Disease relevance of Tim

• In mouse models of asthma and multiple sclerosis, affecting the function of Tim molecules altered disease phenotype [1].

High impact information on Tim

• In addition, expression cloning shows that the Sema4A receptor is Tim-2, a member of the family of T-cell immunoglobulin domain and mucin domain (Tim) proteins that is expressed on activated T cells [2].
• Identification of the T cell immunoglobulin mucin-domain containing (Tim) gene family introduced a new family of cell surface molecules that is involved in the regulation of immune responses [3].
• The mammalian Tim genes are widely expressed in a variety of tissues; however, unlike Drosophila, mTim mRNA levels do not oscillate in the suprachiasmatic nucleus (SCN) or retina [4].
• Organization and function of the small Tim complexes acting along the import pathway of metabolite carriers into mammalian mitochondria [5].
• A dominant induced mutation in the mouse, tightly associated with a reciprocal chromosomal translocation between Chrs 4 and 17, causes abnormal head tossing and circling behavior (the translocation induced circling mutation, Tim) [6].

Biological context of Tim

• Because the small translocation chromosome appears to be inseparably associated with the mutant phenotype, we have named the mutation translocation induced circling mutation symbol, Tim [7].

Associations of Tim with chemical compounds

• Human Tim-3 is a 301-residue type I membrane protein whose extracellular region contains a Cys-rich Ig-like domain and a mucin domain, the characteristics of Tim proteins [8].

References