<?xml version="1.0" encoding="UTF-8"?>
<feed xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://www.w3.org/2005/Atom">
<title>Prof. Pratima Sinha</title>
<link href="http://192.168.1.40:8080/xmlui/handle/123456789/1127" rel="alternate"/>
<subtitle/>
<id>http://192.168.1.40:8080/xmlui/handle/123456789/1127</id>
<updated>2026-05-31T13:43:55Z</updated>
<dc:date>2026-05-31T13:43:55Z</dc:date>
<entry>
<title>Constitutive association of Mcm2-3-5 proteins with chromatin in Entamoeba histolytica</title>
<link href="http://192.168.1.40:8080/xmlui/handle/123456789/2204" rel="alternate"/>
<author>
<name>Das, S.</name>
</author>
<author>
<name>Mukherjee, C.</name>
</author>
<author>
<name>Sinha, Pratima</name>
</author>
<author>
<name>Lohia, Anuradha</name>
</author>
<id>http://192.168.1.40:8080/xmlui/handle/123456789/2204</id>
<updated>2013-03-21T11:12:30Z</updated>
<published>2005-02-01T00:00:00Z</published>
<summary type="text">Constitutive association of Mcm2-3-5 proteins with chromatin in Entamoeba histolytica
Das, S.; Mukherjee, C.; Sinha, Pratima; Lohia, Anuradha
Eukaryotic cells duplicate their genome once and only once per cell cycle. Our earlier studies with the protozoan parasite, Entamoeba histolytica, have shown that genome reduplication may occur several times without nuclear or cellular division. The Mcm2-7 protein complex is required for licensing of DNA replication. In an effort to understand whether genome reduplication occurs due to absence or failure of the DNA replication licensing system, we analysed the function of Mcm2-3-5 proteins in E. histolytica. In this study, we have cloned E. histolytica (Eh) MCM2 and Eh MCM5 genes, while Eh MCM3 was cloned earlier. The sequence of Eh MCM2-3-5 genes is well conserved with other eukaryotic homologues. We have shown that Eh Mcm2,3 proteins are functional in Saccharomyces cerevisiae. Our studies in E. histolytica showed that Eh Mcm2-3-5 proteins are associated with chromatin constitutively in cycling cells and during arrest of DNA synthesis induced by serum starvation. Alternation of genome duplication with mitosis is regulated by association-dissociation of Mcm2-7 proteins with chromatin in other eukaryotes. Our results suggest that constitutive association of Mcm proteins with chromatin could be one of the reasons why genome reduplication occurs in E. histolytica.
DOI: 10.1111/j.1462-5822.2004.00456.x
</summary>
<dc:date>2005-02-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Mrg19 depletion increases S. cerevisiae lifespan by augmenting ROS defence</title>
<link href="http://192.168.1.40:8080/xmlui/handle/123456789/2203" rel="alternate"/>
<author>
<name>Kharade, S. V.</name>
</author>
<author>
<name>Mittal, N.</name>
</author>
<author>
<name>Das, S.P.</name>
</author>
<author>
<name>Roy, N.</name>
</author>
<author>
<name>Sinha, Pratima</name>
</author>
<id>http://192.168.1.40:8080/xmlui/handle/123456789/2203</id>
<updated>2013-03-14T05:49:51Z</updated>
<published>2005-12-19T00:00:00Z</published>
<summary type="text">Mrg19 depletion increases S. cerevisiae lifespan by augmenting ROS defence
Kharade, S. V.; Mittal, N.; Das, S.P.; Roy, N.; Sinha, Pratima
Caloric restriction (CR) is the most compelling example of lifespan extension by external manipulation. Although the molecular mechanisms remain unknown, the theory of hormesis has been invoked to explain the life promoting effects of CR. Hormesis is defined as the beneficial effects of low intensity stressor on a cell or organism. Mrg19 is a putative transcription factor that regulates carbon and nitrogen metabolism in yeast. In this study, we have found that deletion of MRG19 gene causes metabolic shift in yeast cells, leading to higher intracellular reactive oxygen species, augmentation of scavenging enzymes and longer lifespan compared to wild-type cells. All these results together suggest that similar to CR, depletion of Mrg19 leads to a condition of mild stress which in turn enhances vitality. (c) 2005 Federation of European Biochemical Societies.
