General Information of the Molecule (ID: Mol04310)
Name
Ferritin heavy chain (FTH1) ,Homo sapiens
Synonyms
Cell proliferation-inducing gene 15 protein
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Molecule Type
Protein
Gene Name
FTH1
Gene ID
2495
Sequence
MTTASTSQVRQNYHQDSEAAINRQINLELYASYVYLSMSYYFDRDDVALKNFAKYFLHQS
HEEREHAEKLMKLQNQRGGRIFLQDIKKPDCDDWESGLNAMECALHLEKNVNQSLLELH
K LATDKNDPHLCDFIETHYLNEQVKAIKELGDHVTNLRKMGAPESGLAEYLFDKHTLGD
SD NES
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Function
Stores iron in a soluble, non-toxic, readily available form.Important for iron homeostasis. Has ferroxidase activity. Iron is taken up in the ferrous form and deposited asferric hydroxides after oxidation . Also plays a rolein delivery of iron to cells . Mediates iron uptake incapsule cells of the developing kidney . Delivery tolysosomes is mediated by the cargo receptor NCOA4 for autophagicdegradation and release of iron .{ECO:0000250|UniProtKB:P09528, ECO:0000269|PubMed:24695223,ECO:0000269|PubMed:26436293, ECO:0000269|PubMed:9003196}.
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Uniprot ID
FRIH_HUMAN
Ensembl ID
ENSG0000016799616
HGNC ID
HGNC:3976
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Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens
Type(s) of Resistant Mechanism of This Molecule
  EADR: Epigenetic Alteration of DNA, RNA or Protein
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
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Alectinib
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Drug Resistance Data Categorized by Their Corresponding Mechanisms
  Epigenetic Alteration of DNA, RNA or Protein (EADR) Click to Show/Hide
Disease Class: Lung adenocarcinoma [ICD-11: 2C25.0] [1]
Resistant Disease Lung adenocarcinoma [ICD-11: 2C25.0]
Resistant Drug Alectinib
Molecule Alteration Expression
Up-regulation
Experimental Note Revealed Based on the Cell Line Data
In Vitro Model ALK1903 cells N.A. Homo sapiens (Human) N.A.
DTP cells N.A. Homo sapiens (Human) N.A.
Experiment for
Molecule Alteration
Western blot assay
Experiment for
Drug Resistance
CellTiter-Glo 3D cell viability assay
Mechanism Description DTP cells evade ALK-TKI-induced ROS-mediated cell death through GPX4 activity. From these data showing elevated levels of ROS that arise through decreased levels of various antioxidant factors and decreased GSH synthesis, it might be expected that ROS-mediated cell death should occur in alectinib-induced DTP cells. However, DTP cells concurrently upregulated GPX4 protein, suggesting that ALK1903 DTP cells are able to evade ROS-mediated cell death by reducing ROS level in a GPX4-dependent manner.
References
Ref 1 Combined blockade of GPX4 and activated EGFR/HER3 bypass pathways inhibits the development of ALK-inhibitor-induced tolerant persister cells in ALK-fusion-positive lung cancer. Mol Oncol. 2025 Feb;19(2):519-539.

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