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  • ISSN: 2373-9436
    Volume 1, Issue 1
    July/August 2013
    Editorial
    Zhenming Fu*
    US biomedical research including epidemiology research has been criticized that a majority of the research findings are not translational. That is, researches have limited direct impact on improving patient care and public health [1]. In a move to expedite the process for impact, NIH has newly established the National Center for Advancing Translational Sciences (NCATS).
    Jeremy Chien*
    Abstract: Advances in genomic sequencing technologies and computational and analytical methods are now allowing us to characterize at single base-pair resolution of cancer genomes and amass an unprecedented amount of cancer genomic information. However, the gap between genomic information and genomic knowledge and biological insights have been widening as functional characterization of cancer genes are relatively low throughput compared to next-generation sequencing and data analysis. Advances in functional genomics must keep pace with ever advancing genomic sequencing technologies. Functional genomics tools, such as RNAi screens for critical components in cancer pathway and therapeutic targets and ORF screens to identify driver genes in cancer pathway, may allow the gap between information and knowledge to be bridged. In this brief review, I will discuss a few examples of high-throughput functional genomics and provide a modified approach in ORF screenings that we are currently performing to identify tumor-derived transcripts that functionally contribute to chemotherapy resistance in ovarian cancer.
    Research Article
    Eui Young So and Toru Ouchi*
    Abstract: BRCA1-associated ATM activator-1 (BRAT1) was identified by our group as a DNA damage response (DDR) protein, which can bind with many DDR proteins and regulates their functions after DNA damage. However, previous study has also implicated BRAT1 as a regulator of cell growth and apoptosis. In this study, targeted gene deletion showed that BRAT1 is critical in stability and serum-induced expression of mTOR and downstream protein. Conditional deletion of BRAT1 of mouse embryonic fibroblasts suppressed serum-induced cell cycling progress. Our results suggest that BRAT1 is essential factor for PIKK signaling cascades.
    Eui Young So, Martin Kozicki and Toru Ouchi*
    Abstract: ATM, ATR and DNA-PK are critical for DNA damage response (DDR) and sequential repair, leading to genomic stability. In this study, we found the expression of these proteins is markedly induced by PMA during THP1 differentiation without the change in the level of transcripts. Also, inhibitors of these protein activity suppressed PMA-induced morphological change of THP1 cells. Our results suggest the potential roles of these DDR proteins in cellular differentiation.
    Review Article
    Awad Shamma*
    The findings that the retinoblastoma tumor suppressor gene product (pRB) controls gene expression by physically interacting with several epigenetic regulators reveals another potential form of the RB functions in global regulation of the epigenome beyond its well known functions in regulation of the E2F and tissue specific transcription factors. This plethora of novel RB functions may explain why RB should be inactivated in the vast majority of human cancers, and will provide insights for better understanding the future rationale for the epigenetic therapy of cancers.
  • Current Issue Highlights
  • BRAT1 was originally identified as a BRCA1 interacting protein [1], however, subsequent studies showed that it also binds to ATM, DNA-PK, and SMC1,
    Readmore...

    Mechanisms of detecting and repairing damaged DNA are conserved and controlled through the DNA damage response (DDR).
    Readmore...

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