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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