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11篇 您的检索式：作者名="Durcan L"

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		题名	作者	年代	出处	被引量
	1	Predictive vale of soluble intercellular adhesion molecule-1 for risk of ischemic event in individuals with cerebrovascular disease 显示文摘	Ehrensperger E Minuk J Durcan L	2005	Cerebrovasc Dis2005，20，6：	1
	2	Predictive value of soluble intercellular adhesion molecule-1 for risk of ischemic events in individuals with cerebrovascular disease 显示文摘	Ehrensperger E Minuk J Durcan L	2005	Cerebrovasc Dis2005，20，6：	1
	3	Predictive value of soluble intercellular adhesion molecule-1 for risk of ischemic events in indi- viduals with cerebrovascular disease 显示文摘	Ehrensperger E Minuk J Durcan L	2005	Cerebrova~ Dis2005，20，6：	1
	4	Centrosome duplication pro- ceeds during mimosine-induced Gl cell cycle arrest 显示文摘	Durcan TM Halpin ES Casaletti L	2008	J Cell Physiol2008，215，：	1
	5	Centro2 some duplication proceeds during mimosine-induced G1 cell cycle arrest显示文摘	Durcan TM Halpin ES Casaletti L	2008	J Cell Physiol2008，215，：	1
	6	Centrosome duplication proceeds during mimosine-induced G: cell cycle arrest 显示文摘	Durcan TM Halpin ES Casaletti L	2008	J Cell Physiol2008，215，1：	1
	7	Predictive value of soluble intercellular adhesion molecule-I for risk of iachemic events in individuals with cerebrovaseular disease显示文摘	Minuk J Durcan L	2005	Cerebrovaac Dis2005，20，6：	1
	8	Predictive value of soluble intercellular adhesion molecule-1 for risk of ischemic events in individuals with cerebrovascular disease显示文摘	Ehrensperger E Minuk J Durcan L	2005	Cerebrovasc Dis2005，20，6：	1
	9	Chromosomal localiza tion,and partial genomic structure of the human peroxisome proliferator-activated receptor-γ(h PPARγ) gene显示文摘	Negri C Yen C J Gavrilova O Rumberger J M Durcan M J Yarnall D P Hawkins A L Griffin C A Burns D K Roth J Reitman M Shuldiner A R	1997	Biochem Biophys Res Commun1997，233，：	1
	10	Centrosome duplication proceeds during mimosine - induced G1 cell cycle arrest 显示文摘	DURCAN T M HALPIN E S CASALETrl L	2008	J Cell Physiol2008，215，1：	1
	11	TDP-43 dysregulation and neuromuscular junction disruption in amyotrophic lateral sclerosis显示文摘Amyotrophic lateral sclerosis(ALS)is a disease characterized by upper and lower motor neuron(MN)loss with a signature feature of cytoplasmic aggregates containing TDP-43,which are detected in nearly all patients.Mutations in the gene that encodes TDP-43(TARBDP)are known to result in both familial and sporadic ALS.In ALS,disruption of neuro-muscular junctions(NMJs)constitutes a critical event in disease pathogenesis,leading to denervation atrophy,motor impairments and disability.Morphological defects and impaired synaptic transmission at NMJs have been reported in several TDP-43 animal models and in vitro,linking TDP-43 dysregulation to the loss of NMJ integrity in ALS.Through the lens of the dying-back and dying-forward hypotheses of ALS,this review discusses the roles of TDP-43 related to synaptic function,with a focus on the potential molecular mechanisms occurring within MNs,skeletal muscles and glial cells that may contribute to NMJ disruption in ALS.	Sarah Lépine Maria José Castellanos-Montiel Thomas Martin Durcan	2022	Translational Neurodegeneration2022，11，1：	0

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