Human Phenotype Ontology (HPO) gene set. This set contains genes that have been annotated to the HPO term "Multiple impacted teeth", which is defined as "The presence of multiple impacted teeth." This gene set was automatically constructed using annotation and ontology data provided by HPO and includes gene-phenotypes annotations from all HPO sources. The transitive closure of this term is taken into account using is_a relationships. For more information: The Human Phenotype Ontology Consortium (HPOC), http://human-phenotype-ontology.org This gene set was generated using the GeneWeaver HPO loader v. 0.1.5, HPO OBO v. hp/releases/2020-03-27, and HPO Genes to Phenotypes (all sources, all frequencies) v. 2020.05.06.
Authors:
S Köhler, SC Doelken, CJ Mungall, S Bauer, HV Firth, I Bailleul-Forestier, GC Black, DL Brown, M Brudno, J Campbell, DR FitzPatrick, JT Eppig, AP Jackson, K Freson, M Girdea, I Helbig, JA Hurst, J Jähn, LG Jackson, AM Kelly, DH Ledbetter, S Mansour, CL Martin, C Moss, A Mumford, WH Ouwehand, SM Park, ER Riggs, RH Scott, S Sisodiya, S Van Vooren, RJ Wapner, AO Wilkie, CF Wright, AT Vulto-van Silfhout, N de Leeuw, BB de Vries, NL Washingthon, CL Smith, M Westerfield, P Schofield, BJ Ruef, GV Gkoutos, M Haendel, D Smedley, SE Lewis, PN Robinson
Human Phenotype Ontology (HPO) gene set. This set contains genes that have been annotated to the HPO term "Impacted tooth", which is defined as "A tooth that has not erupted because of local impediments (overcrowding or fibrous gum overgrowth)." This gene set was automatically constructed using annotation and ontology data provided by HPO and includes gene-phenotypes annotations from all HPO sources. The transitive closure of this term is taken into account using is_a relationships. For more information: The Human Phenotype Ontology Consortium (HPOC), http://human-phenotype-ontology.org This gene set was generated using the GeneWeaver HPO loader v. 0.1.5, HPO OBO v. hp/releases/2020-03-27, and HPO Genes to Phenotypes (all sources, all frequencies) v. 2020.05.06.
Authors:
S Köhler, SC Doelken, CJ Mungall, S Bauer, HV Firth, I Bailleul-Forestier, GC Black, DL Brown, M Brudno, J Campbell, DR FitzPatrick, JT Eppig, AP Jackson, K Freson, M Girdea, I Helbig, JA Hurst, J Jähn, LG Jackson, AM Kelly, DH Ledbetter, S Mansour, CL Martin, C Moss, A Mumford, WH Ouwehand, SM Park, ER Riggs, RH Scott, S Sisodiya, S Van Vooren, RJ Wapner, AO Wilkie, CF Wright, AT Vulto-van Silfhout, N de Leeuw, BB de Vries, NL Washingthon, CL Smith, M Westerfield, P Schofield, BJ Ruef, GV Gkoutos, M Haendel, D Smedley, SE Lewis, PN Robinson
To monitor the expression levels of a large number of genes and to identify genes not previously implicated in traumatic brain injury pathophysiology, a high-density oligonucleotide array containing 8,800 genes was interrogated. RNA samples were prepared from ipsilateral hippocampi 3 hr and 24 hr following lateral cortical impact injury and compared to samples from sham-operated controls.
Authors:
Matzilevich DA, Rall JM, Moore AN, Grill RJ, Dash PK
Study subjected wild-type and mu opioid receptor knockout mice to an escalating morphine regimen to investigate whether overstimulation of mu opioid receptors impacts on lateral hypothalamus function. This gene set comprises the 29 mu opioid receptor-dependent genes found by the study to alter morphine expression in the lateral hypothalamus.
Authors:
Befort K, Filliol D, Darcq E, Ghate A, Matifas A, Lardenois A, Muller J, Thibault C, Dembele D, Poch O, Kieffer BL
This gene set comprises the 7 lateral hypothalamus genes found by the study to upregulate gene expression in wild-type mice during chronic morphine treatment. Background: Study subjected wild-type and mu opioid receptor knockout mice to an escalating morphine regimen to investigate whether overstimulation of mu opiod receptors impacts on lateral hypothalamus function.
