Experts and Doctors on humans in Kanpur, Uttar Pradesh, India


Locale: Kanpur, Uttar Pradesh, India
Topic: humans

Top Publications

  1. Gupta J. Land use planning in India. J Hazard Mater. 2006;130:300-6 pubmed
    ..level of industrialization in different parts, need for creation of jobs, eco-sensitive regions, tribal regions, historical monuments, etc. This paper discusses the current scene in India and the near future aspects. ..
  2. Jena A, Duggal R. Atypical goldenhar syndrome: a case report. J Clin Pediatr Dent. 2006;31:118-22 pubmed
    ..The hypotrophy of left hemisphere with localized calcification in the occipital and parietal regions of brain is also an additional finding in this patient...
  3. Sengupta S, Badhwar I, Upadhyay M, Singh S, Ganesh S. Malin and laforin are essential components of a protein complex that protects cells from thermal stress. J Cell Sci. 2011;124:2277-86 pubmed publisher
    ..This study demonstrates that laforin and malin are key regulators of HSF1 and that defects in the HSF1-mediated stress response pathway might underlie some of the pathological symptoms in LD. ..
  4. Dubey D, Ganesh S. Modulation of functional properties of laforin phosphatase by alternative splicing reveals a novel mechanism for the EPM2A gene in Lafora progressive myoclonus epilepsy. Hum Mol Genet. 2008;17:3010-20 pubmed publisher
    ..Thus, our findings reveal a novel mechanism for the EPM2A gene function, regulated by alternative splicing, in normal as well as disease conditions. ..
  5. Roy S, Fox M, Curcic J, Schwizer W, Pal A. The gastro-esophageal reflux barrier: biophysical analysis on 3D models of anatomy from magnetic resonance imaging. Neurogastroenterol Motil. 2012;24:616-25, e269 pubmed publisher
    ..Changes in these parameters during respiration and on eating support the hypothesis that structural components of a functional 'flap valve' like mechanism contribute to reflux protection. ..
  6. Singh P, Singh S, Ganesh S. The laforin-malin complex negatively regulates glycogen synthesis by modulating cellular glucose uptake via glucose transporters. Mol Cell Biol. 2012;32:652-63 pubmed publisher
    ..Loss of laforin or malin, however, did not affect glycogen catabolism. Thus, the excessive cellular glucose level appears to be the primary trigger for the abnormally higher levels of cellular glycogen seen in LD. ..
  7. Gupta S, Singh R. Analysis of the virus dynamics model reveals that early treatment of HCV infection may lead to the sustained virological response. PLoS ONE. 2012;7:e41209 pubmed publisher
    ..Moreover, the analysis predicts that the drug that blocks new infections is more effective than the drug that blocks the virus production. ..
  8. Singh S, Singh P, Bhadauriya P, Ganesh S. Lafora disease E3 ubiquitin ligase malin is recruited to the processing bodies and regulates the microRNA-mediated gene silencing process via the decapping enzyme Dcp1a. RNA Biol. 2012;9:1440-9 pubmed publisher
    ..Our study suggests that malin is one of the critical regulators of processing bodies and that defects in the mRNA processing might underlie some of the disease symptoms in LD. ..
  9. Ghosh R, Sharma A. Determinants of tetanus and sepsis among the last neonatal deaths at household level in a peri-urban area of India. Postgrad Med J. 2011;87:257-63 pubmed publisher

