Northwestern University

Mon 4:00 PM

Research Works-in-Progress: Kotaro Hori, Ph.D. and Nurmaa Dashzeveg, Ph.D.

When: Monday, February 26, 2018
4:00 PM - 5:00 PM  

Where: Ward Building, 5-230, 303 E. Chicago Avenue, Chicago, IL 60611 map it

Audience: Faculty/Staff - Student - Post Docs/Docs - Graduate Students

Contact: Liz Barrera Murphy   312.503.4892

Group: Department of Pharmacology Seminars

Category: Lectures & Meetings


Please join the Department of Pharmacology for a Works-in-Progress presentation by Kotaro Hori, Ph.D. and Nurmaa Dashzeveg, Ph.D.

Kotaro Hori, Ph.D., Postdoctoral Fellow, Laboratory of Dr. Murali Prakriya
"Store-operated calcium channels: potential roles in regulating neuronal excitability and seizures?"

Abstract: Store-operated Ca2+ release-activated Ca2+ (CRAC) channels are a major pathway for calcium signaling in many cells and serve numerous functions, including gene expression, the production release of cytokines, and cell motility. Orai1, the protein encoding the channel pore, is highly expressed in hippocampal neurons, however, the role of Orai1 in regulating hippocampal neuronal function is not well understood. A widely used model of neuronal injury and seizures used intraperitoneal injections of kainic acid, a potent agonist of neuronal kainite receptors. We found that mice lacking Orai1 in the brain exhibit significantly stronger seizures and mortality compared to wildtype littermates. Correspondingly, measurements of inhibitory neuronal activity using CA1 slice electrophysiology revealed markedly reduced spontaneous inhibitory post synaptic currents (IPSCs) in the Orai1 knockout mice. The decrease in GABAergic output in response to kainic acid stimulation could potentially alter excitatory/inhibitory balance in the hippocampus and increase propensity of the Orai1 knockout mice for seizures. These results suggest novel roles of Orai1 channels in regulating hippocampal neuronal activity.

Nurmaa Dashzeveg, Ph.D., Postdoctoral Fellow, Laboratory of Dr. Huiping Liu.
"CD44 regulates glycosylation of breast cancer cells in metastasis"

Abstract: Breast cancer is the most common female cancer in the United States and ninety percent of the mortality in breast cancer is caused by metastasis. Circulating tumor cells (CTCs) with stemness or cancer stem cell (CSC) properties are considered the seeds of distant metastasis. Previously, our laboratory demonstrated that CD44+ CSCs mediate spontaneous metastasis in patient tumor-derived xenograft (PDX) models. Moreover, CD44 mediates CTC cluster formation that is correlated with increased metastasis and worse prognosis than single CTCs. The multiple steps driving metastasis require dynamic modifications of the cell surface glycoproteins, such as glycosylation. One of the most important glycosylation in cell adhesion is sialylation, which mediates cell detachment from the tumor mass by inhibiting cell-cell adhesion and increases migration of tumor cells. Our preliminary data identified that CD44 inhibits α2-6-sialylation by suppressing the expression of ST6 beta-galactosamide α2-6-sialyltransferase (ST6Gal1), thereby promoting cluster formation. I aim to examine the role of CD44 mediated ST6Gal1 suppression in metastasis. Elucidating the molecular mechanism by which CD44 mediates CTC cluster formation via glycosylation will provide new insights in metastasis.

Add Event to Calendar

Add Event To My Group:

Please sign-in