Authors:
Befort K, Filliol D, Darcq E, Ghate A, Matifas A, Lardenois A, Muller J, Thibault C, Dembele D, Poch O, Kieffer BL
This gene set comprises the 7 lateral hypothalamus genes found by the study to upregulate gene expression mu opioid receptor knockout mice during chronic morphine treatment. Background: Study subjected wild-type and mu opioid receptor knockout mice to an escalating morphine regimen to investigate whether overstimulation of mu opiod receptors impacts on lateral hypothalamus function.
Authors:
Befort K, Filliol D, Darcq E, Ghate A, Matifas A, Lardenois A, Muller J, Thibault C, Dembele D, Poch O, Kieffer BL
This gene set comprises the 4 lateral hypothalamus genes found by the study to downregulate gene expression in wild-type mice during chronic morphine treatment. Background: Study subjected wild-type and mu opioid receptor knockout mice to an escalating morphine regimen to investigate whether overstimulation of mu opiod receptors impacts on lateral hypothalamus function.
Authors:
Befort K, Filliol D, Darcq E, Ghate A, Matifas A, Lardenois A, Muller J, Thibault C, Dembele D, Poch O, Kieffer BL
This gene set comprises the 4 lateral hypothalamus genes found by the study to downregulate gene expression mu opioid receptor knockout mice during chronic morphine treatment. Background: Study subjected wild-type and mu opioid receptor knockout mice to an escalating morphine regimen to investigate whether overstimulation of mu opiod receptors impacts on lateral hypothalamus function.
Authors:
Befort K, Filliol D, Darcq E, Ghate A, Matifas A, Lardenois A, Muller J, Thibault C, Dembele D, Poch O, Kieffer BL
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Cholesterol, total. The EFO term total cholesterol measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
I Surakka, M Horikoshi, R Mägi, AP Sarin, A Mahajan, V Lagou, L Marullo, T Ferreira, B Miraglio, S Timonen, J Kettunen, M Pirinen, J Karjalainen, G Thorleifsson, S Hägg, JJ Hottenga, A Isaacs, C Ladenvall, M Beekman, T Esko, JS Ried, CP Nelson, C Willenborg, S Gustafsson, HJ Westra, M Blades, AJ de Craen, EJ de Geus, J Deelen, H Grallert, A Hamsten, AS Havulinna, C Hengstenberg, JJ Houwing-Duistermaat, E Hyppönen, LC Karssen, T Lehtimäki, V Lyssenko, PK Magnusson, E Mihailov, M Müller-Nurasyid, JP Mpindi, NL Pedersen, BW Penninx, M Perola, TH Pers, A Peters, J Rung, JH Smit, V Steinthorsdottir, MD Tobin, N Tsernikova, EM van Leeuwen, JS Viikari, SM Willems, G Willemsen, H Schunkert, J Erdmann, NJ Samani, J Kaprio, L Lind, C Gieger, A Metspalu, PE Slagboom, L Groop, CM van Duijn, JG Eriksson, A Jula, V Salomaa, DI Boomsma, C Power, OT Raitakari, E Ingelsson, MR Järvelin, U Thorsteinsdottir, L Franke, E Ikonen, O Kallioniemi, V Pietiäinen, CM Lindgren, K Stefansson, A Palotie, MI McCarthy, AP Morris, I Prokopenko, S Ripatti
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Triglycerides. The EFO term triglyceride measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
I Surakka, M Horikoshi, R Mägi, AP Sarin, A Mahajan, V Lagou, L Marullo, T Ferreira, B Miraglio, S Timonen, J Kettunen, M Pirinen, J Karjalainen, G Thorleifsson, S Hägg, JJ Hottenga, A Isaacs, C Ladenvall, M Beekman, T Esko, JS Ried, CP Nelson, C Willenborg, S Gustafsson, HJ Westra, M Blades, AJ de Craen, EJ de Geus, J Deelen, H Grallert, A Hamsten, AS Havulinna, C Hengstenberg, JJ Houwing-Duistermaat, E Hyppönen, LC Karssen, T Lehtimäki, V Lyssenko, PK Magnusson, E Mihailov, M Müller-Nurasyid, JP Mpindi, NL Pedersen, BW Penninx, M Perola, TH Pers, A Peters, J Rung, JH Smit, V Steinthorsdottir, MD Tobin, N Tsernikova, EM van Leeuwen, JS Viikari, SM Willems, G Willemsen, H Schunkert, J Erdmann, NJ Samani, J Kaprio, L Lind, C Gieger, A Metspalu, PE Slagboom, L Groop, CM van Duijn, JG Eriksson, A Jula, V Salomaa, DI Boomsma, C Power, OT Raitakari, E Ingelsson, MR Järvelin, U Thorsteinsdottir, L Franke, E Ikonen, O Kallioniemi, V Pietiäinen, CM Lindgren, K Stefansson, A Palotie, MI McCarthy, AP Morris, I Prokopenko, S Ripatti
