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Neuroscience 2005 Abstract

Presentation Number: 788.10
Abstract Title: Further characterization of AMG-1 (associated molecule of GAPDH-1): a potential role in modulating the GAPDH/Siah death signaling.
Authors: Cascio, M. B.*1 ; Hara, M. R.1 ; Snyder, S. H.1,2,3 ; Sawa, A.1,2
1Neuroscience, Johns Hopkins Univ., Baltimore, MD
2Psychiatry, Johns Hopkins Univ., Baltimore, MD
3Pharmacology, Johns Hopkins Univ., Baltimore, MD

Primary Theme and Topics Disorders of the Nervous System
- Neurotoxicity, Inflammation, and Neuroprotection
-- Cell death mechanisms
Session: 788. Neurotoxicity: Apoptosis
Poster
Presentation Time: Tuesday, November 15, 2005 2:00 PM-3:00 PM
Location: Washington Convention Center - Hall A-C, Board # TT45
Keywords: apoptosis, GAPDH, Siah, NO
We have studied a role of GAPDH in neuronal cell death, especially focusing on the protein binding of GAPDH with an E3 ligase Siah as the key component of the death signaling. The existence of a novel GAPDH binding protein, Associated Molecule of GAPDH (AMG) was previously reported by our group which exists in several isoforms including 62kDa and 50kDa proteins (Cascio et al, SFN abstract 2004). Results of in vitro binding experiments indicate that the binding of AMG and GAPDH is increased upon treatment of GAPDH with nitric oxide (NO) generators, such as SNP or GSNO. Further in vitro binding studies were performed to explore the function of AMG which revealed inhibition of the GAPDH/Siah binding in the presence of AMG. These effects are being confirmed in cellular systems. Additionally, both AMG over-expression and AMG RNAi treatment lead to morphological changes in several cell types, though it is still unclear if these changes are directly associated with GAPDH. AMG may act to inhibit the recently described GAPDH/Siah death signaling pathway, and may play additional cytoskeletal roles such as actin regulation.
Supported by NIH (AS), NIH (SHS)

Sample Citation:

[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.

Copyright © 2005-2026 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.

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