DOI: 10.1016/j.febslet.2005.11.017
</summary>
<dc:date>2005-12-19T00:00:00Z</dc:date>
</entry>
<entry>
<title>The budding yeast protein Chl1p has a role in transcriptional silencing, rDNA recombination, and aging</title>
<link href="http://192.168.1.40:8080/xmlui/handle/123456789/2202" rel="alternate"/>
<author>
<name>Das, S. P.</name>
</author>
<author>
<name>Sinha, Pratima</name>
</author>
<id>http://192.168.1.40:8080/xmlui/handle/123456789/2202</id>
<updated>2013-03-14T05:40:09Z</updated>
<published>2005-11-11T00:00:00Z</published>
<summary type="text">The budding yeast protein Chl1p has a role in transcriptional silencing, rDNA recombination, and aging
Das, S. P.; Sinha, Pratima
We show that the budding yeast protein Chl1p, required for sister-chromatid cohesion, also modulates transcriptional silencing at HMR and telomeres. The absence of this protein results in increased silencing at HMR and, conversely, in decreased silencing at the telomere. The regulation of silencing by Chl1p at these two loci is dependent on the presence of Sir proteins. Chl1p also acts synergistically with Sir2p to suppress rDNA recombination. In the absence of this protein, yeast cells exhibit reduced life span and hypersensitivity to heat stress. These observations suggest a role of Chl1p in regulating chromatin structure.
DOI: 10.1016/j.bbrc.2005.09.034
</summary>
<dc:date>2005-11-11T00:00:00Z</dc:date>
</entry>
<entry>
<title>The budding yeast protein Chl1p is required to preserve genome integrity upon DNA damage in S-phase</title>
<link href="http://192.168.1.40:8080/xmlui/handle/123456789/2137" rel="alternate"/>
<author>
<name>Laha, Suparna</name>
</author>
<author>
<name>Das, Shankar Prasad</name>
</author>
<author>
<name>Hajra, Sujata</name>
</author>
<author>
<name>Sau, Soumitra</name>
</author>
<author>
<name>Sinha, Pratima</name>
</author>
<id>http://192.168.1.40:8080/xmlui/handle/123456789/2137</id>
<updated>2013-03-06T12:25:21Z</updated>
<published>2006-11-01T00:00:00Z</published>
<summary type="text">The budding yeast protein Chl1p is required to preserve genome integrity upon DNA damage in S-phase
Laha, Suparna; Das, Shankar Prasad; Hajra, Sujata; Sau, Soumitra; Sinha, Pratima
The budding yeast protein, Chl1p, is required for sister-chromatid cohesion, transcriptional silencing, rDNA recombination and aging. In this work, we show that Chl1p is also required for viability when DNA replication is stressed, either due to mutations or if cells are treated with genotoxic agents like methylmethane sulfonate (MMS) and ultraviolet (UV) rays. The chl1 mutation caused synthetic growth defects with mutations in DNA replication genes. At semi-permissive temperatures, the double mutants grew poorly, were less viable and showed nuclear fragmentation. They were, however, not limited in their bulk DNA synthesis. When chl1 cells were treated with relatively low levels of MMS in S-phase, they lost viability. The S-phase DNA damage checkpoint pathway, however, remained active in these cells. Agarose gel electrophoresis of genomic DNA isolated from wild-type and chl1 cells, after recovery from MMS treatment, suggested that the wild-type was more proficient in the repair of DNA damage than the mutant. Our work suggests that Chl1p is required for genome integrity when cells suffer endogenously or exogenously induced DNA damage.
DOI: 10.1093/nar/gkl749
</summary>
<dc:date>2006-11-01T00:00:00Z</dc:date>
</entry>
</feed>
