Z
Zsolt Tallóczy
Researcher at Columbia University
Publications - 18
Citations - 8717
Zsolt Tallóczy is an academic researcher from Columbia University. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 14, co-authored 16 publications receiving 8128 citations. Previous affiliations of Zsolt Tallóczy include Novartis & University of Medicine and Dentistry of New Jersey.
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Journal ArticleDOI
Regulation of starvation- and virus-induced autophagy by the eIF2α kinase signaling pathway
Zsolt Tallóczy,Wenxia Jiang,Herbert W. Virgin,David A. Leib,Donalyn Scheuner,Randal J. Kaufman,Eeva-Liisa Eskelinen,Beth Levine +7 more
TL;DR: Autophagy is a novel evolutionarily conserved function of the eIF2α kinase pathway that is targeted by viral virulence gene products.
Journal ArticleDOI
Dopamine-modified α-synuclein blocks chaperone-mediated autophagy
Marta Martinez-Vicente,Zsolt Tallóczy,Susmita Kaushik,Ashish C. Massey,Joseph R. Mazzulli,Eugene V. Mosharov,Roberto Hodara,Ross A. Fredenburg,Du Chu Wu,Antonia Follenzi,William T. Dauer,Serge Przedborski,Harry Ischiropoulos,Peter T. Lansbury,David Sulzer,Ana Maria Cuervo +15 more
TL;DR: It is proposed that dopamine-induced autophagic inhibition could explain the selective degeneration of PD dopaminergic neurons through blockage of CMA, which increases cellular vulnerability to stressors.
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Autophagy protects against Sindbis virus infection of the central nervous system.
TL;DR: A function for autophagy in mammalian antiviral defense is suggested: a cell-autonomous mechanism in which p62 adaptor-mediated autophagic viral protein clearance promotes cell survival.
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PKR-dependent autophagic degradation of herpes simplex virus type 1.
TL;DR: Qualitative morphologic evidence of PKR-dependent xenophagic degradation of herpes simplex virions and biochemical evidence ofPKR and eIF2alpha-dependent degradation of HSV-1 proteins, both of which are blocked by ICP34.5.5 are shown.
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Neuronal pigmented autophagic vacuoles: lipofuscin, neuromelanin, and ceroid as macroautophagic responses during aging and disease.
TL;DR: The most striking morphologic change in neurons during normal aging is the accumulation of autophagic vacuoles filled with lipofuscin or neuromelanin pigments, which may eventually interfere with normal degradative pathways and endocytic/secretory tasks such as appropriate response to growth factors.