Publication for Fth1 and Ftl1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Fth1	ferritin heavy polypeptide 1	14319			[link]
mmu	Ftl1	ferritin light polypeptide 1	14325

Pubmed ID	Priority	Text
31333462	0.99	FtH with ferroxidase activity and FtL that induces iron nucleation.
	0.98	FtL, and FtH and reduced levels of GSH, suggesting a critical protective role against Hb-mediated ROS production and cell toxicity in the kidney.
	0.98	FtL, and FtH were found upregulated in kidneys from wild-type mice after hemolysis or in cultured tubular epithelial cells stimulated with Hb/heme.
	0.97	FtH) ( Supplemental Figure 3A-C ) and light ferritin chain (FtL) ( Figure 2I-L ).These
	0.97	ferritin subunits, light ferritin (FtL) ( Figure 5A-F ) and heavy ferritin (FtH) ( Supplemental Figure 3D ).
	0.95	FtH, and FtL than did wild-type mice with hemolysis.
25629408	0.98	Fth +/-/Ftl +/- mice), we observed a significant decrease in the expression of AcoI, Fxn, Dmt1, Fth, Ftl, Sod1, Sod2, and Trfrc genes, similar to the gene expression patterns observed for Fth +/- and Ftl +/- single heterozygous knock-out mice in the brain.
	0.98	Fth +/-/Ftl +/- double heterozygous knock-out mice showed a significant decrease in the expression of Sod1 and Sod2, the enzymes responsible for destroying free superoxide radicals in the cytoplasm and mitochondria, respectively.
	0.98	Fth +/-/Ftl +/- double heterozygous mice, the decrease in the expression of the Sod genes may lead to a more significant decrease in SOD activity, making them more susceptible to oxidative stress damage compared to single heterozygous knock-out mice.
	0.94	Fth +/-/Ftl +/- double heterozygous knock-out mice showed a liver gene expression pattern similar to the one observed for the single heterozygous knock-out mice, without significant differences with wild-type mice.
	0.94	H-ferritin homopolymers are capable of maintaining brain iron homeostasis, RNA interference could be used as a therapeutic approach even if the inhibition of the expression of the mutant allele suppresses in part (or to a high degree) the expression of the wild-type FTL allele.
	0.93	Fth +/-/Ftl +/- double heterozygous mice did not reveal significant differences with wild-type mice; however, analysis of gene expression in the brain showed significant changes in a number of genes (S5 and S6 Figs.).
	0.87	Fth allele on a wild-type Ftl background was embryonic lethal, whereas knock-out of the Ftl allele (Ftl-/-) led to a significant decrease in the percentage of Ftl-/- newborn mice.
	0.86	FTH1 gene in a Japanese family leads to the development of an autosomal dominant condition (hemochromatosis type 5) presenting with decreased levels of H polypeptides and iron overload, while mutations in the IRE sequence of the FTL gene have been found associated with the development of hereditary hyperferritinemia cataract syndrome, a disorder characterized by high levels of serum ferritin and early onset bilateral cataract, but
	0.85	Fth gene in mice on a wild-type Ftl background causes embryonic lethality.
	0.84	Fth +/-/Ftl +/- double heterozygous model, and whether the decrease in SOD activity observed in heterozygous Fth +/-
	0.77	Ftl allele on a wild-type Fth background caused embryonic lethality in approximately 50% of the expected Ftl -/- embryos.
	0.74	Fth and Ftl alleles revealed that some degree of complementation between the subunits must occur since we observed complete embryonic lethality when only one Fth allele was present (Fth +/-) in the Ftl -/- knock-out background (Fth +/-/Ftl -/- mice).
29749404	0.98	L-ferritin and H-ferritin and increased levels of intracellular oxidative stress in hamp silenced cells would suggest increased yield of reactive iron from heme, which could have led to mechanisms of cell death characterized as ferroptosis.
	0.97	H-ferritin and stored by L-ferritin or exported by ferroportin-1 (FPN1/SLC40A1/IREG1).
	0.96	H-ferritin, L-ferritin, C/ebpalpha).
	0.96	L-ferritin (p < 0.001), H-ferritin (p < 0.01), and C/ebpalpha (p < 0.001), and reduced Hif1alpha mRNA expression (p < 0.05).
