Keytam S. Awad, MS, PhD

PhD, Kent State University
MS, Youngstown State University

Dr. Awad received her Bachelor of Science and Master’s degrees in biology at Youngstown State University. She then trained as a cellular and molecular biologist at Kent State University where she received her PhD. After a post-doctoral fellowship at the University of Florida, Dr. Awad came to NIH as an IRTA Postdoctoral Fellow in Dr. Robert Danner’s lab. There, she started a project investigating dysregulated signaling pathways in pulmonary arterial hypertension (PAH), the impact of gender on these signaling pathways, and targeted therapies focused on blocking the proliferative, anti-apoptotic vascular remodeling of PAH.

After completing her post-doctoral training, Dr. Awad accepted a biologist position before her later appointment as a Staff Scientist in the Intramural NIH Pulmonary Arterial Hypertension (PAH) Program. Key research areas involve: (1) how the DLL4/NOTCH1 pathway promotes BMPR2 and PPAR signaling to prevent PAH vasculopathy, and (2) the role of tubulin post-translational modifications (PTMs) in PAH pathobiology.

Importantly, DLL4 blockade as therapy for cancer was found to cause pulmonary hypertension in some patients by an unknown mechanism. Dr. Awad has shown that DLL4/NOTCH1 signaling improves BMPR2 and PPAR function and restores endothelial homeostasis, opening up new therapeutic avenues for PAH patients. In other work, she is investigating tubulin PTMs, which regulate microtubule dynamics, organization and interactions with cell signaling pathways. Tyrosination/detyrosination at the COOH terminus of alpha-tubulin is a reversible process involving the addition of tyrosine by tubulin tyrosine ligase (TTL) and removal of tyrosine by vasohibin 1 (VASH1). Understanding how the loss of alpha-tubulin detyrosination contributes to sustained oncogenic signaling in PAH is the basis of an ongoing research project led by Dr. Awad.

• Selected for oral presentation for the Thomas L. Petty Aspen Lung Conference, 2019
• Grover Conference Young Investigator Award, 2015
• Best Poster Award, American College of Cardiology Conference, 2014
• NIH Fellows Award for Research Excellence (FARE), 2013
• Kirschstein-NRSA training grant in Cancer Biology, 2008 - 2010
• Colloquium Award of Excellence for Outstanding Poster, 2005
• Recipient of an NIH Travel Award for the 22nd International Papillomavirus Conference and Clinical Workshop, Vancouver, B.C., 2005

Gairhe S, Awad KS, Dougherty EJ, Ferreyra GA, Wang S, Yu ZX, Takeda K, Demirkale CY, Torabi-Parizi P, Austin ED, Elinoff JM, Danner RL. 2021. Type I interferon activation and endothelial dysfunction in caveolin-1 insufficiency-associated pulmonary arterial hypertension. PNAS; Mar 16, 118(11):e2010206118

Elinoff JM, Chen L, Dougherty EJ, Awad KS, Wang S, Biancotto A, Siddiqui AH, Weir NA, Cai R, Sun J, Preston IR, Solomon MA, Danner RL. 2018. Spinorolactone-induced degradation of the TFIIH core complex XPB subunit suppresses NFkB and AP-1 signaling. Cardiovascular Research, Jan 1; 114(1):65-76

Awad KS, West JD, de Jesus Perez, MacLean M. 2016. Novel signaling pathways in pulmonary arterial hyperstension (2015 Grover Conference Series). Pulmonary Circulation; Sep; 6(3):285-94

Awad KS, Elinoff JM, Wang S, Gairhe S, Ferreyra GA, Cai R, Sun J, Solomon MA, Danner RL. 2016. Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells. American Journal Physiology-Lung Cellular and Molecular Physiology; Nov; 310(2):L187-L201

Wang S, Awad KS, Elinoff JM, Dougherty EJ, Ferreyra GA, Wang JY, Cai R, Sun J, Ptasinska A, Danner RL. 2015. G protein-Coupled Receptor 40 (GPCR40) and Peroxisome Proliferator-Activated Receptor γ (PPAR γ): An Integrated two-receptor Signaling Pathway. J Biol Chemistry; Jun 23

Visit Scopus for a full list of Dr. Awad's publications.