Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Canine marrow cells were incubated with transferrin-bound (59)Fe, and the partition of cellular iron was studied by chromatographic and gel filtration methods. Splitting-off of iron from the stromal fraction was avoided by lysing the cells in Tris HCl buffer at pH 8.6. Cellular iron was divided into four major compartments: stroma, microsomes, main hemoglobin, and fraction I. The iron in fraction I was found in ferritin, heme proteins, and low molecular weight iron. With incubation times of 3-10 min, (59)Fe appeared promptly in the main hemoglobin. The entry of (59)Fe into ferritin paralleled that of hemoglobin but was smaller in amount. When the marrow cells were incubated with (59)Fe for 15-20 min and reincubated without radioactive iron, movement of (59)Fe into main hemoglobin was observed, and essentially all this iron came from the particulate fraction (stroma, mitochondria, and microsomes). In these chase experiments there was no change in the total quantity of (59)Fe in ferritin. There was no evidence of a significant hemoglobin precursor other than low molecular weight iron. DEPENDING UPON CONCENTRATION, LEAD WAS OBSERVED TO INHIBIT CELLULAR IRON METABOLISM AT SEVERAL POINTS: uptake of iron by the cell, movement of iron from stroma to the soluble intracellular compartment, and synthesis of hemoglobin. The most pronounced inhibitory effect of lead was always on hemoglobin synthesis with an increase in ferritin: hemoglobin ratio. Bipyridine appeared to trap intracellular ferrous iron and to inhibit synthesis of both hemoglobin and ferritin. It was concluded that iron moves from the stroma into the soluble intracellular compartment as low molecular weight iron, probably as a complex of ferrous iron with low molecular weight components of the cytoplasm, that serves as the source of iron for both hemoglobin and ferritin synthesis.
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PMID:Studies on the partition of iron in bone marrow cells. 496 2

We searched for metastasis-related genes in adenoid cystic carcinoma by suppression subtractive hybridization analysis of high and low metastasis cell lines. Twelve genes (ten previously identified and two novel sequences) were identified as being expressed at lower levels in high metastasis cell line Acc-M when compared to low metastasis cell line Acc-2. The known sequences corresponded to the genes for cysteine-rich angiogenesis induction factor (cyr61), chromosome 7 RP11-52501 clone, G-protein, WAS familial ferritin I heavy chain, jumping translocation breakpoint, eukaryotic translation elongation, folate receptor and three ribosomal proteins. Among them, the G protein and ferritin I heavy chain genes contained mutations in the high metastasis cell line. The two novel gene sequences have been named ACC metastasis-associated RNH and ACC metastasis-associated suspected protein (GenBank # AF522024 and AF522025, respectively). Taken together, these results suggest that reduced expression and/or mutation of several genes in the tumor cell line Acc-M are associated with high tumor metastasis, providing important molecular biological materials for further study of metastasis control and possible targets for cancer gene therapy.
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PMID:Study of the difference of high and low metastasis cell line's gene expression map and metastasis-related genes of adenoid cystic carcinoma. 1450 62