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Sushama Sivakumar

Researcher at University of Texas Southwestern Medical Center

Publications -  19
Citations -  1686

Sushama Sivakumar is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Kinetochore & Mitosis. The author has an hindex of 11, co-authored 16 publications receiving 1360 citations. Previous affiliations of Sushama Sivakumar include University of Oklahoma & Oklahoma Medical Research Foundation.

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Noncoding RNA NORAD Regulates Genomic Stability by Sequestering PUMILIO Proteins.

TL;DR: The initial functional analysis of a poorly characterized human lncRNA that is induced after DNA damage is described, introducing a mechanism that regulates the activity of a deeply conserved and highly dosage-sensitive family of RNA binding proteins and reveal unanticipated roles for a lnc RNA and PUMILIO proteins in the maintenance of genomic stability.
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Spatiotemporal regulation of the anaphase-promoting complex in mitosis

TL;DR: The appropriate timing of events that lead to chromosome segregation during mitosis and cytokinesis is essential to prevent aneuploidy, and defects in these processes can contribute to tumorigenesis.
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Ska3 Is Required for Spindle Checkpoint Silencing and the Maintenance of Chromosome Cohesion in Mitosis

TL;DR: It is suggested that this network plays a major role in silencing the spindle checkpoint when chromosomes are aligned at metaphase to allow timely anaphase onset and mitotic exit.
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Cohesion Fatigue Induces Chromatid Separation in Cells Delayed at Metaphase

TL;DR: During experimentally induced metaphase delay, spindle pulling forces can cause asynchronous chromatid separation, a phenomenon the authors term "cohesion fatigue" that constitutes a previously overlooked source for chromosome instability in mitosis and meiosis.
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Mitotic progression becomes irreversible in prometaphase and collapses when Wee1 and Cdc25 are inhibited

TL;DR: Inhibition of positive feedback prevents rapid Cdk1 activation and induces a mitotic “collapse” phenotype characterized by the dephosphorylation of mitotic substrates without cyclin B proteolysis.