genetics ; Pain/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Sodium Channel Blockers/pharmacology ; Sodium Channel Blockers/therapeutic use ; Sodium Channels/genetics ; Sodium Channels/metabolism ; Sodium Channels/physiology
    Chemische Substanzen Neuropeptides ; Sodium Channel Blockers ; Sodium Channels
    Sprache Englisch
    Erscheinungsdatum 2004-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 300903-8
    ISSN 1097-4695 ; 0022-3034
    ISSN (online) 1097-4695
    ISSN 0022-3034
    DOI 10.1002/neu.20094
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Incomplete incorporation of tandem subunits in recombinant neuronal nicotinic receptors.

    Groot-Kormelink, Paul J / Broadbent, Steven D / Boorman, James P / Sivilotti, Lucia G

    The Journal of general physiology

    2004  Band 123, Heft 6, Seite(n) 697–708

    Abstract: Tandem constructs are increasingly being used to restrict the composition of recombinant multimeric channels. It is therefore important to assess not only whether such approaches give functional channels, but also whether such channels completely ... ...

    Abstract Tandem constructs are increasingly being used to restrict the composition of recombinant multimeric channels. It is therefore important to assess not only whether such approaches give functional channels, but also whether such channels completely incorporate the subunit tandems. We have addressed this question for neuronal nicotinic acetylcholine receptors, using a channel mutation as a reporter for subunit incorporation. We prepared tandem constructs of nicotinic receptors by linking alpha (alpha2-alpha4, alpha6) and beta (beta2, beta4) subunits by a short linker of eight glutamine residues. Robust functional expression in oocytes was observed for several tandems (beta4_alpha2, beta4_alpha3, beta4_alpha4, and beta2_alpha4) when coexpressed with the corresponding beta monomer subunit. All tandems expressed when injected alone, except for beta4_alpha3, which produced functional channels only together with beta4 monomer and was chosen for further characterization. These channels produced from beta4_alpha3 tandem constructs plus beta4 monomer were identical with receptors expressed from monomer alpha3 and beta4 constructs in acetylcholine sensitivity and in the number of alpha and beta subunits incorporated in the channel gate. However, separately mutating the beta subunit in either the monomer or the tandem revealed that tandem-expressed channels are heterogeneous. Only a proportion of these channels contained as expected two copies of beta subunits from the tandem and one from the beta monomer construct, whereas the rest incorporated two or three beta monomers. Such inaccuracies in concatameric receptor assembly would not have been apparent with a standard functional characterization of the receptor. Extensive validation is needed for tandem-expressed receptors in the nicotinic superfamily.
    Mesh-Begriff(e) Acetylcholine/pharmacology ; Animals ; Cloning, Molecular/methods ; Dimerization ; Dose-Response Relationship, Drug ; Genes, Reporter ; Humans ; Ion Channel Gating/drug effects ; Ion Channel Gating/physiology ; Neurons/metabolism ; Oocytes/physiology ; Patch-Clamp Techniques/methods ; Protein Engineering/methods ; Protein Subunits ; Receptors, Nicotinic/chemistry ; Receptors, Nicotinic/genetics ; Receptors, Nicotinic/metabolism ; Recombinant Fusion Proteins/chemistry ; Recombinant Fusion Proteins/metabolism ; Structure-Activity Relationship ; Transfection/methods ; Xenopus laevis
    Chemische Substanzen Protein Subunits ; Receptors, Nicotinic ; Recombinant Fusion Proteins ; Acetylcholine (N9YNS0M02X)
    Sprache Englisch
    Erscheinungsdatum 2004-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3118-5
    ISSN 1540-7748 ; 0022-1295
    ISSN (online) 1540-7748
    ISSN 0022-1295
    DOI 10.1085/jgp.200409042
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: The effects of beta3 subunit incorporation on the pharmacology and single channel properties of oocyte-expressed human alpha3beta4 neuronal nicotinic receptors.

    Boorman, James P / Beato, Marco / Groot-Kormelink, Paul J / Broadbent, Steven D / Sivilotti, Lucia G

    The Journal of biological chemistry

    2003  Band 278, Heft 45, Seite(n) 44033–44040

    Abstract: We compared the main properties of human recombinant alpha3beta4beta3 neuronal nicotinic receptors with those of alpha3beta4 receptors, expressed in Xenopus oocytes. beta3 incorporation decreased the channel mean open time (from 5.61 to 1.14 ms, after ... ...

