Jorg Kirberg kirberg at nki.nl
Thu Mar 27 09:41:46 EST 1997

In article <199703271238.MAA27981 at holyrood.ed.ac.uk>,
xxzang at HOLYROOD.ED.AC.UK (Xing-Xing Zang) wrote:

> Dear all
> Dose anyone know the key sequence in FasL which is essential to bind Fas.
> Thanks.
> X X Zang

Dear X X,
for simplicity I would assume it is somewhere close to the point where
the point mutation in the gld allel of FasL occured.
It should be possible to find out about that one by searching medline, e.g.:

@C Takahashi, T.//Tanaka, M.//Brannan, C. I.//Jenkins, N. A.//Copeland, N.
G.//Suda, T.//Nagata, S.         Generalized lymphoproliferative disease
in mice, caused by a point mutation in the Fas ligand               Cell 
1994  76 6  969-76         Mar 25   Mice homozygous for lpr
(lymphoproliferation) or gld (generalized lymphoproliferative disease)
develop lymphadenopathy and suffer from autoimmune disease. The lpr mice
have a mutation in a cell-surface protein, Fas, that mediates apoptosis.
Fas ligand (FasL) is a tumor necrosis factor (TNF)-related type II
membrane protein and binds to Fas. Here, mouse Fasl gene was isolated and
localized to the gld region of mouse chromosome 1. Activated splenocytes
from gld mice express Fasl mRNA. However, FasL in gld mice carries a point
mutation in the C-terminal region, which is highly conserved among members
of the TNF family. The recombinant gld FasL expressed in COS cells could
not induce apoptosis in cells expressing Fas. These results indicate that
lpr and gld are mutations in Fas and Fasl, respectively, and suggest
important roles of the Fas system in development of T cells as well as
cytotoxic T lymphocyte-mediated cytotoxicity. 


Joerg Kirberg                              Tel. 0031 - 20 - 512 19 98
The Netherlands Cancer Institute           FAX  0031 - 20 - 512 20 11
Div. Molecular Genetics (H4)               E_mail kirberg at nki.nl
Plesmanlaan 121
NL - 1066 CX Amsterdam
The Netherlands

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