Brijesh Singh

Dr. Brijesh Singh

Columbia University Irving Medical Center, New York, NY, USA
orcid

Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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27 May 2020 in Molecular Neurobiology
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Journal Article
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Sachchida Nand RaiSachchida Nand Rai
Sachchida Nand Rai
CSCharan Singh
Charan Singh
ASArti Singh
Arti Singh
Mohan Prasad SinghMohan Prasad Singh
Mohan Prasad Singh
BSBrijesh Singh
Brijesh Singh

1 April 2014 in Chemistry – A European Journal
Verified
Journal Article
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SPSharbari Palmal
Sharbari Palmal
AMAmit Ranjan maity
Amit Ranjan maity
BSBrijesh Singh
Brijesh Singh
SBSreetama Basu
Sreetama Basu
NJNikhil Ranjan Jana
Nikhil Ranjan Jana

10 November 2020 in 3 Biotech
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Journal Article
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Sachchida Nand RaiSachchida Nand Rai
Sachchida Nand Rai
VIVEK K CHATURVEDIVIVEK K CHATURVEDI
VIVEK K CHATURVEDI
PSPayal Singh
Payal Singh
BSBrijesh Singh
Brijesh Singh
Mohan Prasad SinghMohan Prasad Singh
Mohan Prasad Singh

25 January 2021 in Neural Regeneration Research
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Journal Article
Open access
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Sachchida Nand RaiSachchida Nand Rai
Sachchida Nand Rai
PSPayal Singh
Payal Singh
RVRitu Varshney
Ritu Varshney
VCVivek K. Chaturvedi
Vivek K. Chaturvedi
Emanuel VamanuEmanuel Vamanu
Emanuel Vamanu
BSBrijesh Singh
Brijesh Singh
Parkinson’s disease (PD) is one of the most debilitating brain diseases. Despite the availability of symptomatic treatments, response towards the health of PD patients remains scarce. To fulfil the medical needs of the PD patients, an efficacious and etiological treatment is required. In this review, we have compiled the information covering limitations of current therapeutic options in PD, novel drug targets for PD, and finally, the role of some critical beneficial natural products to control the progression of PD.

4 July 2014 in Human Molecular Genetics
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Journal Article
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MMMegha Maheshwari
Megha Maheshwari
SSShashi Shekhar
Shashi Shekhar
BSBrijesh Singh
Brijesh Singh
IJImran Jamal
Imran Jamal
NVNaman Vatsa
Naman Vatsa
NJNikhil Ranjan Jana
Nikhil Ranjan Jana
Huntington's disease (HD) is an inherited neurodegenerative disorder caused by abnormal expansion of CAG repeats in the gene encoding huntingtin. Mutant huntingtin undergoes proteolytic processing and its N-terminal fragment containing polyglutamine repeat accumulates as inclusion not only in nucleus but also in cytoplasm and neuronal processes. Here, we demonstrate that removal of ubiquitin ligase Ube3a selectively from HD mice brain resulted in accelerated disease phenotype and shorter lifespan in comparison with HD mice. The deficiency of Ube3a in HD mice brain also caused significant increase in global aggregates load, and these aggregates were less ubiquitinated when compared with age-matched HD mice. These Ube3a-maternal deficient HD mice also showed drastic reduction of DARPP-32, a dopamine-regulated phoshphoprotein in their striatum. These results emphasize the crucial role of Ube3a in the progression of HD and its immense potential as therapeutic target.

1 September 2017 in Neurobiology of Disease
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Journal Article
Closed access
IJImran Jamal
Imran Jamal
VKVipendra Kumar
Vipendra Kumar
NVNaman Vatsa
Naman Vatsa
SSShashi Shekhar
Shashi Shekhar
BSBrijesh Singh
Brijesh Singh
NJNikhil Ranjan Jana
Nikhil Ranjan Jana