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Asa Abeliovich
Researcher at Columbia University
Publications - 43
Citations - 5918
Asa Abeliovich is an academic researcher from Columbia University. The author has contributed to research in topics: Parkinson's disease & Neurodegeneration. The author has an hindex of 21, co-authored 43 publications receiving 5465 citations. Previous affiliations of Asa Abeliovich include NewYork–Presbyterian Hospital & Watson School of Biological Sciences.
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Journal ArticleDOI
A MicroRNA Feedback Circuit in Midbrain Dopamine Neurons
Jongpil Kim,Keiichi Inoue,Keiichi Inoue,Jennifer Ishii,Jennifer Ishii,William B. Vanti,William B. Vanti,Sergey V. Voronov,Sergey V. Voronov,Elizabeth P. Murchison,Elizabeth P. Murchison,Gregory J. Hannon,Gregory J. Hannon,Asa Abeliovich,Asa Abeliovich +14 more
TL;DR: AmiR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3, and a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion is proposed.
Journal ArticleDOI
DJ-1 Is a Redox-Dependent Molecular Chaperone That Inhibits α-Synuclein Aggregate Formation
TL;DR: It is demonstrated that DJ-1 functions as a redox-sensitive molecular chaperone that is activated in an oxidative cytoplasmic environment and extends to α-synuclein, a protein implicated in PD pathogenesis.
Journal ArticleDOI
The Familial Parkinsonism Gene LRRK2 Regulates Neurite Process Morphology
TL;DR: It is shown that PD-associated LRRK2 mutations display disinhibited kinase activity and induce a progressive reduction in neurite length and branching both in primary neuronal cultures and in the intact rodent CNS.
PatentDOI
Rab7l1 interacts with lrrk2 to modify intraneuronal protein sorting and parkinson' s disease risk
TL;DR: These studies implicate retromer and lysosomal pathway alterations in PD risk and show that the consequences of variants at 2 such loci, PARK16 and LRRK2, are highly interrelated, both in terms of their broad impacts on human brain transcriptomes of unaffected carriers and in their associations with PD risk.
Journal ArticleDOI
Parkin Is a Component of an SCF-like Ubiquitin Ligase Complex and Protects Postmitotic Neurons from Kainate Excitotoxicity
John F. Staropoli,Caroline McDermott,Cécile Martinat,Brenda A. Schulman,Elena Y. Demireva,Asa Abeliovich +5 more
TL;DR: Parkin deficiency potentiates the accumulation of cyclin E in cultured postmitotic neurons exposed to the glutamatergic excitotoxin kainate and promotes their apoptosis, and parkin overexpression attenuates the accumulation in toxin-treated primary neurons, including midbrain dopamine neurons, and protects them from apoptosis.