Disease relevance of Ftl1

• PURPOSE: Employing an in vitro model system of human melanoma progression, we previously reported ferritin light chain (L-ferritin) gene overexpression in the metastatic phenotype [1].

High impact information on Ftl1

• Untreated M1Egr-1 cells also exhibited cell adherence, expression of Fc and C3 receptors, and upregulation of the myeloid differentiation primary response genes c-Jun, junD, and junB and the late genetic markers ferritin light-chain and lysozyme [2].
• A small group of antioxidative defense genes were found in this population, including catalase, members of the glutathione (GSH)-S-transferase family, NAD(P)H menadione oxidoreductase 1, and the ferritin light chain [3].
• These results provided evidence that changes in cellular Ca(2+) and iron pool by SAAD increased cellular oxidative stress and that the down-regulation of FLC protein by SAAD would further enhance prooxidant production in spite of the increase in FLC mRNA [4].
• Genetic mapping of the mouse ferritin light chain gene and 11 pseudogenes on 11 mouse chromosomes [5].
• Multiple homologous sequences for the ferritin L subunit are present in mammalian genomes, but so far, only one expressed gene has been described [6].

Biological context of Ftl1

• Alterations in cellular Ca(2+) and free iron pool by sulfur amino acid deprivation: the role of ferritin light chain down-regulation in prooxidant production [4].

Anatomical context of Ftl1

• Here we report the isolation of a cDNA from a mouse bone marrow library, corresponding to an isoform of the mouse ferritin L subunit [6].

Analytical, diagnostic and therapeutic context of Ftl1

• We typed the progeny of two sets of genetic crosses to determine the map locations for loci containing sequences related to the ferritin light chain (Ft11) gene [5].

References