{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTransferrin receptor (TFRC, also known as CD71) is a central membrane receptor responsible for the cellular uptake of iron by binding iron‐loaded transferrin and, in some contexts, H‐ferritin. Structural and biochemical studies have delineated how TFRC forms a defined complex with transferrin—with conformational changes and pH‐dependent mechanisms promoting iron release—and established its pivotal role in maintaining iron homeostasis and supporting erythropoiesis. Moreover, TFRC expression is tightly controlled at the mRNA level via iron–responsive elements that ensure proper synthesis and recycling of the receptor, thereby regulating intracellular iron levels necessary for cell growth and metabolism."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTFRC also functions as a point of vulnerability that is exploited in various disease settings. Several pathogenic viruses—including New World arenaviruses, hepatitis C virus and Plasmodium vivax—hijack TFRC to gain cell entry, while in celiac disease TFRC mediates the retro‐transcytosis of gliadin–IgA complexes, thereby contributing to immune activation. In oncogenic settings, TFRC is transcriptionally upregulated by factors such as c‐Myc and MYCN, fueling iron uptake that supports rapid tumor cell proliferation; likewise, mutations that disrupt TFRC internalization can lead to immunodeficiency. Collectively, these findings underscore TFRC’s role in diverse pathological processes ranging from viral infections and iron overload disorders to cancer and neurodegenerative syndromes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "17"}, {"type": "fg_f", "ref": "15"}, {"type": "fg_fs", "start_ref": "18", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its extracellular interactions, TFRC’s function is intricately regulated by its intracellular trafficking, recycling and post–translational modifications. Endocytic sorting mechanisms–mediated by clathrin, dynamin and members of the SNX‐BAR family—as well as modifications such as ubiquitination and palmitoylation, fine–tune TFRC surface expression and stability. These processes not only impact iron delivery and activation of downstream signaling pathways (including effects on mitochondrial fusion and autophagy) but also render TFRC a reliable diagnostic marker for proliferative and erythroid precursor cells as well as certain immune and inflammatory conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Huizhong Feng, Kenji Schorpp, Jenny Jin, et al. 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