Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
about
Neuroprotective Transcription Factors in Animal Models of Parkinson DiseaseDisorders of Upper Limb Movements in Ataxia-TelangiectasiaBehavioral genetic contributions to the study of addiction-related amphetamine effects.Investigation of the functional link between ATM and NBS1 in the DNA damage response in the mouse cerebellum.Neuroanatomical phenotyping in the mouse: the dopaminergic system.Ataxia-telangiectasia, cancer and the pathobiology of the ATM gene.The ATM cofactor ATMIN protects against oxidative stress and accumulation of DNA damage in the aging brain.Elevated Cu/Zn-SOD exacerbates radiation sensitivity and hematopoietic abnormalities of Atm-deficient miceReduced synchronization persistence in neural networks derived from atm-deficient mice.ATM is a cytoplasmic protein in mouse brain required to prevent lysosomal accumulation.Aspects of innate immunity and Parkinson's disease.Cell division in the CNS: protective response or lethal event in post-mitotic neurons?Malignant melanoma, breast cancer and other cancers in patients with Parkinson's disease.Mithramycin is a gene-selective Sp1 inhibitor that identifies a biological intersection between cancer and neurodegeneration.Chromatin modifications associated with DNA double-strand breaks repair as potential targets for neurological diseases.Dissecting the role of Engrailed in adult dopaminergic neurons--Insights into Parkinson disease pathogenesisNeurodegeneration in ataxia-telangiectasia: Multiple roles of ATM kinase in cellular homeostasis.Targeting p38 mitogen-activated protein kinase signaling restores subventricular zone neural stem cells and corrects neuromotor deficits in Atm knockout mouse.Whole genome expression analyses of single- and double-knock-out mice implicate partially overlapping functions of alpha- and gamma-synuclein.A role for vascular deficiency in retinal pathology in a mouse model of ataxia-telangiectasia.Malfunctioning DNA damage response (DDR) leads to the degeneration of nigro-striatal pathway in mouse brain.Elevated DNA double strand breaks and apoptosis in the CNS of scid mutant mice.Behavioural profiles of inbred mouse strains used as transgenic backgrounds. I: motor tests.Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing
P2860
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P2860
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@ast
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@en
type
label
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@ast
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@en
prefLabel
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@ast
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@en
P2093
P2860
P356
P1476
Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice
@en
P2093
P2860
P304
12653-12656
P356
10.1073/PNAS.95.21.12653
P407
P577
1998-10-01T00:00:00Z