Zinc induces depletion and aggregation of endogenous TDP-43.

[1]  C. Lemere,et al.  Regional distribution of TDP‐43 inclusions in Alzheimer disease (AD) brains: Their relation to AD common pathology , 2009, Neuropathology : official journal of the Japanese Society of Neuropathology.

[2]  L. Fenart,et al.  Involvement of LRP1 and RAGE in the transport of β-amyloid (Aβ) peptide across the blood-brain barrier: Use of an in vitro model , 2009, Alzheimer's & Dementia.

[3]  L. Petrucelli,et al.  Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity , 2009, Proceedings of the National Academy of Sciences.

[4]  A. Goate,et al.  VCP Mutations Causing Frontotemporal Lobar Degeneration Disrupt Localization of TDP-43 and Induce Cell Death* , 2009, Journal of Biological Chemistry.

[5]  J. Trojanowski,et al.  Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 Proteinopathies* , 2009, Journal of Biological Chemistry.

[6]  Leah M. Williams,et al.  Potentiation of Amyotrophic Lateral Sclerosis (ALS)-associated TDP-43 Aggregation by the Proteasome-targeting Factor, Ubiquilin 1* , 2009, Journal of Biological Chemistry.

[7]  H. Akiyama,et al.  Phosphorylated and ubiquitinated TDP‐43 pathological inclusions in ALS and FTLD‐U are recapitulated in SH‐SY5Y cells , 2009, FEBS letters.

[8]  C. Masters,et al.  Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation , 2009, Proceedings of the National Academy of Sciences.

[9]  H. Akiyama,et al.  Phosphorylated TDP-43 in Alzheimer’s disease and dementia with Lewy bodies , 2009, Acta Neuropathologica.

[10]  S. Sakoda,et al.  Nuclear TAR DNA Binding Protein 43 Expression in Spinal Cord Neurons Correlates With the Clinical Course in Amyotrophic Lateral Sclerosis , 2009, Journal of neuropathology and experimental neurology.

[11]  N. Bresolin,et al.  The NOS3 G894T (Glu298Asp) polymorphism is a risk factor for frontotemporal lobar degeneration , 2009, European journal of neurology.

[12]  M. Portero-Otín,et al.  Type-Dependent Oxidative Damage in Frontotemporal Lobar Degeneration: Cortical Astrocytes Are Targets of Oxidative Damage , 2008, Journal of neuropathology and experimental neurology.

[13]  C. Masters,et al.  Rapid Restoration of Cognition in Alzheimer's Transgenic Mice with 8-Hydroxy Quinoline Analogs Is Associated with Decreased Interstitial Aβ , 2008, Neuron.

[14]  A. Isaacs,et al.  TDP-43 is a culprit in human neurodegeneration, and not just an innocent bystander , 2008, Mammalian Genome.

[15]  J. Trojanowski,et al.  Disturbance of Nuclear and Cytoplasmic TAR DNA-binding Protein (TDP-43) Induces Disease-like Redistribution, Sequestration, and Aggregate Formation* , 2008, Journal of Biological Chemistry.

[16]  H. Ohshima,et al.  Remarks on Muscle Contraction Mechanism , 2008, International journal of molecular sciences.

[17]  B. Traynor,et al.  Genetics of sporadic amyotrophic lateral sclerosis. , 2007, Human molecular genetics.

[18]  K. Kröncke Cellular stress and intracellular zinc dyshomeostasis. , 2007, Archives of biochemistry and biophysics.

[19]  J. Morris,et al.  TDP-43 in familial and sporadic frontotemporal lobar degeneration with ubiquitin inclusions. , 2007, The American journal of pathology.

[20]  P. Francis,et al.  Metals ions and neurodegeneration , 2007, BioMetals.

[21]  H. Akiyama,et al.  TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. , 2006, Biochemical and biophysical research communications.

[22]  Bruce L. Miller,et al.  Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis , 2006, Science.

[23]  S. Sensi,et al.  Oxidative stress and brain aging: is zinc the link? , 2006, Biogerontology.

[24]  W. Maret Zinc coordination environments in proteins as redox sensors and signal transducers. , 2006, Antioxidants & redox signaling.

[25]  Weidong Wu,et al.  Zn2+-induced IL-8 expression involves AP-1, JNK, and ERK activities in human airway epithelial cells. , 2006, American journal of physiology. Lung cellular and molecular physiology.

[26]  D. Handy,et al.  The Short N-terminal Domains of STIM1 and STIM2 Control the Activation Kinetics of Orai1 Channels* , 2006, The Journal of Biological Chemistry.

[27]  S. Pantano,et al.  Human, Drosophila, and C.elegans TDP43: nucleic acid binding properties and splicing regulatory function. , 2005, Journal of molecular biology.

[28]  C. Masters,et al.  Tyrosine gated electron transfer is key to the toxic mechanism of Alzheimer's disease β‐amyloid , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[29]  L. Pettigrew,et al.  Rapid expression of neuronal and inducible nitric oxide synthases during post-ischemic reperfusion in rat brain , 2001, Brain Research.

[30]  C. T. Aravindakumar,et al.  Nitric oxide induces Zn2+ release from metallothionein by destroying zinc-sulphur clusters without concomitant formation of S-nitrosothiol. , 1999, The Biochemical journal.

[31]  C. Masters,et al.  Syndromes of amyotrophic lateral sclerosis and dementia: Relation to transmissible Creutzfeldt‐Jakob disease , 1983, Annals of neurology.

[32]  A. Bush Drug development based on the metals hypothesis of Alzheimer's disease. , 2008, Journal of Alzheimer's disease : JAD.

[33]  C. Masters,et al.  Mechanisms of A beta mediated neurodegeneration in Alzheimer's disease. , 2008, The international journal of biochemistry & cell biology.

[34]  C. Masters,et al.  Neurotoxicity from glutathione depletion is mediated by Cu-dependent p53 activation. , 2008, Free radical biology & medicine.

[35]  C. Masters,et al.  Mechanisms of Aβ mediated neurodegeneration in Alzheimer's disease , 2008 .

[36]  Weidong Wu,et al.  Zn 2-induced IL-8 expression involves AP-1 , JNK , and ERK activities in human airway epithelial cells , 2006 .

[37]  S. Sensi,et al.  Zinc dyshomeostasis: a key modulator of neuronal injury. , 2005, Journal of Alzheimer's disease : JAD.