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Publications

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Research papers in last 5 years....

Decreased Anterograde Transport Coupled with Sustained Retrograde Transport Contributes to Reduced Axonal Mitochondrial Density in Tauopathy neurons

Front. Mol. Neurosci. Sec. Brain Disease Mechanisms doi: 10.3389/fnmol.2022.927195

Findings from this study indicate that decreased kinesin-mediated transport coupled with sustained retrograde transport might reduce axonal mitochondria in tauopathy neurons, thus contributing to the synaptic deficits in Alzheimer’s Disease (AD) and other tauopathies.

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Pleiotropic roles of evolutionarily conserved signaling intermediate in toll pathway (ECSIT) in pathophysiology

J Cell Physiol, 2022 Sep;237(9):3496-3504. doi: 10.1002/jcp.30832.

This review summarizes the diverse functions of ECSIT and its involvement in pathophysiological conditions such as Alzheimer's, oxidative stress, and infection.

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Broad activation of the Parkin pathway induces synaptic mitochondrial deficits in early tauopathy

Brain, 2022 Mar 29;145(1):305-323. doi: 10.1093/brain/awab243.

In this paper we have shown new mechanistic insights into how parkin activation-enhanced Miro1 degradation and impaired mitochondrial anterograde transport drive tauopathy-linked synaptic pathogenesis and establish a foundation for future investigations into new therapeutic strategies to prevent synaptic deterioration in Alzheimer's disease and other tauopathies.

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Growth hormone induces mitotic catastrophe of glomerular podocytes and contributes to proteinuria

Cell Death Dis. 2021 Apr 1;12(4):342.doi: 10.1038/s41419-021-03643-6.

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Rotenone-induced reactive oxygen species signal the recruitment of STAT3 to mitochondria

FEBS Lett 2020 May;594(9):1403-1412.doi: 10.1002/1873-3468.13741. Epub 2020 Feb 18.

This work demonstrates a novel STAT3-mediated feedback mechanism to maintain redox homeostasis during oxidative stress.

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Genetic variants in the bipolar disorder risk locus SYNE1 that affect CPG2 expression and protein function

Mol Psychiatry 2021 Feb;26(2):508-523. doi: 10.1038/s41380-018-0314-z. Epub 2019 Jan 4.

In this work we identify genetic variants within the CPG2 promoter region, and show that they negatively affect gene expression. We also identify missense single nucleotide polymorphisms (SNPs) in CPG2 coding regions that affect CPG2 expression, localization, and synaptic function. Our findings link genetic variation in the CPG2 region of SYNE1 with a mechanism for glutamatergic synapse dysfunction that could underlie susceptibility to BD in some individuals. .

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Impaired axonal retrograde trafficking of the retromer complex augments lysosomal deficits in Alzheimer's disease neurons

Hum Mol Genet. 2017 Nov 15;26(22):4352-4366.doi: 10.1093/hmg/ddx321.

Our study provides new insights into the regulation of retromer trafficking through retrograde axonal transport to fulfil its function in promoting lysosome biogenesis in the soma, suggesting a potential approach for rescuing lysosomal proteolysis deficits in AD.

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Releasing Syntaphilin Removes Stressed Mitochondria from Axons Independent of Mitophagy under Pathophysiological Conditions

Neuron, 2017 May 3;94(3):595-610.e6.doi: 10.1016/j.neuron.2017.04.004.

Our study provides new mechanistic insights into the maintenance of axonal mitochondrial quality through SNPH-mediated coordination of mitochondrial stress and motility before activation of Parkin-mediated mitophagy

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Regulation of Synaptic Amyloid-β Generation through BACE1 Retrograde Transport in a Mouse Model of Alzheimer's Disease

J Neurosci. 2017 Mar 8;37(10):2639-2655. doi: 10.1523/JNEUROSCI.2851-16.2017.

Our study uncovers a new pathway that controls synaptic APP processing by enhancing axonal BACE1 trafficking, thereby advancing our fundamental knowledge critical for ameliorating Aβ-linked synaptic pathology.

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Impaired retrograde transport of axonal autophagosomes contributes to autophagic stress in Alzheimer's disease neurons

Elife. 2017 Jan 13;6:e21776.doi: 10.7554/eLife.21776.

This study shows that autophagosomes predominantly accumulate in the axons and at the ends of axons during Alzheimer’s disease. Amyloid-β aggregates associate with autophagosomes in the axons and interact with dynein motors. This disrupts the interaction between dynein and Snapin and impairs dynein binding to the autophagosomes, trapping the autophagosomes in the axons. Increasing the production of Snapin proteins inside the mouse neurons enhances dynein binding to autophagosomes and thus helps these structures move to the cell body.

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SNX-1 and RME-8 oppose the assembly of HGRS-1/ESCRT-0 degradative microdomains on endosomes

Proc Natl Acad Sci U S A. 2017 Jan 17;114(3):E307-E316. doi: 10.1073/pnas.1612730114.

In this study we show that retromer cross-regulates ESCRT to maintain an appropriate balance of each activity within a given endosome. The ESCRT and retromer pathways drive opposing endosomal functions that must somehow coexist; therefore, understanding the segregation of ESCRT and retromer domains on the endosome may be particularly relevant to understanding endosome function. We propose that an antagonistic relationship between retromer-associated proteins and ESCRT is important for maintaining a balance of opposing sorting activities within an endosome. These activities may be particularly important to rebalance such activities as cargo load distribution change and cellular physiology changes to keep pace with the cellular environment.

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Autophagy-mediated Regulation of BACE1 Protein Trafficking and Degradation

J Biol Chem 2017 Feb 3;292(5):1679-1690. doi: 10.1074/jbc.M116.766584. Epub 2016 Dec 27.

This study provides new insights into autophagy-mediated regulation of BACE1 turnover and APP processing, thus building a foundation for future development of potential Alzheimer's disease therapeutic strategies.

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