V
Venkata Prasuja Nakka
Researcher at University of Wisconsin-Madison
Publications - 12
Citations - 1086
Venkata Prasuja Nakka is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Unfolded protein response & Endoplasmic reticulum. The author has an hindex of 8, co-authored 9 publications receiving 933 citations. Previous affiliations of Venkata Prasuja Nakka include University of Hyderabad & Central Drug Research Institute.
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Journal ArticleDOI
Molecular Mechanisms of Apoptosis in Cerebral Ischemia: Multiple Neuroprotective Opportunities
TL;DR: This review briefly focuses I/R injury-induced multiple mechanisms of apoptosis, involving key apoptotic regulators and their emerging roles in orchestrating cell death programme and the role of autophagy in modulating cell survival/death during cerebral ischemia.
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Endoplasmic Reticulum Stress Plays Critical Role in Brain Damage After Cerebral Ischemia/Reperfusion in Rats
TL;DR: The enhanced expression of GRP78, Caspase-12, CHOP/GADD153, ATF4 and processing of xbp1 mRNA in the affected brain regions clearly indicate the critical involvement of ER-mediated cell death/survival mechanisms and also collectively demonstrated the activation of unfolded protein response (UPR).
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Crosstalk Between Endoplasmic Reticulum Stress, Oxidative Stress, and Autophagy: Potential Therapeutic Targets for Acute CNS Injuries.
TL;DR: The existing and developing therapeutic options aimed to reduce ER stress to protect the CNS after acute injuries are discussed, highlighting the diverse molecular mechanisms associated with ER stress and its relation to oxidative stress and autophagy.
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Effect of Focal Ischemia on Long Noncoding RNAs
TL;DR: Stroke significantly alters cerebral lncRNAs expression profiles and promoters of stroke-responsive lncRNA genes and their homologous protein-coding genes showed highly overlapping transcription factor binding sites despite presence of open reading frames.
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MicroRNA miR-29c down-regulation leading to de-repression of its target DNA methyltransferase 3a promotes ischemic brain damage.
TL;DR: It is suggested that miR-29c is a pro-survival miRNA and its down-regulation is a promoter of ischemic brain damage by acting through its target DNMT3a.