Disease relevance of TF

• Segregation at the loci coding for the K88ab and K88ac small intestinal receptors to E. coli adhesins (K88abR, K88acR) and at the transferrin (TF) locus was studied in 38 pig families including 273 piglets [1].
• In uterine flushings, AP, RBP, and TF were low on Day 7, and then increased markedly (p < 0.01) by Day 13 in both cyclic and pregnant gilts [2].
• The effects of experimental Salmonella cholerae-suis inoculation with a virulent and an avirulent strain on serum iron (SI), total iron-binding capacity (TIBC), and transferrin (TF) were evaluated [3].
• The authors repeatedly treated 59 patients with thoracic sarcoidosis with transfer factor (TF) since 1976 [4].
• In this study, we determined the efficacy of TF as immunotherapy to treat experimental glioblastoma [5].

High impact information on TF

• Previous work has shown that the Pseudomonas-derived protease, pseudomonas elastase (PAE), can modify transferrin to form iron complexes capable of catalyzing the formation of hydroxyl radical (.OH) from neutrophil (PMN)-derived superoxide (.O2-) and hydrogen peroxide (H2O2) [6].
• We conclude .OH formation resulting from protease alteration of transferrin may serve as a mechanism of tissue injury at sites of bacterial infection and other processes characterized by increased proteolytic activity [6].
• A transferrin-like GPI-linked iron-binding protein in detergent-insoluble noncaveolar microdomains at the apical surface of fetal intestinal epithelial cells [7].
• By its NH2-terminal amino acid sequence, iron-binding capacity and partial immunological cross-reactivity with serum transferrin, the 80-kD protein was shown to belong to the transferrin family, and it is probably homologous to melanotransferrin, a human melanoma-associated antigen [7].
• Iron uptake from transferrin by copper-deficient reticulocytes was 52% of normal, and the rate of heme synthesis was 33% of normal [8].

Chemical compound and disease context of TF

• The best dose (product of 4x10(6) cells) of TF was also combined with carmustine for experimental therapy in rats with C6 malignant glioma [5].
• Eighteen Dunkin-Hartley guinea pigs and 50 NMRI mice were inoculated with Helicobacter pylori and the infection followed by culture, histopathology, antibody response, and plasma levels of the acute-phase proteins albumin, C3, and transferrin for up to 7 weeks [9].
• Comparison of liver, spleen, adrenals, gastrocnemius, and carcass weights, cell-mediated immunity as determined by contact sensitivity to DNFB, and transferrin showed no significant differences [10].
• The pulmonary DTPA clearance and the intrapulmonary transferrin accumulation were significantly increased in the peritonitis group (29.4 +/- 8.2 x 10(-3) min-1, p less than 0.02, and 15.1 +/- 3.1 x 10(-3) min-1, p less than 0.02) when compared with the control group (3.1 +/- 0.8 x 10(-3) min-1 and 4.5 +/- 0.5 x 10(-3) min-1) [11].
• Sequential assessment of pulmonary epithelial diethylene triamine penta-acetate clearance and intrapulmonary transferrin accumulation during Escherichia coli peritonitis [11].

Biological context of TF

• This linkage thus localizes the K88 loci, as the TF locus, on chromosome 13 [1].
• The TF and ALB probes were also used for restriction fragment length polymorphism (RFLP) analysis [12].
• The TF locus showed a segregation deviation towards the B variant while each of the K88 receptors behaved as a single autosomal dominant gene [1].
• Nucleotide sequence of porcine liver transferrin [13].
• Transfer factors (TF) are low molecular weight dialysable products extracted from immune cells which transmit the ability to express delayed-type hypersensitivity and cell mediated immunity from sensitized donors to nonimmnune recipients [5].

Anatomical context of TF

• They utilized this therapy with TF from human tonsil lymphocytes (TFh) on account of the ineffectiveness of the corticosteroid treatment, because of the side effects of the corticosteroids, and as primary TF therapy, and to test an animal TF preparation from pig tonsil lymphocytes (TFp) [4].
• Intratumoral TF reduced significantly the tumour size, and increased CD2+, CD4+, CD8+ and NK cell counts, it also increased the percentage of apoptotic tumour cells and the percentage of tumour tissue expressing Th1 cytokines [5].
• When [59Fe]uteroferrin was introduced into the allantoic sacs of five fetuses at Day 60 of pregnancy, its iron was transferred to another protein, identified as transferrin [14].
• The structure of the expressible VH gene from a hybridoma producing monoclonal antibodies against porcine transferrin [15].
• The method is based on the intravascular and extravascular distribution of indium-113m labelled transferrin compared with the intravascular distribution of technetium-99m labelled red blood cells [16].

Associations of TF with chemical compounds

• Tg production was increased > or = 5-fold by chronic exposure to thyrotropin (TSH), and > or = 25-fold by exposure to a mixture of TSH, insulin, transferrin, and hydrocortisone (4H) [17].
• Iron on uteroferrin is relatively stable to pH and is not readily lost to transferrin at around neutral pH unless low molecular iron chelators such as citrate, pyrophosphate, ATP, or ascorbate are present [14].
• Iron uptake was monitored after the application of 59Fe-labeled ferric citrate or pig transferrin [18].
• This glycoprotein belongs to the transferrin family and differed from the serum transferrin of the same adhesive-phenotype piglets [19].
• Transferrin GP74 contained one monosialylated and monofucosylated glycan chain of the N-acetyllactosamine type [19].

Regulatory relationships of TF

• Transferrin induces maturation of neutrophil granulocyte precursors in vitro [20].

Other interactions of TF

• The ALB gene was assigned to the q12 band of chromosome 8 and the TF gene to the q31 band of chromosome 13 [12].
• Linkage between the loci for transferrin and ceruloplasmin in pigs [21].
• Most of the TF and AFP (100 and 85-90%, respectively) reacted with Con A during the entire developmental period [22].
• The simple organization of the uteroferrin gene, which contrasts with those of the transferrin gene family, and the progesterone induction of uteroferrin mRNA expression suggest that, although this protein may have evolved in a manner distinct from other iron binding proteins, its regulation by steroid hormones may be similar [23].
• Escherichia coli grown in chemically defined iron-deficient media or in fluids containing the iron-binding proteins transferrin, lactoferrin, or ovotransferrin have well-characterized alterations in the chromatographic properties of tRNA's containing the modified nucleoside 2-methylthio-N6-(delta2-isopentenyl)-adenosine [24].

Analytical, diagnostic and therapeutic context of TF

• In situ hybridization mapping and restriction fragment length polymorphism analysis of the porcine albumin (ALB) and transferrin (TF) genes [12].
• We observed an additive antitumoral effect when TF was combined with chemotherapy [5].
• Hemin could inhibit transferrin binding of the recombinant protein in the competitive ELISA, whereas hemoglobin and synthetic iron chelators failed to do so [25].
• These iron binding substances were identified as ferritin, transferrin and a low molecular weight form by elution characteristics on chromatography and by immunological technique [26].
• The conformation of porcine serum ferric transferrin (Tf) and its stability against denaturation were studied by circular dichroism [27].

References