| Description |
Mice homozygous for the Fyntm1Sor targeted mutation are
viable and fertile displaying no overt phenotype. T cell
receptor signaling is defective in homozygous mutant mice
and are characterized by a reduction in levels of
tyrosine-phosphorylated proteins, failure to flux calcium in
response to TCR cross-linking, and a reduction in production
of calcium-related IL2. THY-1-induced proliferation is also
reduced in thymocytes but not in splenic T cells.
Neurological defects include blunted long-term potentiation
(LTP), impaired special learning, and altered hippocampal
development.
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