    Abstract We compared the main properties of human recombinant alpha3beta4beta3 neuronal nicotinic receptors with those of alpha3beta4 receptors, expressed in Xenopus oocytes. beta3 incorporation decreased the channel mean open time (from 5.61 to 1.14 ms, after approximate correction for missed gaps) and burst length. There was also an increase in single channel slope conductance from 28.8 picosiemens (alpha3beta4) to 46.7 picosiemens (alpha3beta4beta3; in low divalent external solution). On the other hand, the calcium permeability (determined by a reversal potential method in chloride-depleted oocytes) and the pharmacological properties of beta3-containing receptors differed little from those of alpha3beta4. The main pharmacological difference in alpha3beta4beta3 "triplet" receptors was a 3-fold decrease in the potency of lobeline relative to acetylcholine. Nevertheless, there was no change in the rank order of potency for agonists (epibatidine >> lobeline > cytisine, 1,1-dimethyl-4-phenylpiperazinium iodide, nicotine > acetylcholine > carbachol for both receptors; measured at low agonist concentrations). Sensitivity to the competitive antagonists trimetaphan (0.2-1 microM) and dihydro-beta-erythroidine (30 microM) was similar for the two combinations, with a Schild KB for trimetaphan of 76 and 66 nM on alpha3beta4 and alpha3beta4beta3, respectively. The change in single channel conductance confirms that beta3 replaces a beta4 subunit in the pentamer. The absence of pronounced differences in the pharmacological profile of the triplet receptor argues against a role for the beta3 subunit in the formation of agonist binding sites, whereas the changes in channel kinetics suggest an important effect on receptor gating. The shortening of the burst length of beta3-containing receptors implies that any synaptic currents mediated by such channels would have faster decay kinetics.
    Mesh-Begriff(e) Animals ; Calcium/metabolism ; Electric Conductivity ; Female ; Gene Expression ; Humans ; Ion Channel Gating ; Kinetics ; Neurons/chemistry ; Nicotinic Agonists/pharmacology ; Nicotinic Antagonists/pharmacology ; Oocytes/chemistry ; Protein Subunits/genetics ; Protein Subunits/physiology ; Receptors, Nicotinic/chemistry ; Receptors, Nicotinic/genetics ; Receptors, Nicotinic/physiology ; Recombinant Proteins ; Structure-Activity Relationship ; Transfection ; Xenopus laevis
    Chemische Substanzen Nicotinic Agonists ; Nicotinic Antagonists ; Protein Subunits ; Receptors, Nicotinic ; Recombinant Proteins ; nicotinic receptor alpha3beta4 ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2003-08-11
    Erscheinungsland United States
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M211719200
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants.

