Sandbox Reserved 1654: Difference between revisions
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On the other hand, the CPEB can activate the translation. Indeed, in the cytoplasm, there are some repressed or silenced mRNA with a short polyA tail. They can be activated by cytoplasmic polyadenylation thanks to a hormonal stimulation. This stimulation can lead to the phosphorylation of CPEB which increase its affinity with the [https://en.m.wikipedia.org/wiki/Cleavage_and_polyadenylation_specificity_factor CPSF] (Cleavage and Polyadenylation Specificity Factor) and decrease the binding between CPEB and PARN. CPSF binds to the mRNA at the sequence 3’ of the tail of the mRNA (AAUAAA) and recruits the [https://en.wikipedia.org/wiki/Polynucleotide_adenylyltransferase poly(A) polymerase] which leads to the elongation of the polyA tail and therefore to the activation of the translation<ref name="publi" />. | On the other hand, the CPEB can activate the translation. Indeed, in the cytoplasm, there are some repressed or silenced mRNA with a short polyA tail. They can be activated by cytoplasmic polyadenylation thanks to a hormonal stimulation. This stimulation can lead to the phosphorylation of CPEB which increase its affinity with the [https://en.m.wikipedia.org/wiki/Cleavage_and_polyadenylation_specificity_factor CPSF] (Cleavage and Polyadenylation Specificity Factor) and decrease the binding between CPEB and PARN. CPSF binds to the mRNA at the sequence 3’ of the tail of the mRNA (AAUAAA) and recruits the [https://en.wikipedia.org/wiki/Polynucleotide_adenylyltransferase poly(A) polymerase] which leads to the elongation of the polyA tail and therefore to the activation of the translation<ref name="publi" />. | ||
== | == Diseases == | ||
CPEB proteins play a key role in some diseases, especially in cancers. Indeed, in some humans tumors the level of CPEB 1 is lower than in healthy cells and this leads to the growth of these tumors. An overexpression of CPEB 4 can lead to tumor growth too. Some researches try to find a cancer treatment thanks to CPEB mutations. | |||
Other diseases, like Fragile X syndrome, could be treated by regulating the expression of CPEB. Indeed, this disease is due to a mutation on FRM1 gene, which is bind to X chromosome. Because of this mutation, FMRP, which is a translational repressor protein, isn’t expressed. So, proteins are overexpressed and it could be the cause of some dysfunctions observed for this disease. That’s why the regulation of the level of CPEB could treat this syndrome. | |||
== References == | == References == | ||
<references/> | <references/> | ||
