| 20529 |
Q8K211 |
COPT1_MOUSE |
High affinity copper uptake protein 1 (Copper transporter 1) (CTR1) (Solute carrier family 31 member 1) [Cleaved into: Truncated CTR1 form] |
DISRUPTION PHENOTYPE |
Homozygous mice lacking Slc31a1 exhibit profound growth and developmental defects and die in utero in mid-gestation (PubMed:11391005, PubMed:11391004). Homozygous embryos exhibit a dramatic reduction in size at E7.5, which is exacerbated during the progression of in utero development through day E10.5 (PubMed:11391005). Although the fundamental mouse embryonic structures are conserved at E7.5, homozygous embryos show that many structures including the neural ectoderm and mesoderm cell layers are poorly developed (PubMed:11391005). Conditionnal knockout mice lacking Slc31a1 in intestinal epithelial cells, are born at the expected frequency and exhibit normal growth rate and mass for the first 6-8 days postpartum, poor growth and lethality occurred beginning approximately 10 days after birth (PubMed:16950140). Conditionnal knockout mice lacking Slc31a1 in germ cells (GCs) seem normal in appearance (PubMed:31002737). Conditionnal knockout mice lacking Slc31a1 in Sertoli cells (SCs) exhibit normal fertility and display similar appearance as their wild-type littermates; no obvious behavioral deficit are noted (PubMed:31002737). {ECO:0000269|PubMed:11391004, ECO:0000269|PubMed:11391005, ECO:0000269|PubMed:16950140, ECO:0000269|PubMed:31002737}. |