    Burton, Paul R / Clayton, David G / Cardon, Lon R / Craddock, Nick / Deloukas, Panos / Duncanson, Audrey / Kwiatkowski, Dominic P / McCarthy, Mark I / Ouwehand, Willem H / Samani, Nilesh J / Todd, John A / Donnelly, Peter / Barrett, Jeffrey C / Davison, Dan / Easton, Doug / Evans, David M / Leung, Hin-Tak / Marchini, Jonathan L / Morris, Andrew P /
    Spencer, Chris C A / Tobin, Martin D / Attwood, Antony P / Boorman, James P / Cant, Barbara / Everson, Ursula / Hussey, Judith M / Jolley, Jennifer D / Knight, Alexandra S / Koch, Kerstin / Meech, Elizabeth / Nutland, Sarah / Prowse, Christopher V / Stevens, Helen E / Taylor, Niall C / Walters, Graham R / Walker, Neil M / Watkins, Nicholas A / Winzer, Thilo / Jones, Richard W / McArdle, Wendy L / Ring, Susan M / Strachan, David P / Pembrey, Marcus / Breen, Gerome / St Clair, David / Caesar, Sian / Gordon-Smith, Katharine / Jones, Lisa / Fraser, Christine / Green, Elaine K / Grozeva, Detelina / Hamshere, Marian L / Holmans, Peter A / Jones, Ian R / Kirov, George / Moskivina, Valentina / Nikolov, Ivan / O'Donovan, Michael C / Owen, Michael J / Collier, David A / Elkin, Amanda / Farmer, Anne / Williamson, Richard / McGuffin, Peter / Young, Allan H / Ferrier, I Nicol / Ball, Stephen G / Balmforth, Anthony J / Barrett, Jennifer H / Bishop, Timothy D / Iles, Mark M / Maqbool, Azhar / Yuldasheva, Nadira / Hall, Alistair S / Braund, Peter S / Dixon, Richard J / Mangino, Massimo / Stevens, Suzanne / Thompson, John R / Bredin, Francesca / Tremelling, Mark / Parkes, Miles / Drummond, Hazel / Lees, Charles W / Nimmo, Elaine R / Satsangi, Jack / Fisher, Sheila A / Forbes, Alastair / Lewis, Cathryn M / Onnie, Clive M / Prescott, Natalie J / Sanderson, Jeremy / Matthew, Christopher G / Barbour, Jamie / Mohiuddin, M Khalid / Todhunter, Catherine E / Mansfield, John C / Ahmad, Tariq / Cummings, Fraser R / Jewell, Derek P / Webster, John / Brown, Morris J / Lathrop, Mark G / Connell, John / Dominiczak, Anna / Marcano, Carolina A Braga / Burke, Beverley / Dobson, Richard / Gungadoo, Johannie / Lee, Kate L / Munroe, Patricia B / Newhouse, Stephen J / Onipinla, Abiodun / Wallace, Chris / Xue, Mingzhan / Caulfield, Mark / Farrall, Martin / Barton, Anne / Bruce, Ian N / Donovan, Hannah / Eyre, Steve / Gilbert, Paul D / Hilder, Samantha L / Hinks, Anne M / John, Sally L / Potter, Catherine / Silman, Alan J / Symmons, Deborah P M / Thomson, Wendy / Worthington, Jane / Dunger, David B / Widmer, Barry / Frayling, Timothy M / Freathy, Rachel M / Lango, Hana / Perry, John R B / Shields, Beverley M / Weedon, Michael N / Hattersley, Andrew T / Hitman, Graham A / Walker, Mark / Elliott, Kate S / Groves, Christopher J / Lindgren, Cecilia M / Rayner, Nigel W / Timpson, Nicolas J / Zeggini, Eleftheria / Newport, Melanie / Sirugo, Giorgio / Lyons, Emily / Vannberg, Fredrik / Hill, Adrian V S / Bradbury, Linda A / Farrar, Claire / Pointon, Jennifer J / Wordsworth, Paul / Brown, Matthew A / Franklyn, Jayne A / Heward, Joanne M / Simmonds, Matthew J / Gough, Stephen C L / Seal, Sheila / Stratton, Michael R / Rahman, Nazneen / Ban, Maria / Goris, An / Sawcer, Stephen J / Compston, Alastair / Conway, David / Jallow, Muminatou / Rockett, Kirk A / Bumpstead, Suzannah J / Chaney, Amy / Downes, Kate / Ghori, Mohammed J R / Gwilliam, Rhian / Hunt, Sarah E / Inouye, Michael / Keniry, Andrew / King, Emma / McGinnis, Ralph / Potter, Simon / Ravindrarajah, Rathi / Whittaker, Pamela / Widden, Claire / Withers, David / Cardin, Niall J / Ferreira, Teresa / Pereira-Gale, Joanne / Hallgrimsdo'ttir, Ingeleif B / Howie, Bryan N / Su, Zhan / Teo, Yik Ying / Vukcevic, Damjan / Bentley, David / Mitchell, Sarah L / Newby, Paul R / Brand, Oliver J / Carr-Smith, Jackie / Pearce, Simon H S / McGinnis, R / Keniry, A / Deloukas, P / Reveille, John D / Zhou, Xiaodong / Sims, Anne-Marie / Dowling, Alison / Taylor, Jacqueline / Doan, Tracy / Davis, John C / Savage, Laurie / Ward, Michael M / Learch, Thomas L / Weisman, Michael H / Brown, Mathew

    Nature genetics

    2007  Band 39, Heft 11, Seite(n) 1329–1337

    Abstract: We have genotyped 14,436 nonsynonymous SNPs (nsSNPs) and 897 major histocompatibility complex (MHC) tag SNPs from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC). ... ...