	0.96	H-ferritin and L-ferritin), but when intracellular iron levels exceed the capacity for safe storage, excess iron may cause inflammation (IL-6), oxidative stress (Hif1alpha) and ER stress (Chop).
	0.95	L-ferritin, H-ferritin, C/ebpalpha, Chop, Hif1alpha, and IL-6 compared to cells treated with RLUC siRNA.
	0.94	L-ferritin, H-ferritin, and C/ebpalpha, whereas Chop, Hif1alpha and IL-6 were moderately elevated (c).
	0.94	L-ferritin, H-ferritin, C/ebpalpha, Chop, and IL-6, whereas mRNA expression of Hif1alpha was significantly reduced compared to control (ctrl).
	0.93	L-ferritin, Chop, and IL-6 were all significantly elevated after 4 h of 10 microM hemin incubation, whereas H-ferritin was increased by 1 microM hemin.
	0.90	H-ferritin, and L-ferritin (b).
	0.89	H-ferritin (p < 0.01), L-ferritin (p < 0.001), and IL-6 (p < 0.05; Fig. 1b), measured at the end of the study were increased.
19519778	0.98	Ftl, Nramp2, and Cp were found to be increased in the Fth1+/- mice compared with wild-type mice.
	0.97	FTL-Tg) mice showed an increase in the cytoplasmic levels of both FTL and ferritin heavy chain polypeptides, a decrease in the protein and mRNA levels of transferrin receptor-1, and a significant increase in iron levels.
	0.97	FTH1 subunit is thought to play a role in the rapid detoxification of iron, whereas the FTL subunit facilitates iron nucleation, mineralization, and long-term iron storage.
	0.97	FTL-Tg mice, NIs composed of the murine Ftl and Fth1 subunits and the mutated human FTL polypeptide were found throughout the CNS (Fig. 1).
	0.97	Fth1, and pantothenate kinase 2 (Pank2) genes were significantly decreased in both the CTX and CBL of FTL-Tg mice.
	0.89	FTL-Tg mice and non-Tg controls was observed in the levels of endogenous murine Ftl and Fth1 polypeptides (Fig. 1g).
	0.78	Ftl and Fth1 in the CTX of 187 +- 29.7% and 244 +- 8.5%, respectively.
	0.70	FTL-Tg and non-Tg controls showed no differences in the expression of the Ftl subunit and a significant reduction of Fth1 expression in FTL-Tg mice.
	0.66	Ftl and Fth1 mRNAs between transgenic mice and age-matched non-Tg controls (i).
31920471	0.98	Ftl-/- mice show that Fth ferritin homopolymers are capable of maintaining brain iron homeostasis in vivo, paving the way for the development of a potential therapeutic approach for HF using RNA interference to induce sequence-specific post-transcriptional gene silencing of mutant FTL (Li et al.,).
	0.97	Ftl-/- mice show that because FTH1 ferritin homopolymers can maintain brain iron homeostasis in a mouse model, there is the potential for development of a therapeutic approach for HF treatment using RNA interference to induce sequence-specific post-transcriptional gene silencing of mutant FTL or alternatively both, wild-type and mutant FTL alleles (Li et al.,).
	0.96	FTL) and heavy chain (FTH1) subunits, possessing complimentary iron-handling functions and forming three-fold and four-fold pores.
	0.95	Ftl-/- mice are viable (knock-out of the Fth subunit is embryonic lethal) and do not show signs of neurodegeneration, presence of an inflammatory process, noticeable protein aggregates, or iron accumulation as in patients with HF, suggesting that the deleterious effect(s) caused by mutant FTL subunits in HF are driven by disruption of the ferritin pore structure and unraveling of the C-terminus in the heteropolymer rather than by a loss of normal function of the FTL subunit itself.
	0.94	FTL as well as antibodies against ferritin heavy chain (FTH1) and mutant-specific antibodies strongly label ferritin IBs of all sizes in glial cells and in nerve cells (Vidal et al.,).
