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| 1 | Nigrostriatal neuronal death following chronic dichlorvos exposure:crosstalk between mitochondrial impairments,or synuclein aggregation,oxidative damage and behavioral changes 显示文摘 | Binukumar BK Bal A Kandimalla R J | 2010 | Mol Brain2010，3，： | 1 |
| 2 | Mitochondrial energy metabolism impairment and liver dysfunction following chronic exposure to dichlorvos 显示文摘 | Binukumar BK Bal A Kandimalla RJ | 2010 | Toxicology2010，270，23： | 1 |
| 3 | TFP5, a peptide derived from p35, a Cdk5 neuronal activator, rescues cortical neurons from glucose toxicity显示文摘 | Binukumar BK Zheng YL Shukla V | 2014 | J Atzheimers Dis2014，39，4： | 1 |
| 4 | Protective efficacy of co- enzyme Q10 against DDYP-induced cognitive impairments and neurode- generation in rats显示文摘 | Binukumar BK Gupta N Sunkaria A | 2012 | Neurotox Res2012，21，： | 1 |
| 5 | TFP5/TP5 peptide provides neuroprotection in the MPTP model of Parkinson's disease显示文摘Cyclin-dependent kinase 5(Cdk5) is a member of the serine-threonine kinase family of cyclin-dependent kinases. Cdk5 is critical to normal mammalian nervous system development and plays important regulatory roles in multiple cellular functions. Recent evidence indicates that Cdk5 is inappropriately activated in several neurodegenerative conditions, including Parkinson's disease(PD). PD is a chronic neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra, decreased striatal dopamine levels, and consequent extrapyramidal motor dysfunction. During neurotoxicity, p35 is cleaved to form p25. Binding of p25 with Cdk5 leads deregulation of Cdk5 resulting in number of neurodegenerative pathologies. To date, strategies to specifically inhibit Cdk5 hyperactivity have not been successful without affecting normal Cdk5 activity. Here we show that inhibition of p25/Cdk5 hyperactivation through TFP5/TP5, truncated 24-aa peptide derived from the Cdk5 activator p35 rescues nigrostriatal dopaminergic neurodegeneration induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP/MPP+) in a mouse model of PD. TP5 peptide treatment also blocked dopamine depletion in the striatum and improved gait dysfunction after MPTP administration. The neuroprotective effect of TFP5/TP5 peptide is also associated with marked reduction in neuroinflammation and apoptosis. Here we show inhibition of Cdk5/p25-hyperactivation by TFP5/TP5 peptide, which identifies Cdk5/p25 as a potential therapeutic target to reduce neurodegeneration in PD. | Binukumar BK Harish C.Pant | 2016 | Neural Regeneration Research2016，11，5： | 1 |
| 6 | Serum paraoxonase-1(PON1)activities(PONase/AREase)and polymorphisms in patients with type 2 diabetes mellitus in a North-West Indian population显示文摘 | Gupta N Binukumar BK Singh S | 2011 | Gene2011，487，： | 1 |
| 7 | Nigrostriatal neuronal death following chronic dichlorvos exposure:crosstal between mitochondrial impairments,αsynuclein aggregation,oxidative damage and behavioral changes显示文摘 | Binukumar BK Bal A Kandimalla RJ | 2011 | Mol Brain2011，133，11： | 1 |
| 8 | TFP5 a peptide derived from p35 a Cdk5 neuronalactivator rescues cortical neurons from glucose toxicity 显示文摘 | Binukumar BK | 2014 | JAlzheimers Dis2014，39，4： | 1 |
| 9 | Ni-grostriatal neuronal death following chronic dichlorvos dichlorvos expo-sure: crosstalk between mitochondrial impairments, a-synuclein aggregation, axidative damage and behavioral changes显示文摘 | Binukumar BK Amanjit B Ramesh JL | 2010 | Mol Brain2010，3，1： | 1 |
| 10 | Mitochondrial energy metabolism impairment and liver dysfunction following chronic exposure to dichlorvos显示文摘 | Binukumar BK Bal A Kandimalla R | 2010 | Toxicology2010，270，： | 1 |
| 11 | Mitochondrial energy metabolism impairment and liver dysfunction following chronic expo- sure to dichlorvos显示文摘 | Binukumar BK Bal A Kandimalla R | 2010 | Toxicology2010，270，： | 1 |
| 12 | Cerebrospinal flu- id profile of amyloid 1342 ( Aβ42 ) , hTau and ubiquitin in North In- dian Alzheimer's disease patients 显示文摘 | Ramesh JL Prabhakar S Binukumar BK | 2011 | Neurosei Lett2011，487，： | 1 |
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