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Cell Cycle (Georgetown, Tex.)|September 2, 2008
The C-termini of tubulin and the specific geometry of tubulin substrates influence the depolymerization activity of MCAKKathleen M Hertzer, Claire E Walczak
Expert Opinion on Therapeutic Targets|February 22, 2013
CXCR2: a target for pancreatic cancer treatment?Kathleen M Hertzer, Graham W Donald, O Joe Hines
Critical Reviews in Biochemistry and Molecular Biology|December 26, 2003
Kin I kinesins: insights into the mechanism of depolymerizationKathleen M Hertzer, Stephanie C Ems-McClung, Claire E Walczak
Molecular Biology of the Cell|November 10, 2006
The interplay of the N- and C-terminal domains of MCAK control microtubule depolymerization activity and spindle assemblyStephanie C Ems-McClung, Kathleen M Hertzer, Xin Zhang, et al.
Molecular Biology of the Cell|November 18, 2005
Full-length dimeric MCAK is a more efficient microtubule depolymerase than minimal domain monomeric MCAKKathleen M Hertzer, Stephanie C Ems-McClung, Susan L Kline-Smith, et al.
American Journal of Physiology. Cell Physiology|August 28, 2015
Prostaglandin E2 activates the mTORC1 pathway through an EP4/cAMP/PKA- and EP1/Ca2+-mediated mechanism in the human pancreatic carcinoma cell line PANC-1Hui-Hua Chang, Steven H Young, James Sinnett-Smith, et al.
Biochemical and Biophysical Research Communications|August 27, 2013
miR-143 decreases COX-2 mRNA stability and expression in pancreatic cancer cellsHung Pham, C Ekaterina Rodriguez, Graham W Donald, et al.
Pancreas|October 27, 2015
Robust Early Inflammation of the Peripancreatic Visceral Adipose Tissue During Diet-Induced Obesity in the KrasG12D Model of Pancreatic CancerKathleen M Hertzer, Mu Xu, Aune Moro, et al.
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