	0.73	FTH1 and FTL subunit concentrations, respectively, but the increase in total iron content is again modest at 25%.
	0.72	FTH1 subunit contains the ferroxidase center, which oxidizes the ferrous ions in preparation for mineral formation and the FTL subunit contains clusters of negatively charged residues which foster the nucleation and mineral growth.
16203866	0.98	H-ferritin, but not L-ferritin, shows saturable binding to subsets of human T and B cells, and its expression is increased in response to inflammation.
	0.98	H-ferritin, but not for L-ferritin, and expression of TIM-2 permits the cellular uptake of H-ferritin into endosomes.
	0.97	H-ferritin, but not for L-ferritin, and that binding of H-ferritin to TIM-2 leads to the endocytosis of extracellular H-ferritin.
	0.96	H-ferritin, but not L-ferritin.
	0.95	L-ferritin, may serve to regulate levels of serum ferritin, whereas the H-ferritin receptor may subserve independent cellular functions in response to a selective increase in H-ferritin.
	0.92	H-ferritin, but not L-ferritin, shows saturable binding to subsets of human T and B cells.
30364139	0.98	ferritin heavy chain (FTH1) and light chain (FTL) to store iron in the oxidized state and of ferroportin 1 (FPN1) to export intracellular labile iron.
	0.98	FTH1 and FTL expression in wild-type mouse embryonic fibroblasts (MEFs) but not in Nrf2 KO MEFs, and an ARE located 4 kb upstream of the FTH1 transcriptional start site is responsible for the induction by Nrf2.
	0.98	FTH1 and FTL expression are regulated not only by transcription but also by translation; an iron-responsive element (IRE) located in the 5'-untranslated region of target mRNAs is bound to iron regulatory proteins (IRPs) and negatively regulates its translation in the absence of iron.
	0.98	FTH1, and FTL1), as well as upregulation of genes involved in iron uptake (TFR1 and Sec15l1) and mitochondrial import (Mfrn2).
	0.96	FTH1) and light chain (FTL) in various ratios and having differing functions.
	0.96	FTH1 and FTL.
32015337	0.98	FTL and FTH (Fig. 4a, b, d, e).
	0.97	ferritin light chain (FTL) and ferritin heavy chain (FTH).
	0.97	FTL and FTH were obviously increased in the UC tissues (Fig. 1f-h).
	0.97	FTL and FTH (Fig. 2d, e, g, h).
	0.95	FTL and FTH protein levels in colonic IECs were all decreased in the GSK 414-treated colitis mice.
	0.93	FTL, FTH, and PTGS2 (Fig. 5c, d) in the RSL3-treated cells, which implied that ferroptosis had occurred.
30954544	0.98	FTL) and FTH.
	0.98	FTH and FTL mRNA translation, while intracellular Fe accumulation promotes IRP2 degradation and allows for FTH and FTL mRNA translation.
	0.97	FTL is thought to provide the scaffold supporting the ferritin multimeric complex, while the ferroxidase activity of FTH converts redox-active Fe2+ into redox-inactive Fe3+ via a process referred to as Fe nucleation.
	0.97	FTH and FTL mRNA translation.
	0.95	FTH and FTL are encoded by distinct genes, with germline Fth deletion being embryonically lethal in mice and insects.
31263155	0.98	L-ferritin, H-ferritin) and iron import (Tfrc, Dmt1(+IRE)) in astrocytes, especially after iron treatment.
	0.98	L-ferritin, H-ferritin) and import (Tfrc, Dmt1(+IRE)) in oligodendrocytes, especially following the addition of iron.
	0.97	L-ferritin) and heavy chain (H-ferritin) to provide insight into the mechanisms by which iron homeostasis is regulated in astrocytes and oligodendrocytes.
	0.97	L-ferritin and H-ferritin mRNA levels were significantly increased, and Tfrc mRNA levels were substantially decreased, in oligodendrocytes from all three mouse strains after iron treatment (all P < 0.05).
	0.96	L-ferritin and H-ferritin mRNA levels were substantially increased in all three groups after iron treatment (all P < 0.05 vs cells not treated with iron).
31551410	0.98	Ft-L, and Ft-H contents, and reduced expression of ALAS2, FECH, and FLVCR mRNAs in the bone marrow.
