Memory Molecule Pivotal to Brain Functions Revealed by Scientists
A recent study published in the Proceedings of the National Academy of Sciences (PNAS) has unveiled important insights into the function of the gene SLC35F2 and its role in facilitating the entry of the micronutrient queuosine into cells. This discovery could have significant implications for cancer treatment, neurodegenerative diseases, and personalized diets.
SLC35F2 encodes a transporter protein that is highly specific for the nucleobase and nucleoside compounds, queuine and queuosine. Research has demonstrated that SLC35F2 acts as the sole transporter for queuosine in human cells, such as HeLa cells, with a high affinity for the compound, as indicated by a Km of 174 nM.
The study suggests that SLC35F2 mediates the uptake of queuosine across cell membranes, including potentially those of brain cells. This is crucial for proper neuronal function and protein synthesis, as queuosine is involved in the modification of certain transfer RNAs (tRNAs).
In the context of medicine, the findings have promising implications. SLC35F2 has been identified as an oncogene, and its transporter role means it could be a target or biomarker in cancer therapy. Targeting SLC35F2 function could modulate the uptake of drugs or nutrient analogs, offering a route to selectively affect cancer cells expressing this transporter.
In neurodegenerative diseases, since queuosine plays a role in tRNA modification and thus protein translation fidelity, deficiencies or dysfunctions in SLC35F2 could contribute to neurodegenerative conditions by disrupting cellular metabolism and protein synthesis.
Queuosine, a vitamin-like molecule, is responsible for memory retention and cancer protection. Discovered in the 1970s, its structure and functions remained a mystery for a long time. The gene SLC35F2 exists in the simplest organisms, suggesting its fundamental importance.
The new study also revealed that without SLC35F2, queuosine cannot perform its functions in mice. Professor Valerie de Cresci-Lagarde believes that queuosine acts as a fine-tuning in the system of reading genetic information. However, the exact mechanisms by which queuosine affects gene reading remain unclear.
The discovery that the gene SLC35F2 acts as a door for queuosine to enter brain cells, made by scientists from the USA and Ireland, opens up prospects for future research. The potential application of this discovery in practical medicine is yet to be fully realised, but new prospects for medicine could potentially include treatments for cancer and neurodegenerative diseases, as well as personalized diets.
Since humans cannot produce queuosine independently, the body obtains it exclusively from food after it is processed by intestinal flora. Answering the question of how queuosine affects gene reading will help translate the discovery into practical medicine. The new study provides a significant step towards understanding this process.
- The study's findings suggest that the gene SLC35F2, which encodes a transporter protein for the micronutrient queuosine, could have significant implications for health-and-wellness, particularly mental health, as queuosine is responsible for memory retention and cancer protection.
- In light of the study, SLC35F2 may be a potential target for therapies-and-treatments in cancer, neurodegenerative diseases, and personalized diets, considering its role in facilitating the entry of queuosine into cells, including brain cells.
- The discovery of SLC35F2's role in the uptake of queuosine could lead to the development of supplements that enhance queuosine levels, promoting healthier protein synthesis and possibly aiding in the prevention and treatment of various health conditions.
