Ts65Dn, a mouse model of Down syndrome, exhibits increased GABAB-induced potassium current. - Wikidata - awgldk - TriplyDB

Ts65Dn, a mouse model of Down syndrome, exhibits increased GABAB-induced potassium current.

Ts65Dn, a mouse model of Down syndrome, exhibits increased GABAB-induced potassium current.

http://www.wikidata.org/entity/Q48375391

about

Down syndrome: searching for the genetic culprits Prospects for Improving Brain Function in Individuals with Down Syndrome Emerging pharmacotherapies for neurodevelopmental disorders Functional genomic analysis of amniotic fluid cell-free mRNA suggests that oxidative stress is significant in Down syndrome fetuses Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies Pharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.Dysfunctional hippocampal inhibition in the Ts65Dn mouse model of Down syndrome.Prenatal treatment prevents learning deficit in Down syndrome model.Down syndrome--recent progress and future prospects.Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex.Specific targeting of the GABA-A receptor α5 subtype by a selective inverse agonist restores cognitive deficits in Down syndrome mice.Chronic Treatment with a Promnesiant GABA-A α5-Selective Inverse Agonist Increases Immediate Early Genes Expression during Memory Processing in Mice and Rectifies Their Expression Levels in a Down Syndrome Mouse Model Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome Involvement of Potassium and Cation Channels in Hippocampal Abnormalities of Embryonic Ts65Dn and Tc1 Trisomic Mice Molecular and cellular alterations in Down syndrome: toward the identification of targets for therapeutics From abnormal hippocampal synaptic plasticity in down syndrome mouse models to cognitive disability in down syndrome.Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.GIRK channel modulation by assembly with allosterically regulated RGS proteins Absence of Prenatal Forebrain Defects in the Dp(16)1Yey/+ Mouse Model of Down Syndrome.Down syndrome and the molecular pathogenesis resulting from trisomy of human chromosome 21.GABAB receptor-mediated, layer-specific synaptic plasticity reorganizes gamma-frequency neocortical response to stimulation.Infantile spasms: a critical review of emerging animal models.Prevention of developmental delays in a Down syndrome mouse model.A new mouse model for the trisomy of the Abcg1-U2af1 region reveals the complexity of the combinatorial genetic code of down syndrome Aneuploidy: from a physiological mechanism of variance to Down syndrome.Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome.The GABAergic Hypothesis for Cognitive Disabilities in Down Syndrome Is it possible to improve neurodevelopmental abnormalities in Down syndrome?Autism spectrum disorders: the quest for genetic syndromes.New insights into the therapeutic potential of Girk channels.GABAergic dysfunction in pediatric neuro-developmental disorders.G Protein-Gated K+ Channel Ablation in Forebrain Pyramidal Neurons Selectively Impairs Fear Learning.Altered intrinsic and network properties of neocortical neurons in the Ts65Dn mouse model of Down syndrome GABAergic hyperinnervation of dentate granule cells in the Ts65Dn mouse model of down syndrome: Exploring the role of App.The GIRK2 subunit is involved in IS-like seizures induced by GABA(B) receptor agonists.Enriching the environment to disinhibit the brain and improve cognition.G-Protein-Coupled Inwardly Rectifying Potassium (GIRK) Channel Activation by the p75 Neurotrophin Receptor Is Required for Amyloid β Toxicity.Cognitive and pharmacological insights from the Ts65Dn mouse model of Down syndrome The impact of spermine synthase (SMS) mutations on brain morphology.

P2860

Q22241596-C1F4D552-5417-4A0A-9AF3-3F1DFD606FE6 Q22252566-E7D68972-3058-4DC9-A24A-BCA1038E6D7F Q24619170-47CDCE0C-2E1C-465B-98B7-8D1788614D46 Q24654648-BABD2873-C488-48DE-BCF7-569F6B47A098 Q26863005-C6E9945F-CFF6-4F01-A6FD-1439A4322E23 Q27308052-362931A5-CC80-4059-AF7A-FEFBF03EFC82 Q30422188-41F01A31-1FF0-4271-9731-0C0DDB168D28 Q34010790-BD7C0BC3-9A09-460C-B329-637E7B30FC2E Q34500663-18247ED9-148C-4CF3-8EF4-68EB78889BE2 Q34964947-9B6FB401-00AE-46B1-8A23-CF799D27A803 Q34982914-A5E8BC0C-8F4E-459D-9333-A85A72B1B46B Q35177041-E1674FF5-BCC0-4AC9-B1CD-24F276695DD1 Q35418044-F91AEA19-77C3-4539-8049-D07C1D48E2DB Q35675287-54E7961F-5A9B-4AEC-A947-2456885DDBBC Q36106443-83DECF57-2E38-4F16-B6DA-504DC2FE349D Q36111546-2A879CFB-011B-4BE2-9948-4669FDFA200A Q36111747-10B0AEDE-36FD-4A6A-8303-D4326641D338 Q36138353-29B971E1-67A2-437D-AEF3-1D2B796BF0D4 Q36471320-7A37569D-68FB-429A-A3D7-7DB4608099A4 Q36665885-C5FEF476-585D-46A6-A057-33BEC1F7A57A Q36681400-92349168-756C-4060-A1DF-89D3F193B9DA Q36905053-D4872D0D-A5D2-43E4-BAB7-9A6B18E48B59 Q37201308-9E48F3B3-76D3-4B17-904B-4DB08F54117E Q37204848-EAA4DE2F-F995-4E63-90E9-2DF3DE79B130 Q37423613-08DE8956-2A3D-4106-98ED-0B42872DE67F Q37543845-7077934C-AD3E-4D94-A6EE-1A146B381324 Q37548268-A867FF9C-D097-4949-8EA7-F7C49EAF94D9 Q37683060-51033FDE-1738-423A-BE69-0B97F9DC14CC Q37912174-8C95F11B-C5C0-4A95-AB14-F5D31937FFCF Q38104700-55F4BAF0-0B31-4DE4-B544-1DB37188BB75 Q38165545-15D4A11F-0BE5-47DB-9B8F-75F054F9DDEE Q38175971-0A50622A-B01E-4A37-B869-D3A4E0DFDEF3 Q38435508-3E4F61E2-7283-490A-898B-89BC46DDA629 Q38565706-A51505F8-92EF-405E-B486-61E7BA133BB6 Q39324113-6721548A-E188-4976-85B3-1B3D1A92D35F Q40880509-B69BC08E-15E6-4240-AB7B-B59B224929A1 Q41134034-6D8BA005-B430-47D9-863B-BF70F2243B99 Q41334124-6B154ED2-3BF6-4904-ACDE-97B2599682C6 Q41811378-E1DF32A4-42D6-44A4-A4CD-B2567E5AEB7D Q42122757-40EB7945-0A6C-4DB1-AAA3-DDCB2B1D71FA