GWAS: low density lipoprotein cholesterol measurement
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was LDL cholesterol. The EFO term low density lipoprotein cholesterol measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
I Surakka, M Horikoshi, R Mägi, AP Sarin, A Mahajan, V Lagou, L Marullo, T Ferreira, B Miraglio, S Timonen, J Kettunen, M Pirinen, J Karjalainen, G Thorleifsson, S Hägg, JJ Hottenga, A Isaacs, C Ladenvall, M Beekman, T Esko, JS Ried, CP Nelson, C Willenborg, S Gustafsson, HJ Westra, M Blades, AJ de Craen, EJ de Geus, J Deelen, H Grallert, A Hamsten, AS Havulinna, C Hengstenberg, JJ Houwing-Duistermaat, E Hyppönen, LC Karssen, T Lehtimäki, V Lyssenko, PK Magnusson, E Mihailov, M Müller-Nurasyid, JP Mpindi, NL Pedersen, BW Penninx, M Perola, TH Pers, A Peters, J Rung, JH Smit, V Steinthorsdottir, MD Tobin, N Tsernikova, EM van Leeuwen, JS Viikari, SM Willems, G Willemsen, H Schunkert, J Erdmann, NJ Samani, J Kaprio, L Lind, C Gieger, A Metspalu, PE Slagboom, L Groop, CM van Duijn, JG Eriksson, A Jula, V Salomaa, DI Boomsma, C Power, OT Raitakari, E Ingelsson, MR Järvelin, U Thorsteinsdottir, L Franke, E Ikonen, O Kallioniemi, V Pietiäinen, CM Lindgren, K Stefansson, A Palotie, MI McCarthy, AP Morris, I Prokopenko, S Ripatti
GWAS: high density lipoprotein cholesterol measurement
Description:
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was HDL cholesterol. The EFO term high density lipoprotein cholesterol measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
I Surakka, M Horikoshi, R Mägi, AP Sarin, A Mahajan, V Lagou, L Marullo, T Ferreira, B Miraglio, S Timonen, J Kettunen, M Pirinen, J Karjalainen, G Thorleifsson, S Hägg, JJ Hottenga, A Isaacs, C Ladenvall, M Beekman, T Esko, JS Ried, CP Nelson, C Willenborg, S Gustafsson, HJ Westra, M Blades, AJ de Craen, EJ de Geus, J Deelen, H Grallert, A Hamsten, AS Havulinna, C Hengstenberg, JJ Houwing-Duistermaat, E Hyppönen, LC Karssen, T Lehtimäki, V Lyssenko, PK Magnusson, E Mihailov, M Müller-Nurasyid, JP Mpindi, NL Pedersen, BW Penninx, M Perola, TH Pers, A Peters, J Rung, JH Smit, V Steinthorsdottir, MD Tobin, N Tsernikova, EM van Leeuwen, JS Viikari, SM Willems, G Willemsen, H Schunkert, J Erdmann, NJ Samani, J Kaprio, L Lind, C Gieger, A Metspalu, PE Slagboom, L Groop, CM van Duijn, JG Eriksson, A Jula, V Salomaa, DI Boomsma, C Power, OT Raitakari, E Ingelsson, MR Järvelin, U Thorsteinsdottir, L Franke, E Ikonen, O Kallioniemi, V Pietiäinen, CM Lindgren, K Stefansson, A Palotie, MI McCarthy, AP Morris, I Prokopenko, S Ripatti
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Length of menstrual cycle. The EFO term menstrual cycle measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
KS Ruth, RN Beaumont, J Tyrrell, SE Jones, MA Tuke, H Yaghootkar, AR Wood, RM Freathy, MN Weedon, TM Frayling, A Murray
List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Lung cancer. The EFO term lung carcinoma was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.
