Disease relevance of TFRC

• PROCEDURE: Concentrations of TR alpha 2, beta 1, and beta 2 mRNA in the myocardium were determined for clinically normal dogs (n = 7) and dogs with heart failure caused by dilated cardiomyopathy (DCM; 7) or chronic valvular disease (CVD; 7) [1].

High impact information on TFRC

• Early and recycling endosomes were resolved on Optiprep gradients and shown to be differentially associated with rab4, rab11, and transferrin receptor; rab4 was enriched on early endosomes and at least partially depleted from recycling endosomes, with the opposite being true for rab11 and transferrin receptor [2].
• The endocytosis and recycling of E-cadherin and of the transferrin receptor were similarly inhibited by potassium depletion and by bafilomycin treatment, and both proteins were accumulated in intracellular compartments by an 18 degrees C temperature block, suggesting that endocytosis may occur via a clathrin-mediated pathway [3].
• The two populations were also pharmacologically distinct, with AlF4 selectively blocking export of transferrin receptor from recycling endosomes to the basolateral plasma membrane [2].
• At 20 degreesC dIgA-pIgR internalize to interconnected groups of vacuoles and tubules that comprise the endosomal compartment and in which they codistribute with internalized transferrin receptors (TR) and epidermal growth factor receptors (EGFR) [4].
• We have characterized the polarity of the transferrin receptor in the epithelial Madin-Darby canine kidney (MDCK) cell line [5].

Biological context of TFRC

• We used the recycling of transferrin receptor in filter-grown MDCK cells to evaluate the accuracy of the sorting of a basolateral protein during endocytosis [5].
• Here we show that trypanosomes can also adapt to dilute dog serum without switching but by replacing the ESAG7 gene in the 221 ES by one from another ES, by deleting ESAG7 from the 221 ES with concomitant upregulation of transcription of ESAG7 in 'silent' ESs, by grossly overproducing the 221 Tf-R or by combinations of these alterations [6].
• CONCLUSIONS AND CLINICAL RELEVANCE: Altered regulation of transcription of the TR beta gene may be one facet of the myocardial phenotype in heart failure [1].

Anatomical context of TFRC

• The accuracy of transferrin receptor sorting (greater than 99.88%) during a single cycle of transit between the endosome and the plasma membrane is sufficient to maintain the high level of polarity of the cell [5].
• Using video microscopy and correlative electron microscopy to study cells grown thin and flat we show that endosome vacuoles tubulate in response to dIgA/pIgR but that the tubules contain TR as well as pIgR [4].
• Here we demonstrate that both MT1-MMP and MT3-MMP are internalized, transported to the trans-Golgi network through early endosomes, and recycled back to cell surface in 60 min in a manner distinct from the one employed by transferrin receptor [7].
• OBJECTIVE: To investigate whether expression of thyroid hormone receptor (TR) messenger RNA (mRNA) is changed in the myocardium of dogs with heart failure [1].

Analytical, diagnostic and therapeutic context of TFRC

• Western blot analysis of sorted fractions showed enrichment of the early endosomal markers transferrin receptor and the small GTPase Rab5 [8].

References