Syed Babar Ali School of Science and Engineering
Dr Zakir Ullah received his B. Sc (Hons) degree from Agricultural University Peshawar and was awarded a University Gold Medal and a Presidential Award. Dr. Ullah received his M. Sc (Hons) degree from the same university and was once again awarded a University Gold Medal and a Presidential Award for his outstanding academic performance. In 1993, Dr. Ullah was awarded "Aizaz-e-Sabqat" by the President of Pakistan for his academic excellence. In 1994, Dr. Ullah went to Michigan State University (MSU) for his graduate studies. Dr. Ullah received Research Assistantship, Teaching Assistantship and five graduate student awards during his PhD program. After completing his PhD in 2000, Dr Ullah joined Texas A&M University as a postdoctoral researcher. In 2001, Dr Ullah was awarded a postdoctoral fellowship and research funding by the Department of Biochemistry and Molecular Biology at Michigan State University to study the role of tumor suppressor proteins, known as the Retinoblastoma family of proteins, during embryonic development. Work done by Dr. Ullah discovered new roles for RBF family of proteins during embryonic development and resulted in substantial additional funding by the National Institutes of Health. In 2005 Dr. Ullah joined the National Institutes of Health (NIH) in Bethesda, Maryland (USA) where he started a new project to understand the differentiation of trophoblast stem cells into giant cells at the molecular level. Dr. Ullah received two Fellowship Awards for Research Excellence at the NIH and published his findings in highly reputable scientific journals. Dr. Ullah has extensive expertise in various biological systems and is one of the few scientists in the world who have published first author papers in reputable international journals in plants, Drosophila and mammals. In 2012 Dr. Ullah joined LUMS University as an Associate Professor.
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The focus of my research group is to understand the molecular circuits that regulate cell cycle progression and biological signals that trigger exit from the mitotic cell cycle. Mitotic cell cycle is a tightly regulated process that is essential to our survival. Perturbations in cell cycle regulation result in various developmental abnormalities, diseases and death. Cancer is the most common disease resulting from abnormal cell cycle regulation. Orderly exit from mitotic cell cycle is fundamental to human development. As a human body matures, most cells in the adult body exit the mitotic cell cycle and stop proliferation. Many tissues however, contain stem cells which can proliferate and differentiate in response to appropriate molecular signals.
We are using the differentiation of trophoblast stem (TS) cells into terminally differentiated, polyploid giant cells (TG cells) as a model system to identify the molecular events that drive exit from the mitotic cell cycle. We have discovered that differentiation of TS cells into TG cells is triggered by p57 inhibition of Cyclin Dependent Kinase-1 (CDK1) activity (Ullah et al 2008, Genes and Development, Ullah et al 2009, Cell Cycle). p57 is an inhibitor of CDK activity and mutations in p57 result in cancer and developmental abnormalities like placentomegaly and Bekwith-Wiedmann syndrome, a congenital disorder characterized by a large body and organs. We have also discovered that the DNA damage checkpoint kinase CHK1 phosphorylates and targets p57 for degradation in TS cells. When TS cells differentiate into TG cells, CHK1 is degraded which allows for accumulation of p57 thereby resulting in inhibition of CDK1 activity and causing cell cycle exit. Thus we have identified a novel role for CHK1 in stem cell differentiation (Ullah et al 2011 Molecular and Cellular Biology).
Current projects in the lab focus on the role of CDK1 inhibitor p21 in maintaining polyploidy in TG cells and on the biological signals that result in degradation of CHK1 during differentiation of TS cells.