    Abstract We have genotyped 14,436 nonsynonymous SNPs (nsSNPs) and 897 major histocompatibility complex (MHC) tag SNPs from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC). Comparing these data against a common control dataset derived from 1,500 randomly selected healthy British individuals, we report initial association and independent replication in a North American sample of two new loci related to ankylosing spondylitis, ARTS1 and IL23R, and confirmation of the previously reported association of AITD with TSHR and FCRL3. These findings, enabled in part by increased statistical power resulting from the expansion of the control reference group to include individuals from the other disease groups, highlight notable new possibilities for autoimmune regulation and suggest that IL23R may be a common susceptibility factor for the major 'seronegative' diseases.
    Mesh-Begriff(e) Aminopeptidases/genetics ; Autoimmunity/genetics ; Breast Neoplasms/epidemiology ; Breast Neoplasms/genetics ; Case-Control Studies ; Chromosome Mapping ; Genetics, Population ; Genotype ; Haplotypes/genetics ; Humans ; Linkage Disequilibrium ; Minor Histocompatibility Antigens ; Multiple Sclerosis/epidemiology ; Multiple Sclerosis/genetics ; North America/epidemiology ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide/genetics ; Receptors, Immunologic/genetics ; Receptors, Interleukin/genetics ; Spondylitis, Ankylosing/epidemiology ; Spondylitis, Ankylosing/genetics ; Thyroiditis, Autoimmune/epidemiology ; Thyroiditis, Autoimmune/genetics
    Chemische Substanzen FCRL3 protein, human ; IL23R protein, human ; Minor Histocompatibility Antigens ; Receptors, Immunologic ; Receptors, Interleukin ; Aminopeptidases (EC 3.4.11.-) ; ERAP1 protein, human (EC 3.4.11.-)
    Sprache Englisch
    Erscheinungsdatum 2007-10-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Randomized Controlled Trial
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/ng.2007.17
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Replication of Genome-Wide Association Signals in UK Samples Reveals Risk Loci for Type 2 Diabetes

    Zeggini, Eleftheria / Ahmad, Tariq / Ardern-Jones, A / Attwood, Antony P / Ball, Stephen G / Balmforth, Anthony J / Ban, Maria / Barbour, Jamie / Barrett, Jeffrey C / Barrett, Jennifer H / Barton, Anne / Bentley, David / Berg, J / Bishop, D. Timothy / Boorman, James P / Bradbury, Linda A / Bradshaw, N / Brady, A / Braga Marcano, Carolina A /
    Braund, Peter S / Bredin, Francesca / Breen, Gerome / Brewer, C / Brice, G / Brown, Matthew A / Brown, Morris J / Bruce, Ian N / Bullman, B / Bumpstead, Suzannah J / Burke, Beverley / Burton, Paul R / Caesar, Sian / Campbell, J / Cant, Barbara / Cardin, Niall J / Cardon, Lon R / Castle, B / Caulfield, Mark / Cetnarsryj, R / Chaney, Amy / Chapman, C / Chu, C / Clayton, David G / Coates, N / Cole, T / Collier, David A / Compston, Alastair / Compston, Alistair / Connell, John / Conway, David / Craddock, Nick / Cummings, Fraser R / Davidson, R / Davison, Dan / Deloukas, Panos / Dixon, Richard J / Dobson, Richard / Dominiczak, Anna / Donaldson, A / Doney, Alex S.F / Donnelly, Peter / Donovan, Hannah / Dorkins, H / Douglas, F / Downes, Kate / Drummond, Hazel / Duncanson, Audrey / Dunger, David B / Easton, Doug / Eccles, D / Eeles, R / Elkin, Amanda / Ellard, Sian / Elliott, Katherine S / Elmslie, F / Evans, D.G / Evans, David / Everson, Ursula / Eyre, Steve / Farmer, Anne / Farrall, Martin / Farrar, Claire / Ferreira, Teresa / Ferrier, I. Nicol / Fisher, Sheila A / Forbes, Alastair / Franklyn, Jayne A / Fraser, Christine / Frayling, Timothy M / Freathy, Rachel M / Ghori, Mohammed J.R / Gilbert, Paul D / Goff, S / Goodman, S / Gordon-Smith, Katherine / Goris, An / Goudie, D / Gough, Stephen C.L / Gray, J / Green, Elaine K / Greenhalgh, L / Gregory, H / Groves, Christopher J / Grozeva, Detelina / Gungadoo, Johannie / Gwilliam, Rhian / Hall, Alistair S / Hallgrimsdóttir, Ingeleif B / Hamshere, Marian L / Harries, Lorna W / Hattersley, Andrew T / Heward, Joanne M / Hider, Samantha L / Hill, Adrian V.S / Hinks, Anne M / Hitman, Graham A / Hodgson, S.V / Holmans, Peter A / Homfray, T / Houlston, R.S / Howie, Bryan N / Hunt, Sarah E / Hussey, Judith M / Iles, Mark M / Inouye, Michael / Isaacs, John D / Izatt, L / Jackson, L / Jallow, Muminatou / Jeffers, L / Jewell, Derek P / John, Sally L / Johnson-Roffey, V / Jolley, Jennifer D / Jones, Ian R / Jones, Lisa / Jones, Richard W / Kavalier, F / Keniry, Andrew / King, Emma / Kirk, C / Kirov, George / Knight, Alexandra S / Knight, Beatrice / Koch, Kerstin / Kwiatkowski, Dominic P / Lalloo, F / Langman, C / Lango, Hana / Lathrop, G. Mark / Lee, Kate L / Lees, Charles W / Leung, Hin-Tak / Lewis, Cathryn M / Lindgren, Cecilia M / Locke, I / Longmuir, M / Lyons, Emily / Mackay, J / Magee, A / Mangino, Massimo / Mansfield, John C / Mansour, S / Maqbool, Azhar / Marchini, Jonathan L / Mathew, Christopher G / McArdle, Wendy L / McCarthy, Mark I / McGinnis, Ralph / McGuffin, Peter / Meech, Elizabeth / Miedzybrodzka, Z / Miller, J / Mohiuddin, M. Khalid / Morgan, Ann W / Morris, Andrew D / Morris, Andrew P / Morrison, P / Moskvina, Valentina / Munroe, Patricia B / Murday, V / Newhouse, Stephen J / Newport, Melanie / Nikolov, Ivan / Nimmo, Elaine R / Nutland, Sarah / O'Donovan, Michael C / Onipinla, Abiodun / Onnie, Clive M / Ouwehand, Nilesh J / Ouwehand, Willem H / Owen, Katharine R / Owen, Michael J / Parkes, Miles / Paterson, J / Pembrey, Marcus / Pereira-Gale, Joanne / Perry, John R.B / Pichert, G / Pointon, Jennifer J / Porteous, M / Potter, Catherine / Potter, Simon / Prescott, Natalie J / Prowse, Christopher V / Rahman, N / Rahman, Nazneen / Ravindrarajah, Rathi / Rayner, Nigel W / Ring, Susan M / Rockett, Kirk A / Rogers, M / Rowe, S / Saggar, A / Samani, Michael R / Samani, Nilesh J / Sanderson, Jeremy / Satsangi, Jack / Sawcer, Stephen J / Scott, G / Seal, Sheila / Shanley, S / Shields, Beverley / Side, L / Silman, Alan J / Simmonds, Matthew J / Sirugo, Giorgio / Snadden, L / Spencer, Chris C.A / St. Clair, David / Steel, M / Stevens, Helen E / Stevens, Suzanne / Strachan, David P / Stratton, Michael R / Su, Zhan / Symmons, Deborah P.M / Taylor, Niall C / Teo, Yik Ying / Thomas, M / Thomas, S / Thompson, John R / Thomson, Wendy / Timpson, Nicholas J / Tobin, Martin D / Todd, John A / Todhunter, Catherine E / Tremelling, Mark / Vannberg, Fredrik / Vukcevic, Damjan / Walker, Mark / Walker, Neil M / Wallace, Chris / Walters, Graham R / Watkins, Nicholas A / Webster, John / Weedon, Michael N / Whittaker, Pamela / Widden, Claire / Widmer, Barry / Williamson, Richard / Wilson, Gerry D / Winzer, Thilo / Withers, David / Wordsworth, Paul / Worthington, Jane / Xue, Mingzhan / Young, Allan H / Yuldasheva, Nadira

