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Ambreena Siddiq

Researcher at Cornell University

Publications -  13
Citations -  1337

Ambreena Siddiq is an academic researcher from Cornell University. The author has contributed to research in topics: Neuroprotection & Hypoxia-inducible factors. The author has an hindex of 13, co-authored 13 publications receiving 1267 citations. Previous affiliations of Ambreena Siddiq include Harvard University & Burke Rehabilitation Hospital.

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HDAC6 is a target for protection and regeneration following injury in the nervous system

TL;DR: It is shown that pan-HDAC inhibition not only promotes neuronal protection against oxidative stress, a common mediator of injury in many neurological conditions, but also promotes neurite growth on myelin-associated glycoprotein and chondroitin sulfate proteoglycan substrates.
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Selective Inhibition of Hypoxia-Inducible Factor (HIF) Prolyl-Hydroxylase 1 Mediates Neuroprotection against Normoxic Oxidative Death via HIF- and CREB-Independent Pathways

TL;DR: Together, these studies suggest that iron chelators can prevent normoxic oxidative neuronal death through selective inhibition of PHD1 but independent of HIF-1α and CREB; and that Hif-2α, not HIF -PHD, regulates susceptibility to normoxic antioxidant neuronal death.
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Hypoxia inducible factor prolyl 4-hydroxylase enzymes: center stage in the battle against hypoxia, metabolic compromise and oxidative stress.

TL;DR: The possible role of PHDs in regulation of both HIF-dependent and -independent cell survival pathways in the nervous system with particular attention to the co-substrate requirements for these enzymes is discussed.
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Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity: model for the potential involvement of the hypoxia-inducible factor pathway in Parkinson disease.

TL;DR: Novel data is provided extending the possible therapeutic utility of HIF induction to a Parkinson disease model of neurodegeneration, which may prove beneficial not only in this disorder itself but also in other diseases associated with metal-induced oxidative stress.