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Reengineering a receptor footprint of adeno-associated virus enables selective and systemic gene transfer to muscle
Unlike other AAV serotypes, which are preferentially sequestered in the liver, AAV2i8 showed markedly reduced hepatic tropism, suggesting that it is well suited to translational studies in gene therapy of musculoskeletal disorders.
Multiple Cancer Testis Antigens Function To Support Tumor Cell Mitotic Fidelity
- Kathryn M. Cappell, R. Sinnott, Patrick J. Taus, K. Maxfield, Moriah Scarbrough, Angelique W Whitehurst
- BiologyMolecular and Cellular Biology
- 6 August 2012
It is demonstrated that combining paclitaxel with a small-molecule inhibitor of the gametogenic and tumor cell mitotic protein TACC3 leads to enhanced centrosomal abnormalities, activation of death programs, and loss of anchorage-independent growth.
Mechanisms promoting escape from mitotic stress-induced tumor cell death.
It is reported that intrinsic resistance to paclitaxel in NSCLC occurs at a cell-autonomous level because of the uncoupling of mitotic defects from apoptosis, and hypothesize that tumor evolution selects for a permissive mitotic checkpoint, which may promote survival despite chromosome segregation errors.
Differential cell responses to nanoparticle docetaxel and small molecule docetaxel at a sub-therapeutic dose range.
Abstract 4379: Framing therapeutic opportunities in tumor-activated gametogenic programs.
- K. Corcoran, Patrick J. Taus, R. Sinnott, K. Maxfield, J. Wooten, Angelique W Whitehurst
- 15 April 2013
The hypothesis that CTAs are frequently integrated into the tumor cell regulatory environment to support cell division, survival and modulate stress responses by regulating key signaling pathways is supported.
tumor cell death Mechanisms promoting escape from mitotic-stress induced
Therapeutics , Targets , and Chemical Biology MechanismsPromoting Escape fromMitotic Stress – Induced Tumor Cell Death
It is reported that intrinsic resistance to paclitaxel in NSCLC occurs at a cell-autonomous level because of the uncoupling of mitotic defects from apoptosis, and it is hypothesized that tumor evolution selects for a permissivemitotic checkpoint, which may promote survival despite chromosome segregation errors.
Differential Cellular Response to Nanoparticle Docetaxel and Docetaxel at Subtherapeutic Dose Range