Kim Failor

Title
Assistant Head of School, Biology Instructor
Education

B.S., University of Illinois, Urbana-Champaign

Ph.D., University of California, Berkeley

Dr. Failor earned her B.S. in Cell and Structural Biology from the University of Illinois, Urbana-Champaign and her Ph.D. in Molecular and Cell Biology from the University of California, Berkeley. While at UC Berkeley, she worked with Dr. Gary Firestone studying the steroid hormone regulation of cell signaling in mammary epithelium that controls the interaction between cells and the development of the mammary gland.  She also taught a variety of courses including cell biology and prepared students for the Biological Sciences section of the Medical College Admissions Test (MCAT). 

Dr. Failor joined Stanford OHS in 2007 as the Lead Biology Instructor and is currently the Division Head of Science.  She has been involved in the development of numerous OHS courses including AP Biology and Advanced Topics in Biological Research.  In addition, the division has expanded its extracurricular offerings including middle school and high school Science Bowl teams, the OHS Science Fair, and Student Research Colloquium.  For Dr. Failor, working with students is the highlight of the job.

Publications

Failor KL, Desyatnikov Y, Finger LA, Firestone GL. 2007. Glucocorticoid-induced degradation of glycogen synthase kinase-3 protein is triggered by serum- and glucocorticoid-induced protein kinase and Akt signaling and controls beta-catenin dynamics and tight junction formation in mammary epithelial tumor cells. Mol Endocrinol. (10): 2403–15.

Buse P, Maiyar AC, Failor KL, Tran S, Leong ML, Firestone GL. 2007. The stimulus-dependent co-localization of serum- and glucocorticoid-regulated protein kinase (Sgk) and Erk/MAPK in mammary tumor cells involves the mutual interaction with the importin-alpha nuclear import protein. Exp Cell Res. 313 (15): 3261–75.

Guan Y, Rubenstein NM, Failor KL, Woo PL, Firestone GL. 2004. Glucocorticoids control beta-catenin protein expression and localization through distinct pathways that can be uncoupled by disruption of signaling events required for tight junction formation in rat mammary epithelial tumor cells. Mol Endocrinol. 18 (1): 214–27.