More Information


  1. Dhingra M, Pantola C, Agarwal A. Congenital granular cell tumor of the alveolar ridge. Indian J Pathol Microbiol. 2010;53:327-8 pubmed publisher
    ..We report a case of congenital granular cell tumor in a newborn female child that was uneventfully operated. The case is reported here because of its rarity...
  2. Singh S, Ganesh S. Lafora progressive myoclonus epilepsy: a meta-analysis of reported mutations in the first decade following the discovery of the EPM2A and NHLRC1 genes. Hum Mutat. 2009;30:715-23 pubmed publisher
  3. Anand B, Majumdar S, Prakash B. Structural basis unifying diverse GTP hydrolysis mechanisms. Biochemistry. 2013;52:1122-30 pubmed publisher
    ..This understanding would be valuable for experiments in which abolishing GTP hydrolysis or generating constitutively active forms of a GTPase is important. ..
  4. Kumari P, Srivastava A, Ghosh E, Ranjan R, Dogra S, Yadav P, et al. Core engagement with ?-arrestin is dispensable for agonist-induced vasopressin receptor endocytosis and ERK activation. Mol Biol Cell. 2017;28:1003-1010 pubmed publisher
  5. Raj A, Ramesh G, Nagarajappa R, Pandey A, Raj A. Prevalence of odontogenic lesions among the Kanpur population: an institutional study. J Exp Ther Oncol. 2017;12:35-42 pubmed
    ..The relative frequency of these cysts and tumors can be analyzed at a global level to understand their prevalence, incidence, biological behaviour, and distribution. ..
  6. Arora S. Leprosy in a preschool child--a case report. J Indian Med Assoc. 2007;105:140 pubmed
    ..Histopathological examination from the patch revealed it to be a case of indeterminate leprosy. The child responded favourably with antileprosy treatment...
  7. Siwach P, Pophaly S, Ganesh S. Genomic and evolutionary insights into genes encoding proteins with single amino acid repeats. Mol Biol Evol. 2006;23:1357-69 pubmed
    ..Therefore, instability associated with repeats might be driven by processes that are specific to sperm or oocyte development, and the recombination frequency might play a positive role in this process. ..
  8. Majumdar S, Acharya A, Prakash B. Structural plasticity mediates distinct GAP-dependent GTP hydrolysis mechanisms in Rab33 and Rab5. FEBS J. 2017;284:4358-4375 pubmed publisher
    ..Taken together with the mechanisms seen for Rab1, it is evident that the observed variations in Rab and their GAP partners allow structural plasticity, or in other words, the choice of different catalytic mechanisms. ..
  9. Ramesh G, Raj A, Nagarajappa R, Pandey A. Basal cell adenoma of palatal glands. J Exp Ther Oncol. 2017;12:55-59 pubmed
    ..We here report a case of basal cell adenoma of trabecular type in a male patient of age 45 years in the minor salivary glands of left posterior palatal region. ..
  10. Ganesh S, Tsurutani N, Suzuki T, Hoshii Y, Ishihara T, Delgado Escueta A, et al. The carbohydrate-binding domain of Lafora disease protein targets Lafora polyglucosan bodies. Biochem Biophys Res Commun. 2004;313:1101-9 pubmed
    ..This is the first report demonstrating a direct association between the LD gene product and the disease-defining storage product, the Lafora bodies. ..
  11. Gupta A, Verma R, Agarwal V, Vajpai M, Bansal V, Sankararamakrishnan R. MIPModDB: a central resource for the superfamily of major intrinsic proteins. Nucleic Acids Res. 2012;40:D362-9 pubmed publisher
    ..Sequences and structures of selected MIPs can be downloaded from MIPModDB database which is freely available at ..
  12. Puri R, Suzuki T, Yamakawa K, Ganesh S. Dysfunctions in endosomal-lysosomal and autophagy pathways underlie neuropathology in a mouse model for Lafora disease. Hum Mol Genet. 2012;21:175-84 pubmed publisher
  13. Garyali P, Siwach P, Singh P, Puri R, Mittal S, Sengupta S, et al. The malin-laforin complex suppresses the cellular toxicity of misfolded proteins by promoting their degradation through the ubiquitin-proteasome system. Hum Mol Genet. 2009;18:688-700 pubmed publisher
  14. Singh S, Satishchandra P, Shankar S, Ganesh S. Lafora disease in the Indian population: EPM2A and NHLRC1 gene mutations and their impact on subcellular localization of laforin and malin. Hum Mutat. 2008;29:E1-12 pubmed publisher
    ..Our results suggest that the altered subcellular localization of mutant proteins of the EPM2A and NHLRC1 genes could be one of the molecular bases of the LD phenotype. ..
  15. Banerjee I, Gupta V, Ahmed T, Faizaan M, Agarwal P, Ganesh S. Inflammatory system gene polymorphism and the risk of stroke: a case-control study in an Indian population. Brain Res Bull. 2008;75:158-65 pubmed
    ..In conclusion, the -889 C/T and SNP83 T/C SNPs of the IL-1alpha and PDE4D genes, respectively, appear to be genetic risk factors for stroke in our study population. ..
  16. Banerjee I, Gupta V, Ganesh S. Association of gene polymorphism with genetic susceptibility to stroke in Asian populations: a meta-analysis. J Hum Genet. 2007;52:205-19 pubmed
  17. Singh S, Suzuki T, Uchiyama A, Kumada S, Moriyama N, Hirose S, et al. Mutations in the NHLRC1 gene are the common cause for Lafora disease in the Japanese population. J Hum Genet. 2005;50:347-52 pubmed
    ..Our study, in addition to documenting the genetic and molecular heterogeneity observed for LD, suggests that mutations in the NHLRC1 gene may be a common cause of LD in the Japanese population. ..