	0.97	Ft-L and Ft-H contents, and reduced the expression of ALAS2, FECH, and FLVCR mRNAs in the bone marrow
	0.97	Ft-L and Ft-H Proteins (Ft-L: Fig. 2c, e; Ft-H: Fig. 2d, f) and mRNAs (Ft-L: Fig. 2g; Ft-H: Fig. 2h) in the bone marrow of CBS-/- mice, as compared with CBS+/+ and CBS+/- mice.
	0.97	Ft-L and Ft-H proteins and down-regulated Fpn1 and DMT1 in BMDMs
	0.95	Ft-L (Fig. 4d), and Ft-H (Fig. 4e) proteins was significantly higher, while DMT1 (Fig. 4b) and Fpn1 (Fig. 4c) proteins lower in BMDM cells in CBS-/- mice, when compared to CBS+/+ and CBS+/- mice.
31976478	0.98	FTL and FTH protein levels and a trend towards lower TFR1 protein levels (Fig. 1E-H).
	0.98	Ftl1 and Fth1 mRNA levels (SDC Figure 1j-l, Supplemental Digital Content).
	0.96	FTL and FTH) and lower transferrin receptor 1 (TfR1) protein levels.
	0.88	ferritin light chain (FTL), ferritin heavy chain (FTH) and ferroportin (Fpn) mRNA and protein levels (Fig. 1A-D; SDC Fig. 1C-H, Supplemental Digital Content) remained unaltered.
	0.85	Fth and Ftl mRNA and protein levels, suggesting that the iron content remained unaffected (SDC B-G, Supplemental Digital Content), thus excluding the involvement of the Bmpr2 SNP in explaining changes in splenic iron levels.
18755684	0.98	Ftl and Fth1 polypeptides, which are seen to aggregate in neurons and glia throughout the life span of the mice.
	0.98	FTH1 and FTL polypeptide subunits are important for the iron storage function of ferritin, with the former containing the ferroxidase site for ferrous iron oxidation and the latter containing the iron nucleation site .
	0.97	FTH1 subunit has a potent ferroxidase activity that catalyzes the oxidation of ferrous iron, whereas the FTL subunit plays important roles in iron nucleation and protein stability, giving ferritin the dual functions of iron detoxification and iron storage.
	0.59	FTL polypeptides with the p.Phe167SerfsX26 mutation suggest that this mutation is apparently not severe enough to prevent iron incorporation, but it has a C terminus exposed external to the protein shell similar to that associated with the FTL460-461InsA mutation and the extended Fth1 polypeptides.
29774023	0.98	FtL levels in the lungs of Mtb-infected Fth-/- mice at 9 weeks postinfection (Figures 3A,B) which is likely a compensatory response to limiting FtH levels.
	0.98	FtL) and iron export (FPN) proteins, leading to reduced levels of iron in the lungs of Fth-/- mice.
	0.97	FtH) chains and 24 light (FtL) chains, which can bind up to 4,500 Fe3+ ions.
	0.97	FtL was increased in Fth-/- macrophages compared to those from Fth+/+ mice (Figure S1B in Supplementary Material).
28774900	0.98	Ftl1 and Fth1 in the mutant (fig. S8A).
	0.95	Ftl1 and Fth1 mRNAs in wild-type but not mutant reticulocytes (fig. S8B); this result suggested that Ube2o-/- reticulocytes are responding to increased cytosolic iron or heme levels and that reticulocyte iron deficiency is unlikely to be the cause of the anemia.
	0.87	FTL1 and FTH1) were also elevated in Ube2o-/- reticulocytes (Fig. 1E).
30558109	0.98	H-ferritin (FtH) receptor T cell immunoglobulin and mucin domain 2 (TIM2) and light chain L-ferritin (FtL) receptor scavenger receptor, member 5 (Scara5).
	0.98	FtH, FtL, delta-aminolevulinate synthase 1 (ALAS1), aconitase 2 (ACO2), hypoxia-inducible factor 2 (HIF2) mRNAs to mediate the degradation of the transcripts of the IREs to decrease iron storage and export.
	0.91	FtH and FtL. Due to the ferroxidase activity of FtH, cytosolic ferrous iron (Fe2+) is oxidized into ferric iron (Fe3+) prior to storage in the ferritin cavity.
