(i) A novel transporter, i.e., a thiamine transporter, which is referred to herein as ThTr-1; (ii) polynucleotide sequences, genomic and/or cDNA sequences, encoding said ThTr-1, which are referred to herein collectively and/or independently as TRMA (SLC19A2); (iii) oliginucleotides and oligonucleotide analogs derived from said polynucleotide sequences; (v) a display library displaying short peptides derived from said ThTr-1; (v) antibodies raised against/recognizing said ThTr-1; (vi) peptides or peptide analogs derived from said ThTr-1; (vii) methods of employing said peptides or peptide analogs, said oligonucleotides and oligonucleotide analogs, and/or said polynucleotide sequences to up-regulate or down-regulate transporter activity; (viii) the use of a mammalian TRMA (SLC19A2) derived sequence for designing and constructing molecules useful in the research, diagnosis and/or treatment of TRMA syndrome and/or manifestations thereof or those associated with thiamine deficiency and/or defective thiamine transport; (ix) the use of mammalian TRMA (SLC19A2) derived sequence for designing and constructing a two-hybrid system for isolating peptides capable of binding a mammalian TRMA (SLC19A2) gene product, Th-Tr-1; (x) a method of determining whether a subject has a mutated, polymorphic or normal TRMA (SLC19A2) allele; (xi) a method of determining whether a subject has defective, impaired or normal thiamine transport; and, last but not least, (xii) a method of determining a presence or absence of association of a mutated TRMA (SLC19A2) allele with a specific disease (e.g., diabetes mellitus, deafness and/or anemia) or a specific disease manifestation (e.g., diabetes mellitus vascular complications, such as diabetic nephropathy, myocardial infarction, coronary angioplasty associated restenosis, fewer coronary artery collateral blood vessels and myocardial ischemia).
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