    Science. 2007 June 1, v. 316, no. 5829

    2007  

    Abstract: The molecular mechanisms involved in the development of type 2 diabetes are poorly understood. Starting from genome-wide genotype data for 1924 diabetic cases and 2938 population controls generated by the Wellcome Trust Case Control Consortium, we set ... ...

    Abstract The molecular mechanisms involved in the development of type 2 diabetes are poorly understood. Starting from genome-wide genotype data for 1924 diabetic cases and 2938 population controls generated by the Wellcome Trust Case Control Consortium, we set out to detect replicated diabetes association signals through analysis of 3757 additional cases and 5346 controls and by integration of our findings with equivalent data from other international consortia. We detected diabetes susceptibility loci in and around the genes CDKAL1, CDKN2A/CDKN2B, and IGF2BP2 and confirmed the recently described associations at HHEX/IDE and SLC30A8. Our findings provide insight into the genetic architecture of type 2 diabetes, emphasizing the contribution of multiple variants of modest effect. The regions identified underscore the importance of pathways influencing pancreatic beta cell development and function in the etiology of type 2 diabetes.
    Schlagwörter etiology ; genes ; genotype ; islets of Langerhans ; loci ; noninsulin-dependent diabetes mellitus ; risk ; United Kingdom
    Sprache Englisch
    Erscheinungsverlauf 2007-0601
    Umfang p. 1336-1341.
    Erscheinungsort American Association for the Advancement of Science
    Dokumenttyp Artikel
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1142364
    Datenquelle NAL Katalog (AGRICOLA)

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