P2860

Ts65Dn, a mouse model of Down syndrome, exhibits increased GABAB-induced potassium current.

http://www.wikidata.org/entity/Q48375391

description

2006 nî lūn-bûn

@nan

2006年の論文

@ja

2006年学术文章

@wuu

2006年学术文章

@zh

2006年学术文章

@zh-cn

2006年学术文章

@zh-hans

2006年学术文章

@zh-my

2006年学术文章

@zh-sg

2006年學術文章

@yue

2006年學術文章

@zh-hant

name

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@en

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@nl

type

label

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@en

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@nl

prefLabel

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@en

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@nl

P1433

Q48375391-20F2E28F-DCF8-46E3-BB13-CA1F0A61CC90

P1476

Q48375391-ACF37F96-53CB-46E5-B397-C5504B4A72DD

P2093

Q48375391-97ED25F8-55E7-4BF0-904E-290B6849F6D4

Q48375391-BB61B622-3D59-4694-9EE6-8DE459DA78C0

Q48375391-CD940AB2-ABA5-4AE0-BFBC-6D09885D379E

P2860

Q48375391-0045A63B-FECC-42D4-A6D9-50B9B261A005

Q48375391-11E207FE-C14C-40C5-8A2C-006D80CB7968

Q48375391-160C6F15-5282-4DCE-A9EA-E79315D5B06A

Q48375391-180AAE0F-0620-443D-951B-45F72E4C188E

Q48375391-32E5C6C7-34E1-450C-A8F1-D462A028102B

Q48375391-374E713F-B4C8-4056-BB38-3C123BF6C692

Q48375391-3A247C19-6DDA-4F7E-A401-EE33B2D1F98C

Q48375391-3AED388F-1F6C-44AF-B6F8-37E0102339F5

Q48375391-3DDC77A7-169E-452A-814C-9EA3F2CB8957

Q48375391-3FB7DDC1-B2BC-4E5A-825C-0D7B7FEF5574

P304

Q48375391-6B6E0C83-2811-485F-8D8C-D25702856358

P31

Q48375391-FFE19962-AE07-460D-BAC6-466717237940

P356

Q48375391-2A1D2A3D-F4C2-4712-AC2B-FFED8AC92EC3

P407

Q48375391-CA90776C-33D6-454F-9C89-AC2DFA86B8AA

P433

Q48375391-4FFC2D4E-8AA7-43FE-82FD-BAB2765804FC

P478

Q48375391-DF1FEB38-C7A1-4D27-B7DD-3918AA9EF669

P577

Q48375391-1A103A05-E3A7-4392-ABE8-ACB92C7C0BBE

P5875

Q48375391-A8F6CDBC-A87D-4420-B27D-13D030621A40

P698

Q48375391-EDB6C835-C879-492F-B9F7-F0D19F299C13

P356

P1433

Journal of Neurophysiology

P1476

Ts65Dn, a mouse model of Down ...... BAB-induced potassium current.

@en

P2093

Richard J Siarey

http://www.w3.org/2001/XMLSchema#string

Tyler K Best

http://www.w3.org/2001/XMLSchema#string

Zygmunt Galdzicki

http://www.w3.org/2001/XMLSchema#string

P2860

Human gamma-aminobutyric acid type B receptors are differentially expressed and regulate inwardly rectifying K+ channels

The DNA sequence of human chromosome 21

Chromosome 21 and down syndrome: from genomics to pathophysiology

Allosteric interactions between GB1 and GB2 subunits are required for optimal GABA(B) receptor function

A chromosome 21 critical region does not cause specific Down syndrome phenotypes.

A trafficking checkpoint controls GABA(B) receptor heterodimerization.

Function of GB1 and GB2 subunits in G protein coupling of GABA(B) receptors.

Evidence that neuronal G-protein-gated inwardly rectifying K+ channels are activated by G beta gamma subunits and function as heteromultimers.

Tertiapin-Q blocks recombinant and native large conductance K+ channels in a use-dependent manner.

Molecular and cellular diversity of neuronal G-protein-gated potassium channels.

P304

892-900

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1152/JN.00626.2006

http://www.w3.org/2001/XMLSchema#string

P407

P433

1

http://www.w3.org/2001/XMLSchema#string

P478

97

http://www.w3.org/2001/XMLSchema#string

P577

2006-11-08T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

6704429

http://www.w3.org/2001/XMLSchema#string

P698

17093127

http://www.w3.org/2001/XMLSchema#string