High affinity copper transporter involved in Cu(+) import into the cell upon copper-limitating conditions (PubMed:21819456, PubMed:23498952, PubMed:31932719). Functions with BIM1 and probably also FRE4 and FRE7, where FRE4 and FRE7 metalloreductases liberate the Cu(2+) bound to the BIM1 copper-binding site for subsequent import of Cu(+) into the cell by CTR1, via the reduction of BIM1-bound Cu(2+) to Cu(+) to reduce binding affinity for BIM1 but increase affinity for CTR1 (Probable). The BIM1-CTR1 pathway for copper uptake plays a key role in colonization in the brain where copper amounts are low and thus in cryptococcal meningitis (PubMed:25417972, PubMed:31932719). Interacts with the copper acquisition factor BIM1. Expression is induced by copper deficiency and regulated by the CUF1 copper-dependent transcription factor (PubMed:21819456, PubMed:29608794). The CTR1 promoter harbors the Cu-responsive element (CuRE), which is critical for CUF1 binding and activation under copper-limiting conditions (PubMed:29608794). Leads to a severe growth defect in copper deficiency conditions, but does not significantly affect melanin production, nor fungal virulence (PubMed:21819456, PubMed:25417972). However, when both CTR1 and CTR4 are disrupted, the colonization in the brain and subsequent virulence are significantly reduced (PubMed:25417972). Belongs to the copper transporter (Ctr) (TC 1.A.56) family. SLC31A subfamily.