32080266	0.98	Fth1-/- macrophages exhibited similar trends as Fth1+/+ macrophages in the response to the iron treatments, with upregulation of genes involved in iron storage (Ftl) and iron export (Slc40a1) as well as with a decrease in the expression of the iron internalization-related gene Tfrc in response to heme (Table 3).
	0.97	FTH1 differs from L-ferritin (FTL) in its ferroxidase activity, which is responsible for the oxidation of iron Fe2+ to Fe3+, preventing the oxidative damage that could be caused by Fenton reactions involving Fe2+ .
	0.95	H-ferritin the expression of L-ferritin is not increased.
18053288	0.98	L-ferritin and H-ferritin synthesis in H9c2 cardiomyocytes (Ref.) and in mouse hearts (Ref.), with a prominent upregulation of H-ferritin, which has been proposed to have an antioxidant function (Refs).
	0.97	H-ferritin and L-ferritin, respectively) (see Refs for reviews) and of the TFRC gene (Refs) in response to iron has been described, these two proteins are mainly controlled at the post-transcriptional level through the IRE-IRP system.
23781294	0.98	H-ferritin is endowed with a ferroxidase activity and is essential for iron incorporation into the core of large L-ferritin and H-ferritin complexes.
	0.53	H-ferritin and L-ferritin.
25600948	0.98	Fth, Ftl, and Slc40a1.
	0.97	Fth1 and Ftl1 (genes for Ft heavy and light chains, respectively) and Slc40a1 (gene for Fpn1).
26403645	0.98	FTL and FTH1) expression compared to ferroptosis-resistant cells.
	0.98	FTH1, but not FTL and TFR1, is regulated by NRF2 in ferroptosis.
26778957	0.98	H-Ft, L-Ft and Fpn mRNAs, should inhibit their translation.
	0.97	L-ferritin expression clearly shows that only H-Ft is upregulated at the protein level in SOD1G93A mice, not only in tissues primarily affected by ALS (muscles, M. oblongata, and spinal cord) but also in the liver, a tissue, which is not directly related to the ALS pathology.
30930742	0.98	FTH1/FTL) that can store up to 4500 iron atoms.
	0.96	FTL, FTH1) and the HERC2 E3 ubiquitin ligase as NCOA4-interacting partners.
31659150	0.98	ferritin heavy (FTH) and light chains (FTL).
	0.94	FTH1) and a light subunit (FTL).
22003390	0.98	FtH and FtL monomers, an iron exporter, ferroportin, and other transcripts.
27685634	0.98	ferritin heavy chain (FtH) and ferritin light chain (FtL) (at least, P<0.05; Figure 5d).
30200471	0.98	H-ferritin and L-ferritin genes is regulated post-transcriptionally by the IRPs.
31320987	0.98	H-ferritin and L-ferritin, and the twelve pairs of subunits binding head to foot form the 24 subunit ferritin cages.
30287942	0.97	FTL or FTH1, iron further promoted ROS increase and GSDME cleavage (Fig. 1g).
	0.97	FTL or FTH1 knockdown in A375 cells, the cleavage of caspase-9 and -3 was further enhanced by the CCCP/iron treatment (Fig. 2f).
	0.91	FTL- or FTH1-knockdown A375 cells (Supplementary information, Fig. S1b).
	0.91	FTL or FTH1 enhanced the CCCP/FeSO4-induced cleavage of caspase-3 and -9.
	0.90	FTL or FTH1 enhanced LDH release and cell death in response to CCCP/FeSO4 stimulation.
	0.90	FTH1- or FTL-knockdown A375 cells, which could be abolished by DFO pretreatment (Supplementary information, Fig. S1g).
	0.86	FTL- or FTH1-knockdown A375 cells (Supplementary information, Fig. S1c, pyroptotic cells were indicated by red arrows).
	0.86	FTH1- or FTL-knockdown A375 cells (Fig. 1b).
	0.80	FTL or FTH1 enhanced CCCP/FeSO4-induced LDH release and GSDME cleavage.
	0.67	ferritin light chain protein (FTL) or ferritin heavy chain 1 (FTH1), two components of ferritin, was separately knocked down in melanoma A375 cells (Supplementary information, Fig. S1a), and several reagents that activate oxidative stress, including carbonyl cyanide m-chlorophenyl hydrazone (CCCP), NaAsO2, H2O2, antimycin A, and oligomycin, were used to evaluate the role of iron metabolism in cell death.
