coloboma/tyrosine

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Expression of catecholaminergic mRNAs in the hyperactive mouse mutant coloboma.

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The SNAP-25 deficient mouse mutant coloboma (Cm/+) is an animal model for investigating the biochemical basis of locomotor hyperactivity. The spontaneous hyperactivity exhibited by coloboma is three times greater than control mice and is a direct result of the SNAP-25 deletion. SNAP-25 is a

Mouse and human SHPS-1: molecular cloning of cDNAs and chromosomal localization of genes.

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SHPS-1 (SHP substrate-1) is a glycosylated receptor-like protein with three immunoglobulin-like domains in its extracellular region and four YXX(L/V/I) motifs, potential tyrosine phosphorylation and SRC homology 2 (SH2) domain binding sites, in its cytoplasmic region. Various mitogens and cell

Abnormal presynaptic catecholamine regulation in a hyperactive SNAP-25-deficient mouse mutant.

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The consequences of a reduction in the presynaptic protein, SNAP-25, were investigated to determine the neurochemical basis of the marked hyperlocomotor activity in coloboma (Cm/+) mice. SNAP-25 is part of the minimal presynaptic machinery necessary for exocytotic neurotransmitter release. Reserpine

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