Projects

(This page is currently under development.)

 

Proper blood cell development (hematopoiesis) is essential for life and is tightly controlled by a fine-tuned regulatory network that is still incompletely understood. The critical importance of this is reflected in the wide range of diseases that can arise due to defects in the regulation of hematopoiesis, including immunodeficiency, autoimmunity and blood cell cancers.

 

The Schjerven lab studies normal and malignant immune cell development with a focus on transcriptional regulation, and the molecular mechanisms underlying how mutations in key regulatory factors can cause disease. The transcription factor Ikaros, encoded by the IKZF1 gene, is a major focus of ongoing work. Due to the many roles of Ikaros in blood cell development and function, the lab has several diverse and complementary research projects.  

 

IKAROS family zinc finger 1

The development of blood cells (hematopoiesis) depends on a complex series of events that involves many regulatory processes. Blood cancer or immunological diseases can develop if these developing cells have loss of function or gain of function mutations in genes that control development, function, growth or survival. 

Ikaros (encoded by the IKZF1 gene) is a transcription factor that is required for proper development of many different blood cell lineages. It is also an important tumor suppressor in certain subtypes of pre-B ALL (leukemia) and is implicated in other human immunological diseases through recent GWAS studies. 

The overall research interest is in transcriptional regulation in the immune system during development and disease, and the current ongoing and proposed future research is focused on the role of the zinc finger (ZnF) transcription factor Ikaros. Studies use in vitro and in vivo models and also include the use of genome-wide analysis of DNA-binding and chromatin status (ChIP-Seq) as well as gene expression analysis (RNA-Seq). By increasing our knowledge about the molecular mechanism of action of key transcription factors in both normal development and disease, we might guide the development of targeted therapies for diseases where known transcriptional regulators are mutated.