25259650	0.97	H-ferritin possesses ferroxidase activity and enables the oxidation of iron; L-ferritin induces iron nucleation within the central core of the protein.
	0.97	L- and H-ferritin, can cross the inner BRB through L-ferritin binding to Scara5 and H-ferritin binding to TfR1 in retinal blood vessels.
	0.97	H-ferritin also has a nuclear localization in retinal cells (data not shown), the presence of L-ferritin in the nuclei, with its specific iron nucleation function, should be of importance for counteracting the iron oxidative DNA damage.
	0.94	H-ferritin, and some authors even deny the existence of L-ferritin in the nucleus.
	0.92	L-ferritin binds to Scara5, while H-ferritin binds to TIM-2 and transferrin receptor 1 (TfR1).
30428583	0.97	H-ferritin utilizes ferroxidase activity that is necessary for the oxidation of ferrous (Fe2+) to ferric (Fe3+) iron while L-ferritin contains acidic residues on the surface cavity of the protein that facilitate ferroxidase turnover and are crucial for the nucleation of ferric iron within the core of the fully formed protein.
	0.91	L-ferritin has been shown to bind to Scara5, H-ferritin has thus far been shown to bind to Tim-2 in rodents, Tim-1 in humans, as well as CXCR4 and TfR1 (Figure 1).
	0.91	L-ferritin subunit and as such, remain a poor indicator of iron status of the patient in this inflammatory state, as described earlier it is H-ferritin that is mostly responsive to the inflammatory process.
	0.89	H-ferritin, but not L-ferritin, at the Arg23 residue.
31941883	0.97	Fth1, Ftl1), and regulate the stability or translation of these mRNAs.
	0.97	Ftl1 mRNA levels were similar in WT and Irp2-/- islets, but unexpectedly, Fth1 mRNA levels decreased in Irp2-/- islets, which may be a transcriptional response to compensate for increased Fth1 protein (Fig. 4b).
	0.68	Fth1- and Ftl1-subunits, and TfR1 were assessed in WT and Irp2-/- islets.
	0.63	Ftl1 levels were similar in WT and Irp2-/- islets, while Fth1 was not detected in WT islets, but notably increased in Irp2-/- islets (Fig. 4a).
24130337	0.97	Ftl1 and Fth1 and the protein levels of hemoxygenase-1 were reduced in palmitate- but not oleate-treated PPMs.
	0.94	Ftl1 and Fth1, respectively]), and export (ceruloplasmin [Cp] and ferroportin-1 [Slc40a1]) in MFehi compared with MFelo cells.
24791141	0.97	H-ferritin and L-ferritin levels and drastic upregulation of hepcidin expression.
	0.54	H-ferritin and L-ferritin and reverse transcription-polymerase chain reaction (RT-PCR)/quantitative PCR (qPCR) analysis of mRNA levels for various iron-regulatory genes in wild-type and Tmprss6msk/msk mouse retinas.
26160767	0.97	H-ferritin was slightly overexpressed as a result of in vitro FAC accumulation, both H- and L-ferritin were overexpressed in vivo posttransplantation.
	0.96	H-ferritin) participates by converting the more toxic Fe2+ to Fe3+, while light-chain ferritin (L-ferritin) is primarily involved in long-term iron storage.
28622511	0.97	FTH) and light/liver (FTL) genes.
	0.95	FTH/FTL subunits, which can store and convert ~4,500 atoms of Fe2+ into inert Fe3+ through the ferroxidase activity of FTH.
28703745	0.97	L-Ferritin and H-Ferritin in FtMt overexpressing mice were decreased significantly (Figure 6a,c), and those of TfR1 increased (Figure 6d), compared to wild-type mice.
	0.97	L-Ferritin and H-Ferritin expression, and increased TfR1 expression.
26441243	0.97	HFt and L-ferritin (LFt), respectively, in mice.
