In This Section

Alexander Y. Tsygankov, PhD

Associate Professor, Cardiovascular Sciences
Associate Professor, Sol Sherry Thrombosis Research Center
Associate Professor, Fels Cancer Institute for Personalized Medicine
Associate Professor, Microbiology, Immunology and Inflammation 

Alexander Tsygankov
Contact Information

Contact Information





About Me

Research Interests

Dr. Tsygankov’s research interests lie in the area of cell signaling, in particular, of its regulation by protein tyrosine kinases and phosphatases. Previous work of this laboratory with protein kinases of Src and Syk families and adaptor proteins of Cbl family, which is involved in Src- and Syk-mediated signaling, defined the novel protein family TULA. Dr. Tsygankov’s laboratory identified and characterized TULA, a Cbl-associated protein and later demonstrated that TULA-2, but not TULA, is an active protein tyrosine phosphatase capable of dephosphorylating Syk, which along with the highly-related kinase Zap-70 is a bona-fide substrate of TULA-2.

The current interests of Dr. Tsygankov are focused on understanding the role of TULA-family proteins in cell signaling and activation. This issue is addressed in two experimental systems – T lymphocytes and platelets. The results of the laboratory indicate that TULA- and TULA-2-null mice are significantly more responsive to experimentally induced colitis and that this inflammation to a large degree depends on hyper-responsiveness of TULA-deficient T cells to stimulation through T-cell antigen receptor. These results are directly related to understanding of molecular and cellular mechanisms of inflammatory bowel disease.

In collaboration with platelet experts, including Dr. Kunapuli from Temple University School of Medicine, Dr. Tsygankov’s group has also shown that TULA-2-mediated dephosphorylation of Syk significantly reduces platelet signaling mediated by GPVI collagen receptor, thus increasing the platelet activation threshold, which prevents unnecessary and potentially dangerous stimulation of platelet responses by sub-optimal stimuli. These results indicate that TULA-2-null platelet exhibit greatly potentiated responses in vitro and in vivo. Likewise, pharmacological inhibition of TULA-2 by a novel compound appears to exert similar effects on platelets. The current focus of Dr. Tsygankov’s laboratory in these studies is deciphering the molecular mechanism of down-regulatory functions of TULA-2 in GPVI signaling and assessing the therapeutic potential of TULA-2 as a target in treatment of platelet-dependent bleeding disorders.

Education, Training & Credentials

Educational Background

  • Bach Institute of Biochemistry, Moscow

Digital Bibliography

View PubMed Publications

Collingwood TS, Smirnova EV, Bogush M, Carpino N, Annan RS, Tsygankov AY, TULA affects cell death through a functional interaction with AIF, a key factor of caspase-independent apoptosis. J Biol Chem 2007 Aug 20.

Swaminathan G, Feshchenko EA, Tsygankov AY, c-Cbl-facilitated cytoskeletal effects in v-Abl-transformed fibroblasts are regulated by membrane association of c-Cbl. Oncogene 2007 Jun 14;26(28):4095-105)2007.

Swaminathan G, Tsygankov AY, The Cbl family proteins: ring leaders in regulation of cell signaling. J Cell Physiol 2006 Oct;209(1):21-43.

Teckchandani AM, Panetti TS, Tsygankov AY, c-Cbl regulates migration of v-Abl-transformed NIH 3T3 fibroblasts via Rac1. Exp Cell Res 2005 Jul 1;307(1):247-58... Expand