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Articles by A Kumar
Total Records ( 3 ) for A Kumar
  A Kumar and L. Cowen
 

Motivation: While profile hidden Markov models (HMMs) are successful and powerful methods to recognize homologous proteins, they can break down when homology becomes too distant due to lack of sufficient training data. We show that we can improve the performance of HMMs in this domain by using a simple simulated model of evolution to create an augmented training set.

Results: We show, in two different remote protein homolog tasks, that HMMs whose training is augmented with simulated evolution outperform HMMs trained only on real data. We find that a mutation rate between 15 and 20% performs best for recognizing G-protein coupled receptor proteins in different classes, and for recognizing SCOP super-family proteins from different families.

  J Kumar , G Garg , A Kumar , E Sundaramoorthy , K. R Sanapala , S Ghosh , G Karthikeyan , L Ramakrishnan and Sengupta Indian Genome Variation Consortium
 

Background— An elevated level of homocysteine (hyperhomocysteinemia) has been implicated as an independent risk factor for cardiovascular diseases. Deficiency of dietary factors like vitamin B12, folate, and genetic variations can cause hyperhomocysteinemia. The prevalence of hyperhomocysteinemia in the Indian population is likely to be high because most Indians adhere to a vegetarian diet, deficient in vitamin B12. In the background of vitamin B12 deficiency, variations in genes involved in homocysteine metabolism might have a greater impact on homocysteine levels.

Methods and Results— We genotyped 44 nonsynonymous single-nucleotide polymorphisms (nsSNPs) from 11 genes involved in homocysteine metabolism and found only 14 to be polymorphic. These 14 nsSNPs were genotyped in 546 individuals recruited from a tertiary care center in New Delhi, India, and it was found that choline dehydrogenase (CHDH A119C) and methylenetetrahydrofolate reductase (MTHFR C677T) were significantly associated with plasma total homocysteine levels (P=0.009 and P=0.001, respectively). These 2 SNPs were further genotyped in 330 individuals recruited from the same center, and the association remained significant even after increasing the sample size. Furthermore, we found the possibility of a significant interaction between vegetarian diet and the 2 polymorphisms that could explain the variation of homocysteine levels. We also genotyped all the polymorphic nsSNPs in apparently healthy individuals recruited from 24 different subpopulations (based on their linguistic lineage) spread across the country to determine their basal frequencies. The frequencies of these SNPs varied significantly between linguistic groups.

Conclusion— Vegetarian diet along with CHDH A119C and MTHFR C677T play an important role in modulating the homocysteine levels in Indian population.

  Z Tang , P Arjunan , C Lee , Y Li , A Kumar , X Hou , B Wang , P Wardega , F Zhang , L Dong , Y Zhang , S. Z Zhang , H Ding , R. N Fariss , K. G Becker , J Lennartsson , N Nagai , Y Cao and X. Li
 

Platelet-derived growth factor CC (PDGF-CC) is the third member of the PDGF family discovered after more than two decades of studies on the original members of the family, PDGF-AA and PDGF-BB. The biological function of PDGF-CC remains largely to be explored. We report a novel finding that PDGF-CC is a potent neuroprotective factor that acts by modulating glycogen synthase kinase 3β (GSK3β) activity. In several different animal models of neuronal injury, such as axotomy-induced neuronal death, neurotoxin-induced neuronal injury, 6-hydroxydopamine–induced Parkinson’s dopaminergic neuronal death, and ischemia-induced stroke, PDGF-CC protein or gene delivery protected different types of neurons from apoptosis in both the retina and brain. On the other hand, loss-of-function assays using PDGF-C null mice, neutralizing antibody, or short hairpin RNA showed that PDGF-CC deficiency/inhibition exacerbated neuronal death in different neuronal tissues in vivo. Mechanistically, we revealed that the neuroprotective effect of PDGF-CC was achieved by regulating GSK3β phosphorylation and expression. Our data demonstrate that PDGF-CC is critically required for neuronal survival and may potentially be used to treat neurodegenerative diseases. Inhibition of the PDGF-CC–PDGF receptor pathway for different clinical purposes should be conducted with caution to preserve normal neuronal functions.

 
 
 
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