28499927	0.97	ferritin light chain (FtL) and ferritin heavy chain (FtH) as well as for the iron exporter FPN.
29089902	0.97	L-ferritin, Ftl1 and H-ferritin, Fth1); and iron export, as ferroportin (Slc40A1), thereby controlling mRNA stability or translation (Anderson et al.,; Zhang et al.,).
30630985	0.97	FTL, FTH1) that can chelate up to 4,500 iron atoms in a non-toxic ferrihydrite mineral core.
31781351	0.97	ferritin light chain (FTL) and ferritin heavy chain 1 (FTH1).
30555055	0.96	Ft-H and Ft-L in serum (biomarkers for body iron stores) were significantly higher in old mice than in young mice (Fig. 1E, F).
	0.96	Ft-H and Ft-L in the liver, kidney and heart, and up-regulated serum iron level in old mice.
	0.95	Ft-H and Ft-L in the liver (Fig. 1G; J & M), kidney (Fig. 1H; K & N) and heart (Fig. 1I, L &O) were found to be significantly higher in old mice compared to young mice.
	0.95	Ft-H, Ft-L, Tf and CP contents (Fig. 2E & G) in young mice as compared to the isochronic parabiotic mice (Y-Y).
	0.94	Ft-H and Ft-L in the liver, kidney and heart, and down-regulate serum iron level and up-regulate serum Ft-H and Ft-L contents in young mice.
	0.93	Ft-H, Ft-L, Fpn1 and CP in the liver (Fig. 3C & E), reduced expression of Ft-L, TfR1, DMT1, Fpn1 and CP in the kidney (Fig. 4C & E), and reduced expression of Ft-H, Ft-L and Fpn1 in the heart (Fig. 5C & E), as compared with the isochronic parabiotic mice (O-O).
	0.92	Ft-H, Ft-L, Fpn1 and CP contents in the liver (Fig. 3B & D), increased Ft-L, TfR1, DMT1 and CP contents in the kidney (Fig. 4B & D), and increased Ft-H, Ft-L, DMT1, CP and decreased TfR1 in the heart (Fig. 5B & D), as compared with the isochronic parabiotic mice (Y-Y).
	0.88	Ft-H, Ft-L, Tf and CP contents in young mice
	0.70	Ft-H, Ft-L, Tf and CP contents (Fig. 3F & H) as compared to the isochronic parabiotic mice (O-O).
22693571	0.96	ferritin heavy chain (Fth1) expression is increased in Gfap+/R236H/Nrf2+/+ and reduced back to wild-type levels in Gfap+/R236H/Nrf2-/- (Figure 6A), although ferritin light chain transcripts remain unchanged (Ftl1, data not shown).
	0.86	Fth1 or Ftl1 do not seem to change, regardless of Nrf2 activation.
24586712	0.96	FTH and FTL expression in the kidney decreased by half when sham mice were treated with DFO.
	0.92	FTH and FTL expression was approximately 1.5-fold higher in UUO mice than in sham mice.
19154717	0.96	H-ferritin is a ferroxidase and L-ferritin induces polynucleation of iron ], both ferritins can independently incorporate iron into a core.
20817278	0.96	L-ferritin, where the active site is on H-ferritin yet heteropolymers of H and L subunits have a higher ferroxidase activity per H subunit than H homopolymers.
22860010	0.96	Fth1, Ftl1, Table 1).
27188291	0.96	ferritin heavy chain, FtH, and ferritin light chain, FtL) were also found to be significantly elevated in CKO mice.
25220979	0.95	L-ferritin mRNA was found to be twice as high in old rat hearts compared to young ones, presumably upregulated by age-related oxidative stress, while H-ferritin levels did not change.
	0.93	L-ferritin mRNA correlated with heart iron concentration while H-ferritin mRNA was constitutively expressed.
	0.85	H-ferritin mRNA levels were about 2-7 fold higher than those of L-ferritin in both males and females.
	0.81	L-ferritin transcription increases with iron while H-ferritin transcription does not rise significantly.
	0.55	L-ferritin promoter has shown it to be affected by antioxidant inducers as well as high iron concentrations; the H-ferritin promoter did not show the same response to high iron.
