Neuroscience 2004 Abstract
| Presentation Number: | 944.19 |
|---|---|
| Abstract Title: | PI-3 kinase is required for the anti-apoptotic function of a novel glial cell line-derived neurotrophic factor receptor α-like (GRAL) gene. |
| Authors: |
Zhou, J.*1
; Li, Z.1
; Wang, B.1
; Wu, X.1
; Yin, M.1
; Snyder, E. Y.2
1Inst Biochem & Cell Biol, Chinese Acad Sci, Shanghai, China 2CA, 320 Yueyang Rd, 200031, |
| Primary Theme and Topics |
Development - Trophic Factors and Developmental Cell Death -- Trophic factors and cell death |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Other |
| Session: |
944. Trophic Factors and Cell Death V Poster |
| Presentation Time: | Wednesday, October 27, 2004 3:00 PM-4:00 PM |
| Location: | San Diego Convention Center - Hall A-H, Board # D31 |
| Keywords: | GDNF receptor, PC12, APOPTOSIS , C17.2 |
We have previously reported cloning of a novel gene that shares moderate homology with the glial cell line-derived neurotrophic factor (GDNF) receptor a (GFRα) family (SFN 2003 program no. 677.1). The gene contained a putative signal peptide at its N-terminus and shares conserved spacing of cystine residues which are also present in the GFRα receptors family. It was thus designated as GDNF receptor alpha-like (GRAL) gene. It appears to be localized specifically in the central nervous system of adult mouse. To investigate its potential biological function in vitro, we first screened a variety of cell lines to verify the expression of this gene. GRAL mRNA was only found in C17.2 cell line, a neural stem cell line, albeit at low levels. It was, however, absent in other cells examined, such as primary cultures of astrocytes, PC12, B104 and C6 cell lines. Following withdrawal of serum, the number of surviving C17.2 cells was markedly reduced. In contrast, the expression level of GRAL mRNA was significantly increased in these cells, suggesting involvement of GRAL in the self-protection. To further characterize the anti-apoptotic function of GRAL, we used two series of PC12 cells, one with transient transfection and the other with stable transfection. Cell counting on either typan blue or fluorescein diacetate-stained cells showed that overexpression of GRAL effectively reduced apoptosis, as evidenced by marked increase of survived PC cells. Experiments with pharmacological inhibitors indicated that PI 3-kinase but not MAPK mediated GRAL's anti-apoptotic activity. These results suggest that GRAL is able to delay apoptotic death induced by serum withdrawal.
Supported by grants from the Chinese Academy of Sciences (No. KSCX2-SW-209), the National Basic Research Program of China (G1999054000) and the Chinese MOST (No. 2001AA221221).
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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