Answer:
it is expected that FXR1 interacts with mRNAs by inhibiting them before they are translated into the ribosomes, thereby preventing the production of proteins that cause damage in the arteries.
Explanation:
The translation is the cellular process in which a messenger RNA (mRNA) is used as template to synthesize a protein in the ribosomes. During translation, ribosomes catalyze the reaction that joins amino acids in order to create a polypeptide chain (i.e., an ordered sequence of amino acids). Diverse types of either synthetically or naturally occurring molecules can inhibit protein production at the level of translation (e.g., siRNAs, proteins, drugs, etc). In this case, it is expected that FXR1 inhibits the mRNAs that encode proteins capable of causing damage in the arteries, thereby a mutation that results in reduced and/or abolished FXR1 function (i.e., a loss of function mutation) will lead to a phenotype with high levels of these proteins.
Binding of FRX1 protein to mRNA will block the translation process of mRNA, thereby inhibiting protein synthesis.
mRNA or messenger RNA is made from the transcription of DNA and the information stored in it is translated into amino acids by ribosomes in the process of protein synthesis.
Thus, mRNA serves as a template for protein synthesis.
The binding of the FRX1 protein will most likely block access to the codons present in the mRNA from being read by tRNA, thus inhibiting the synthesis of the proteins that damage arteries.
Therefore, binding of FRX1 protein to mRNA will block the translation process of mRNA, thereby inhibiting protein synthesis.
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