Seminar by Dr. Marius SUDOL. "The role of the WW domain in Golabi syndrome and Hippo tumor suppressor pathway."

Dear all,

Cell Signal Unit(Yamamoto Unit) would like to invite you to a seminar by Dr. Marius SUDOL.

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Date: Thursday, June 27th

Time: 11:00 – 12:00

Venue: C016, Lab1

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Speaker: Prof. Marius SUDOL

Adjunct Associate Professor at Department of Medicine, Mount Sinai School of Medicine, NYC

Staff Scientist at Laboratory of Signal Transduction and Proteomic Profiling, Weis Center for Research, Danville, PA

Title: The role of the WW domain in Golabi syndrome and Hippo tumor suppressor pathway.

Abstract: The goal of the Sudol laboratory is to elucidate signaling networks that use a modular protein domain, known as the WW domain, which mediates well-defined protein-protein interactions with proline motif-containing ligands. Missense point mutations mapped within the domain or its ligand have been implicated in several human diseases including Golabi-Ito-Hall syndrome of intellectual disability and Liddle syndrome of hypertension. Our aim is to characterize signaling changes caused by genetic lesions that affect the WW domain complexes and result in human disease. The ultimate goal of our research is to predict and design molecular tools for interventions in WW domain-mediated pathways to correct pathological states.


In my seminar I will discuss in detail two projects:

(I)              The function of the WW domain-containing protein YAP (Yes kinase-associated protein), a potent oncogene and stemness factor in the Hippo tumor suppressor pathway. YAP is a transforming gene of the chromosome 11q22 amplicon, and its expression is elevated at a high frequency in human cancers, including cancers of liver, breast, ovary and prostate. Understanding the mechanism of YAP function should identify new drug targets and have direct implications for cancer management.

(II)          The PQBP1 (Poly-glutamine tract-binding protein 1) gene encodes a brain-enriched protein that contains a WW domain and regulates pre-mRNA splicing. Mutations in the PQBP1 gene were reported in several X chromosome-linked intellectual disability disorders including Golabi-Ito-Hall (GIH) syndrome. The mutation that causes GIH syndrome maps within the WW domain of PQBP1 and substitutes Tyrosine 65 (Y65) with Cysteine (C). We are generating human neuronal stem cell and mouse models of GIH syndrome in order to study the mRNA splicing defect globally.

Host: 

Tadashi Yamamoto, Cell Signal Unit

We look forward to seeing many of you.

Sincerely,

Kaori Yamashiro

Cell Signal Unit (Yamamoto Unit)