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Journal of Postdoctoral Research (JPR) - Vol. 6, No. 1, January 2018
 
EDITORIAL: Mining gold to treat the untreatable: Design, Synthesis and Characterization of Gold Based Nucleosidic Compounds
Sharmistha Mitra, PhD
6-Mercaptopurine Nucleoside Complexes of Gold(I): Synthesis and Cytotoxicity
Ayan Maity, Nihal Deligonul, Anthony J. Berdis, and Thomas G. Gray
Recent discoveries of Cohesin Establishment and Maintenance in Eukaryotes
Debjani Pal, PhD
EDITORIAl: Rot1 is degraded by ERAD: new insights into protein homeostasis of an essential gene
Nimrat Chatterjee, PhD
Rot1, an essential yeast protein, is degraded through the ER-associated protein degradation system (ERAD)
M. Angeles Juanes, PhD, Carlos A. Martínez-Garay, PhD, and M. Carmen Bañó, PhD
Scanning Electron Microscopy Techniques For Preservation and Observation Of Microbe-Mineral Assemblages and Biominerals
Wendy Smythe, PhD
Recommendations for improving international study programs in South Korea: a literature review
Justin Fendos, PhD
Noncoding RNA in cancer
Isabel Calvo, PhD
Research Highlight: Neoadjuvant chemotherapy exacerbates breast cancer metastasis
Chinmay R. Survey, PhD
EDITORIAL: Targeting DNA repair as cancer therapy: TLS comes into focus
Jia Zhou, Ph.D.
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Author(s)
Sharmistha Mitra, PhD
Address
Department of Pediatrics, Division of Neurology, UTSMC, Dallas, TX 75390, USA.
Abstract:

The current field of anticancer therapy is dominated by organic molecules. However, after FDA approval of the platimum based drug Cisplatin in 1978 and its positive effects to treat testicular and ovarian cancer, there came an urge to design more metal based anticancer drugs which would be more selective, non-toxic to non-targeting cells and will have reduced side effects. Following the success of Cisplatin, came the gold based anti cancer drug Auranofin, which showed immunosuppressory properties as well. Gold’s oxidation state +3 is similar in chemical configation as platinum and on the top gold complexes show antiinflammatory and immunospressory properties5. Therefore, there were several reports afterwards which emphasized the synthesis and use of gold based complexes as potetial drugs against cancer. Most of the gold complexes described so far targets enzymes or proteins inside the cells. Gold complexes targeting DNA are rare. 


Author(s)
Ayan Maity, Nihal Deligonul, Anthony J. Berdis, and Thomas G. Gray
Address
MIT, Cambridge, MA 02139.
Case Western Reserve University, Cleaveland, OH 44106.
Cleveland State University, Cleveland, OH 44115, USA,
Abstract:

Molecular gold compounds have shown intermittent promise as human pharmaceuticals, mostly in in vitro as-says.  Rational approaches to gold prodrugs are essential for desired cytotoxicity.  This work describes non-natural nucleosides of 6-mercaptopurine.  Binding to (organophosphine)- and (N-heterocyclic carbene)gold(I) proceeds in high-yield reactions at room temperature.  Three such metallonucleosides were prepared.  They dif-fer in the phosphine or carbene ligand on gold.  New compounds are characterized by multinuclear NMR spec-troscopy, mass spectrometry, and elemental analysis.  One complex is crystallographically characterized; gold(I) is bound to the sulfur atom of the mercaptopurine moiety, and aurophilic interactions are absent.  Experiments in human cell lines showed evidence of mitochondrial swelling, programmed cell death, and inhibition of rat liver thioredoxin reductase.


Author(s)
Debjani Pal, PhD
Address
WMS, Columbus, OH 43210
Abstract:

Cohesin is multi-subunit protein that encompasses naked DNA.  In eukaryotes, cohesin is es-sential for accurate segregation of the sister chromatids during mitosis and meiosis. Majority of cohesin complexes are removed from chromosomes during prophase in higher eukaryotes. WAPL mediated opening of the cohesin ring at the junction between the SMC3 ATPase do-main and the N-terminal domain of cohesin's α-kleisin subunit has been shown in flies and human.
Cohesin complex also plays a role in DNA damage repair, regulation of gene expression and chromosome condensation. In this commentary, recent discoveries of the mode of mecha-nism of cohesin establishment and maintenance in higher eukaryotes has been highlighted.

 


Author(s)
Nimrat Chatterjee, PhD
Address
Department of Biology, MIT, Cambridge, MA 02139, USA

Author(s)
M. Angeles Juanes, PhD, Carlos A. Martínez-Garay, PhD, and M. Carmen Bañó, PhD
Address
ERI BIOTECMED, Universitat de València, Burjassot, Valencia, 46100, Spain
Rosenstiel Basic Medical Science Research Center, Brandeis University, Waltham, MA, 02454, USA

Author(s)
Wendy Smythe, PhD
Address
BEACON Center for the Study of Evolution in Action, 1441 East Lansing MI, 48824, USA

Author(s)
Justin Fendos, PhD
Address
Fudan University, Shanghai, China 508915
Dongseo University, Busan, South Korea 617716

Author(s)
Isabel Calvo, PhD
Address
MGH Cancer Center and Department of Medicine, HMS, Charlestown, MA 02129, USA
Centro de Investigación Médica Aplicada (CIMA) - Universidad de Navarra, Pío XII, 55 E-31008 Pamplona, Spain.

Author(s)
Chinmay R. Survey, PhD
Address
Department of Anatomy and Structural Biology, Albert Einstein college of Medicine, Bronx, NY, USA

Author(s)
Jia Zhou, Ph.D.
Address
Department of Radiation Oncology, DFCI, Harvard Medical School, MA, 02115, USA. 
Abstract:

DNA repair plays critical roles in maintaining genome stability. There are six major DNA repair pathways that handle different types of DNA damages, namely base excision repair (BER), nucleotide excision repair (NER), mis-match repair (MMR), homologous recombination repair (HR), non-homologous end joining (NHEJ), and translesion synthesis (TLS). Numerous studies have shown that alteration in DNA repair genes, including deletions, mutations, and copy number alterations, and altered gene expression, is one of the major causes of mutagenesis and cancer. In fact, cancer cells are often defective in one of their six major DNA repair pathways. For example, approximately half of the epithelial ovarian cancers have alterations in genes that regulate HR, which accounts for their genomic instability and thus aggressiveness. The cancer risk dramatically increases in the population who carry mutations in HR genes, including the well-known breast cancer susceptibility genes (BRCA1 and BRCA2). 

 
     
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