Authors:
P Broderick, Y Wang, J Vijayakrishnan, A Matakidou, MR Spitz, T Eisen, CI Amos, RS Houlston
Human Phenotype Ontology (HPO) gene set. This set contains genes that have been annotated to the HPO term "Perseveration", which is defined as "Perseveration can be defined as the contextually inappropriate and unintentional repetition of a response or behavioral unit. In other words, the observed repetitiveness does not meet the demands of the situation, is not the product of deliberation, and may even unfold despite counterintention. Perseveration can therefore be differentiated from goal-directed and intentional forms of repetition, such as linguistic redundancies designed to enhance communicative or poetic impact." This gene set was automatically constructed using annotation and ontology data provided by HPO and includes gene-phenotypes annotations from all HPO sources. The transitive closure of this term is taken into account using is_a relationships. For more information: The Human Phenotype Ontology Consortium (HPOC), http://human-phenotype-ontology.org This gene set was generated using the GeneWeaver HPO loader v. 0.1.5, HPO OBO v. hp/releases/2020-03-27, and HPO Genes to Phenotypes (all sources, all frequencies) v. 2020.05.06.
Authors:
S Köhler, SC Doelken, CJ Mungall, S Bauer, HV Firth, I Bailleul-Forestier, GC Black, DL Brown, M Brudno, J Campbell, DR FitzPatrick, JT Eppig, AP Jackson, K Freson, M Girdea, I Helbig, JA Hurst, J Jähn, LG Jackson, AM Kelly, DH Ledbetter, S Mansour, CL Martin, C Moss, A Mumford, WH Ouwehand, SM Park, ER Riggs, RH Scott, S Sisodiya, S Van Vooren, RJ Wapner, AO Wilkie, CF Wright, AT Vulto-van Silfhout, N de Leeuw, BB de Vries, NL Washingthon, CL Smith, M Westerfield, P Schofield, BJ Ruef, GV Gkoutos, M Haendel, D Smedley, SE Lewis, PN Robinson
Cocaine exposure to escalation of cocaine intake and glutamatergic gene expression
Description:
Here, we investigated the contribution of behavioral contingency of cocaine administration on escalation of cocaine intake and gene expression in the dorsal medial prefrontal cortex (dmPFC) in adult male rats. Rats were allowed to self-administer intravenous cocaine (0.25 mg/infusion) under either limited cocaine-(1 h/day), prolonged cocaine-(6 h/day), or limited cocaine-(1 h/day) plus yoked cocaine-access (5 h/day); a control group received access to saline (1 h/day). One day after the final self-administration session, the rats were euthanized and the dmPFC was removed for quantification of mRNA expression of critical glutamatergic signaling genes, Homer2, Grin1, and Dlg4, as these genes and brain region have been previously implicated in addiction, learning, and memory. All groups with cocaine-access showed escalated cocaine intake during the first 10 min of each daily session, and within the first 1 h of cocaine administration. Additionally, the limited-access + yoked group exhibited more non-reinforced lever responses during self-administration sessions than the other groups tested. Lastly, Homer2, Grin1, and Dlg4 mRNA were impacted by both duration and mode of cocaine exposure. Only prolonged-access rats exhibited increases in mRNA expression for Homer2, Grin1, and Dlg4 mRNA.
Authors:
Kyle L Ploense, Philip Vieira, Lana Bubalo, Gema Olivarria, Amanda E Carr, Karen K Szumlinski, Tod E Kippin
QTL associated with radiation induced gastroschisis 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (72726204)
QTL associated with T cell ratio modifier QTL 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (146377508)
Authors:
Myrick C, DiGuisto R, DeWolfe J, Bowen E, Kappler J, Marrack P, Wakeland EK
McKnite AM, Perez-Munoz ME, Lu L, Williams EG, Brewer S, Andreux PA, Bastiaansen JW, Wang X, Kachman SD, Auwerx J, Williams RW, Benson AK, Peterson DA, Ciobanu DC
McKnite AM, Perez-Munoz ME, Lu L, Williams EG, Brewer S, Andreux PA, Bastiaansen JW, Wang X, Kachman SD, Auwerx J, Williams RW, Benson AK, Peterson DA, Ciobanu DC
McKnite AM, Perez-Munoz ME, Lu L, Williams EG, Brewer S, Andreux PA, Bastiaansen JW, Wang X, Kachman SD, Auwerx J, Williams RW, Benson AK, Peterson DA, Ciobanu DC
McKnite AM, Perez-Munoz ME, Lu L, Williams EG, Brewer S, Andreux PA, Bastiaansen JW, Wang X, Kachman SD, Auwerx J, Williams RW, Benson AK, Peterson DA, Ciobanu DC
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