TFRC Antibodies

Structure of TFRC

The transferrin receptor protein (CD71) encoded by the TFRC gene is a type II transmembrane glycoprotein with a molecular weight of approximately 85 kDa. Its actual molecular weight fluctuates within the range of 84-95 kDa depending on the degree of glycosylation modification.

This protein is composed of 760 amino acids and forms a typical topological structure of type II membrane proteins. Its extracellular C-terminal region presents a spherical conformation and forms transferrin binding sites through a large number of β -folds. A single transmembrane region is composed of 22 hydrophobic amino acids. The intracellular N-terminal fragment contains the key internalized signal sequence of YTRF. The secondary structure of this receptor is dominated by β -folding, a feature that significantly distinguishes it from myoglobin, which is mainly composed of α -helix, in terms of structural classification.

Fig. 1 Predict the structure of TFRC through UniProt.¹

Key structural properties of TFRC:

• A heterodimer transmembrane structure composed of α and β subunits
• Extracellular into tapered transferrin combined cavity
• Intracellular domains of iron-containing responsive elements
• A stable ligand binding interface with disulfide bonds

Functions of TFRC

The transferrin receptor encoded by the TFRC gene mainly mediates iron uptake in cells and is also involved in the regulation of various cellular physiological processes.

The iron uptake kinetics of this receptor exhibits typical ligand-dependent endocytosis characteristics, which are different from the linear kinetics of free iron diffusion, indicating its precise regulatory role in maintaining iron homeostasis. Its expression is regulated by the negative feedback of intracellular iron levels through the IRP/IRE system. This mechanism has similar physiological significance to the oxygen-binding property of myoglobin in maintaining metabolic balance.

Applications of TFRC and TFRC Antibody in Literature

1. Yi, Lu, et al. "TFRC upregulation promotes ferroptosis in CVB3 infection via nucleus recruitment of Sp1." Cell death & disease 13.7 (2022): 592. https://doi.org/10.1038/s41419-022-05027-w

This study is the first to confirm that CVB3 infection can induce ferroptosis and reveal its mechanism: the transcription factor Sp1 binds to the TFRC promoter, upregulates TFRC expression and promotes its nuclear translocation, exacerbating intracellular iron overload and lipid peroxidation, and ultimately leading to ferroptosis. The Sp1/TFRC/Fe axis may become a new therapeutic target for CVB3.

2. Li, Rong, et al. "FTO deficiency in older livers exacerbates ferroptosis during ischaemia/reperfusion injury by upregulating ACSL4 and TFRC." Nature Communications 15.1 (2024): 4760. https://doi.org/10.1038/s41467-024-49202-3

Research has revealed the mechanism by which the liver in the elderly is prone to ischemia-reperfusion injury: down-regulation of the FTO gene, enhanced stability of ACSL4 and TFRC mRNA through the m6A method, and promotion of ferroptosis. Supplementing NMN can activate FTO, inhibit ferroptosis, and provide a new target for improving donor liver function in the elderly.

3. Zhou, Xing, et al. "RAB17 promotes endometrial cancer progression by inhibiting TFRC-dependent ferroptosis." Cell Death & Disease 15.9 (2024): 655. https://doi.org/10.1038/s41419-024-07013-w

Research has revealed that RAB17 promotes tumor progression in endometrial cancer by ubiquitinating and degrading TFRC protein, inhibiting ferroptosis. Especially under conditions of glucose deficiency, the expression of RAB17 is upregulated, enhancing the survival ability of cancer cells through this axis.

4. Wang, Xinyuan, et al. "Knockdown of ANXA10 induces ferroptosis by inhibiting autophagy-mediated TFRC degradation in colorectal cancer." Cell death & disease 14.9 (2023): 588. https://doi.org/10.1038/s41419-023-06114-2

Studies have revealed that ANXA10 is highly expressed in colorectal cancer and is associated with a poor prognosis. It promotes the survival and metastasis of cancer cells by inhibiting autophagy-mediated TFRC degradation and preventing intracellular ferroptosis. ANXA10 may become a potential therapeutic target.

5. Wei, Xue-biao, et al. "Exosome-derived lncRNA NEAT1 exacerbates sepsis-associated encephalopathy by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis." Molecular Neurobiology 59.3 (2022): 1954-1969. https://doi.org/10.1007/s12035-022-02738-1

Studies have found that sepsis highly expresses NEAT1 in serum exosomes, which acts as ceRNA to adsorb miR-9-5p, thereby upregulating the expression of TFRC and GOT1, inducing ferroptosis and exacerbating sepsis-related encephalopathy. Targeting this axis may be a new therapeutic strategy.

Creative Biolabs: TFRC Antibodies for Research

Creative Biolabs specializes in the production of high-quality TFRC antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom TFRC Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our TFRC antibodies, custom preparations, or technical support, contact us at email.