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The knockout mouse project 总被引:1,自引:0,他引:1
Austin CP Battey JF Bradley A Bucan M Capecchi M Collins FS Dove WF Duyk G Dymecki S Eppig JT Grieder FB Heintz N Hicks G Insel TR Joyner A Koller BH Lloyd KC Magnuson T Moore MW Nagy A Pollock JD Roses AD Sands AT Seed B Skarnes WC Snoddy J Soriano P Stewart DJ Stewart F Stillman B Varmus H Varticovski L Verma IM Vogt TF von Melchner H Witkowski J Woychik RP Wurst W Yancopoulos GD Young SG Zambrowicz B 《Nature genetics》2004,36(9):921-924
Mouse knockout technology provides a powerful means of elucidating gene function in vivo, and a publicly available genome-wide collection of mouse knockouts would be significantly enabling for biomedical discovery. To date, published knockouts exist for only about 10% of mouse genes. Furthermore, many of these are limited in utility because they have not been made or phenotyped in standardized ways, and many are not freely available to researchers. It is time to harness new technologies and efficiencies of production to mount a high-throughput international effort to produce and phenotype knockouts for all mouse genes, and place these resources into the public domain. 相似文献
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How will we view schizophrenia in 2030? Schizophrenia today is a chronic, frequently disabling mental disorder that affects about one per cent of the world's population. After a century of studying schizophrenia, the cause of the disorder remains unknown. Treatments, especially pharmacological treatments, have been in wide use for nearly half a century, yet there is little evidence that these treatments have substantially improved outcomes for most people with schizophrenia. These current unsatisfactory outcomes may change as we approach schizophrenia as a neurodevelopmental disorder with psychosis as a late, potentially preventable stage of the illness. This 'rethinking' of schizophrenia as a neurodevelopmental disorder, which is profoundly different from the way we have seen this illness for the past century, yields new hope for prevention and cure over the next two decades. 相似文献
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Increased affiliative response to vasopressin in mice expressing the V1a receptor from a monogamous vole. 总被引:8,自引:0,他引:8
Arginine vasopressin influences male reproductive and social behaviours in several vertebrate taxa through its actions at the V1a receptor in the brain. The neuroanatomical distribution of vasopressin V1a receptors varies greatly between species with different forms of social organization. Here we show that centrally administered arginine vasopressin increases affiliative behaviour in the highly social, monogamous prairie vole, but not in the relatively asocial, promiscuous montane vole. Molecular analyses indicate that gene duplication and/or changes in promoter structure of the prairie vole receptor gene may contribute to the species differences in vasopressin-receptor expression. We further show that mice that are transgenic for the prairie vole receptor gene have a neuroanatomical pattern of receptor binding that is similar to that of the prairie vole, and exhibit increased affiliative behaviour after injection with arginine vasopressin. These data indicate that the pattern of V1a-receptor gene expression in the brain may be functionally associated with species-typical social behaviours in male vertebrates. 相似文献
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Vacic V McCarthy S Malhotra D Murray F Chou HH Peoples A Makarov V Yoon S Bhandari A Corominas R Iakoucheva LM Krastoshevsky O Krause V Larach-Walters V Welsh DK Craig D Kelsoe JR Gershon ES Leal SM Dell Aquila M Morris DW Gill M Corvin A Insel PA McClellan J King MC Karayiorgou M Levy DL DeLisi LE Sebat J 《Nature》2011,471(7339):499-503
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New models of collaboration in genome-wide association studies: the Genetic Association Information Network 总被引:7,自引:0,他引:7
GAIN Collaborative Research Group Manolio TA Rodriguez LL Brooks L Abecasis G;Collaborative Association Study of Psoriasis Ballinger D Daly M Donnelly P Faraone SV;International Multi-Center ADHD Genetics Project Frazer K Gabriel S Gejman P;Molecular Genetics of Schizophrenia Collaboration Guttmacher A Harris EL Insel T Kelsoe JR;Bipolar Genome Study Lander E McCowin N Mailman MD Nabel E Ostell J Pugh E Sherry S 《Nature genetics》2007,39(9):1045-1051
The Genetic Association Information Network (GAIN) is a public-private partnership established to investigate the genetic basis of common diseases through a series of collaborative genome-wide association studies. GAIN has used new approaches for project selection, data deposition and distribution, collaborative analysis, publication and protection from premature intellectual property claims. These demonstrate a new commitment to shared scientific knowledge that should facilitate rapid advances in understanding the genetics of complex diseases. 相似文献
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Collins PY Patel V Joestl SS March D Insel TR Daar AS;Scientific Advisory Board the Executive Committee of the Grand Challenges on Global Mental Health Anderson W Dhansay MA Phillips A Shurin S Walport M Ewart W Savill SJ Bordin IA Costello EJ Durkin M Fairburn C Glass RI Hall W Huang Y Hyman SE Jamison K Kaaya S Kapur S Kleinman A Ogunniyi A Otero-Ojeda A Poo MM Ravindranath V Sahakian BJ Saxena S Singer PA Stein DJ 《Nature》2011,475(7354):27-30
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Social amnesia in mice lacking the oxytocin gene 总被引:20,自引:0,他引:20
The development of social familiarity in rodents depends predominantly on olfactory cues and can critically influence reproductive success. Researchers have operationally defined this memory by a reliable decrease in olfactory investigation in repeated or prolonged encounters with a conspecific. Brain oxytocin (OT) and vasopressin (AVP) seem to modulate a range of social behaviour from parental care to mate guarding. Pharmacological studies indicate that AVP administration may enhance social memory, whereas OT administration may either inhibit or facilitate social memory depending on dose, route or paradigm. We found that male mice mutant for the oxytocin gene (Oxt-/-) failed to develop social memory, whereas wild-type (Oxt+/+) mice showed intact social memory. Measurement of both olfactory foraging and olfactory habituation tasks indicated that olfactory detection of non-social stimuli is intact in Oxt-/- mice. Spatial memory and behavioural inhibition measured in a Morris water-maze, Y-maze, or habituation of an acoustic startle also seemed intact. Treatment with OT but not AVP rescued social memory in Oxt-/- mice, and treatment with an OT antagonist produced a social amnesia-like effect in Oxt+/+ mice. Our data indicate that OT is necessary for the normal development of social memory in mice and support the hypothesis that social memory has a neural basis distinct from other forms of memory. 相似文献
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