Institute for Integrative Genome Biology

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Iryna Ethell

Associate Professor

Mailing Address:

Biomedical Sciences
Webber Hall /2263
University of California
Riverside, CA 92521

Phone: (951) 827-2186
Fax: (951) 827-7121
Email: iryna.ethell@ucr.edu

Degree(s):

PhD 1991 Dnipropetrovsk National University, Ukraine
BS 1988 Dnipropetrovsk National University, Ukraine

College/Division Affiliation:

College of Natural and Agricultural Sciences

Center/Inst Affiliation(s):

Center for Glial-Neuronal Interactions

Areas Of Expertise:

Brain Development; Synaptic Plasticity; Signal Transduction; Fragile X

Awards / Honors:

2002  Regents’ Faculty Fellowships and Faculty Development Award, UCR, Riverside, CA
1995  Max Planck Gesellschaft Post-Doctoral Fellowship, Martinsried (Munich), Germany.
1993  Jeanne Timmins Scholarship Fund for postdoctoral fellowship position at the Montreal Neurological Institute, Montreal, Canada.
1993  The Wellcome Trust research travel grant for a two month visit to The Open University, Milton Keynes, UK for collaborative research on N-CAM expression in chick forebrain, following training in the framework of passive-avoidance paradigm.
1992  FEBS travel grant for participation in the advanced biochemistry course
1992  Award by the Ukranian Biochemical Society presented at the Ukrainian Biochemical Meeting, Kiev.
1988  Red Diploma (Summa cum laude equivalent)

Research Summary:

In our laboratory we are interested in understanding how the neuronal network develops and applying these principles to identifying the mechanistic perturbations which underlie various neurodevelopmental diseases such as mental retardation and the autism spectrum of disorders.  Toward this end, we are currently working to more clearly define the mechanistic role of ephrins and Eph receptors in the formation of functional synaptic connections.  Dendritic spines are small protrusions that extend from the dendritic shafts of neurons to form excitatory synaptic connections with the axons of adjacent neurons.  The development of mature dendritic spines involves a number of interacting molecular and cellular factors (Ethell and Pasquale, 2005), including the interactions between Eph receptors, which are generally postsynaptic, and their cognate ligands, the ephrins, which are presynaptic.  We have recently documented the importance of Eph/ephrin interactions in dendritic spine/synapse formation (Henkemeyer et al., 2003). However, little is known concerning the downstream mechanisms involved.  We propose that EphB2 receptor activation results in the activation of two complementary mechanistic pathways.  The first pathway is centered on the assembly of a focal adhesion complex (FAC) or FAC-like protein complex which associates with EphB2 receptor upon its activation.  This protein complex is believed to stimulate the reorganization of actin filaments.  The second pathway relies on EphB receptor dependent activation of small Rho GTPases promoting the formation of new actin filaments.

Another area of ongoing interest is to investigate the role of EphB receptors in the progression of melanoma. Malignant melanomas are hard to treat compared to the other types of skin cancer. The incidence of malignant melanoma is increasing faster than that of any other malignancy in the United States, and therefore this disease represents a significant health threat now and in the future. Several studies have demonstrated the expression of B class Eph/ephrin molecules in different tumors and suggested a functional relationship between Eph/ephrin expression and tumor progression. Our recent results show that EphB family of receptor tyrosine kinases play an important role in the melanoma progression. We show that the ability of Eph receptors and ephrins to promote cell migration in vitro, as well as melanoma growth, angiogenesis and metastasis in vivo.

Selected Publications:

Lab Personnel: +

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