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Dr. Siva Sundara Kumar Durairajan
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Academic Career Length
23Years (2004-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 December 2012 in Neurobiology of Aging
Journal Article
SDSiva Sundara Kumar Durairajan
Siva Sundara Kumar DurairajanLLLiang-Feng Liu
Liang-Feng Liu
JLJiahong Lu
Jiahong LuLCLei-Lei Chen
Lei-Lei Chen
QYQiuju Yuan
Qiuju Yuan
MLMin LI
Min LI +4
1 July 2016 in Autophagy
Journal Article
JSJu-Xian Song
Ju-Xian SongYSYue-Ru Sun
Yue-Ru Sun
IPIvana Peluso
Ivana Peluso
YZYu Zeng
Yu Zeng
XYXing Yu
Xing Yu
MLMin LI
Min LI +14
Autophagy dysfunction is a common feature in neurodegenerative disorders characterized by accumulation of toxic protein aggregates. Increasing evidence has demonstrated that activation of TFEB (transcription factor EB), a master regulator of autophagy and lysosomal biogenesis, can ameliorate neurotoxicity and rescue neurodegeneration in animal models. Currently known TFEB activators are mainly inhibitors of MTOR (mechanistic target of rapamycin [serine/threonine kinase]), which, as a master regulator of cell growth and metabolism, is involved in a wide range of biological functions. Thus, the identification of TFEB modulators acting without inhibiting the MTOR pathway would be preferred and probably less deleterious to cells. In this study, a synthesized curcumin derivative termed C1 is identified as a novel MTOR-independent activator of TFEB. Compound C1 specifically binds to TFEB at the N terminus and promotes TFEB nuclear translocation without inhibiting MTOR activity. By activating TFEB, C1 enhances autophagy and lysosome biogenesis in vitro and in vivo. Collectively, compound C1 is an orally effective activator of TFEB and is a potential therapeutic agent for the treatment of neurodegenerative diseases.
1 January 2012 in Autophagy
Journal Article
JLJiahong Lu
Jiahong LuJTJie-Qiong Tan
Jie-Qiong TanSDSiva Sundara Kumar Durairajan
Siva Sundara Kumar DurairajanLLLiang-Feng Liu
Liang-Feng LiuZZZhuo-Hua Zhang
Zhuo-Hua ZhangMLMin LI
Min LI +3
Accumulation of α-synuclein (α-syn) in the brain is a pathogenic feature and also a causative factor of Parkinson disease. Isorhynchophylline (IsoRhy) is a major tetracyclic oxindole alkaloid isolated from the Chinese herbal medicine Uncaria rhynchophylla (Miq.)Jacks (Gouteng in Chinese), which has been used for the treatment of neurological diseases in East Asia for centuries. Here we report a novel function of IsoRhy as a neuronal autophagy inducer. IsoRhy induced autophagy in different neuronal cell lines, including N2a, SH-SY5Y and PC12 cells, and also in primary cortical neurons. Furthermore, IsoRhy induced autophagy in the fat bodies of Drosophila. IsoRhy promoted clearance of wild-type, A53T and A30P α-syn monomers, α-syn oligomers and α-syn/synphilin-1 aggresomes in neuronal cells via the autophagy-lysosome pathway. More importantly, IsoRhy was able to decrease the expression levels of wild-type and A53T α-syn protein in differentiated human dopaminergic neurons. Notably, IsoRhy-induced autophagy was independent of the mTOR pathway but dependent on the function of Beclin 1. Taken together, data from this study raise the possibility that oxindole alkaloid derivatives may serve as a means to stimulate autophagy in neuronal cells, thereby exerting preventive and therapeutic values against neurodegenerative diseases such as Parkinson disease by reducing pathogenic protein aggregates in neurons.
26 January 2011 in ChemBioChem
Journal Article
JLJiahong Lu
Jiahong LuMAMustafa Taleb Ardah
Mustafa Taleb Ardah
SDSiva Sundara Kumar Durairajan
Siva Sundara Kumar DurairajanLLLiang‐Feng Liu
Liang‐Feng Liu
LXLi‐Xia Xie
Li‐Xia Xie
MLMin LI
Min LI +4
19 December 2019 in Aging Cell
Journal Article
JSJu‐Xian Song
Ju‐Xian Song
SMSandeep Malampati
Sandeep Malampati
YZYu Zeng
Yu Zeng
SDSiva Sundara Kumar Durairajan
Siva Sundara Kumar DurairajanCYChuanbin Yang
Chuanbin YangMLMin LI
Min LI +9
Accumulating studies have suggested that targeting transcription factor EB (TFEB), an essential regulator of autophagy‐lysosomal pathway (ALP), is promising for the treatment of neurodegenerative disorders, including Alzheimer's disease (AD). However, potent and specific small molecule TFEB activators are not available at present. Previously, we identified a novel TFEB activator named curcumin analog C1 which directly binds to and activates TFEB. In this study, we systematically investigated the efficacy of curcumin analog C1 in three AD animal models that represent beta‐amyloid precursor protein (APP) pathology (5xFAD mice), tauopathy (P301S mice) and the APP/Tau combined pathology (3xTg‐AD mice). We found that C1 efficiently activated TFEB, enhanced autophagy and lysosomal activity, and reduced APP, APP C‐terminal fragments (CTF‐β/α), β‐amyloid peptides and Tau aggregates in these models accompanied by improved synaptic and cognitive function. Knockdown of TFEB and inhibition of lysosomal activity significantly inhibited the effects of C1 on APP and Tau degradation in vitro. In summary, curcumin analog C1 is a potent TFEB activator with promise for the prevention or treatment of AD.
1 March 2008 in Neurochemistry International
Journal Article
SDSiva Sundara Kumar Durairajan
Siva Sundara Kumar DurairajanQYQiuju Yuan
Qiuju Yuan
LXLixia Xie
Lixia Xie
WCWing-Sai Chan
Wing-Sai Chan
WKWan-Fung Kum
Wan-Fung Kum
MLMin LI
Min LI +5
About Me
Dr. D.Siva Sundara Kumar is as Associate Professor at the Department of Microbiology, Central University of Tamil Nadu, India. Prior to this role, He held a position as a Research Assistant Professor at Hong Kong Baptist University (HKBU) in Hong Kong. During hi tenure at HKBU, my responsibilities encompassed both teaching and research endeavours, with a primary focus on microbiology and neurodegenerative diseases. I earned my doctoral degree in fungal biotechnology from the University of Hong Kong (HKU) in 2004. During my initial postdoctoral training at the Vaccine R&D Centre at the National Health Research Institutes in Taiwan (2005-2006), I actively contributed to a project titled "Identification of an alternative receptor for the SARS CoV virus." Subsequently, sought to further enhance my expertise in neuroprotective strategies for addressing neurodegenerative diseases, prompting my decision to assume a postdoctoral fellow position at the School of Chinese Medicine at HKBU from 2006 to 2012. In recognition of my achievements, I was honoured with an outstanding research award in fungal biotechnology from the Venus International Foundation in India in 2022My research contributions are also underscored by the publication of 49 papers in peer-reviewed journalsreflecting an H-index of 29. Additionally, I have secured two patents in the United States and two in China, along with receiving nine extramural grants from institutions in Hong Kong and India.