27574973	0.95	Ftl (DFP100; p = 0.0233), without significant changes in Fth1, Cp, Tfrc, Tf, and Sod1 levels.
	0.94	Ftl (DFP50; p = 0.0049, DFP100; p = 0.0199) and Fth1 (DFP50; p = 0.0006, DFP100; p = 0.0007), without significant changes in Hamp or Tfrc mRNA levels.
	0.89	Ftl (p < 0.0001), Fth1 (p < 0.05), hepcidin (Hamp) (p < 0.001), AcoI (p < 0.05), Sod1 (p < 0.05), and Hmox1 (p < 0.05) mRNA was observed.
32205843	0.95	H-ferritin and L-ferritin levels are significantly higher in Prx5-/- mice compared to WT mice with HFe.
	0.94	H-ferritin and L-ferritin mRNA levels and decreases TfR mRNA levels compared to ND in both WT and Prx5-/- mice.
19513908	0.94	H-ferritin but not L-ferritin levels.
	0.92	H-ferritin gene knockout, which is associated with a compensatory increase in L-ferritin, had no effect on astrocyte vulnerability to hemin.
	0.87	H-ferritin by gene transfer, but that L-ferritin had no effect per se.
	0.82	H-ferritin in the CNS but compensate by increasing L-ferritin expression.
19416716	0.94	FtL and FtH, both of which are encoded by transcripts that contain 5' IREs as well.
	0.91	FtL and FtH proteins were observed in animals on a low-iron diet (Figure 1C).
	0.55	FtL and FtH decreased.
23455710	0.94	FTL1 and FTH1 or ferritin light and heavy chains (FTL and FTH)), and export (SLC40A1 or ferroportin (FPN)).
24349383	0.94	H-ferritin has a ferroxidase centre that promotes the conversion of Fe2+ to Fe3+, and L-ferritin facilitates nucleation and mineralization of the iron core.
25447222	0.92	FtL and FtH than WT-FVB, respectively (Fig. 2A, middle and lower panels).
	0.90	FtH/FtLF167SfsX26 produces more effectively ROS species in physiological solutions compared to FtH/FtL. In these measurements, oxygen reduction is related to the generation of ROS.
	0.81	FtL and FtH increased with age, but they reached a maximum at 12 months.
	0.78	FtH/FtLF167SfsX26 than for the FtH/FtL, proving that in the presence of the variant ferritin iron is less retained and ROS are more efficiently generated.
23044750	0.91	ferritin light polypeptide (Ftl) is up-regulated ~8 fold, and the ferritin heavy chain (Fth1) is up-regulated ~14 fold, when comparing maturation stage to secretory stage amelogenesis.
29052173	0.90	H-ferritin) is responsible for the rapid oxidation of ferrous to ferric iron at a dinuclear center, whereas the L-subunit (L-ferritin) appears to help iron clearance from the ferroxidase center of the H-subunit and support iron nucleation and mineralization.
	0.70	H-ferritin, L-ferritin, and FPN1 (Fig. 7c).
27773819	0.84	FTH1 [ferritin, heavy polypeptide 1], FTL1 [ferritin, light polypeptide 1], GPX4 [glutathione peroxidase 4], HAMP [hepcidin antimicrobial peptide], HSPB1 [heat shock protein family B (small) member 1], NRF2 [nuclear factor, erythroid 2 like 2], SLC40A1 [solute carrier family 40 member 1], STEAP3 [six-transmembrane epithelial antigen of prostate 3], TF [transferrin], and TFRC [transferrin receptor]) involved in iron metabolism and lipid peroxidation was assayed in both FANCD2-deficient and wild type BMSCs (Fig. 4A).
26303407	0.69	L-ferritin and GFAP (n=3), and between H-ferritin and MBP (n=3), as well as between H-ferritin and F4/80 (n=3).
31568497	0.65	H Ferritin gene (Fth-/-) die during embryogenesis whereas the deletion of the L Ferritin (Ftl-/-) only cause reduced viability with the majority of the embryos being born without obvious defects.
25120486	0.64	H-ferritin, L-ferritin and TfR1 (only the A IRE of TfR1 mRNA is shown).
26707700	0.57	FTL and FTH1) are present as well.