High-resolution immunoelectron microscopy has shown that hnRNPs localize predominantly to the border regions of chromatin, where it has access to these nascent RNAs.
Much of hnRNPs' importance to cell cycle control is evidenced by its role as an oncogene, in which a loss of its functions results in various common cancers.
In response to ionizing radiation, hnRNP C partially localizes to the site of DNA damage, and when depleted, S-phase progression of the cell is impaired.
Through these genes, hnRNP is necessary to induce cell-cycle arrest in response to DNA damage by ionizing radiation.
p53 suppression of genes is often carried out by a number of these lincRNAs, which in turn have been shown to act though hnRNP K. Through physical interactions with these molecules, hnRNP K is targeted to genes and transmits p53 regulation, thus acting as a key repressor within the p53-dependent transcriptional pathway.
[13][14] hnRNP serves a variety of processes in the cell, some of which include: The association of a pre-mRNA molecule with a hnRNP particle prevents formation of short secondary structures dependent on base pairing of complementary regions, thereby making the pre-mRNA accessible for interactions with other proteins.
[15] Several hnRNPs interact with telomeres, which protect the ends of chromosomes from deterioration and are often associated with cell longevity.
[16] hnRNP has also been shown to interact with telomerase, the protein responsible for elongating telomeres and prevent their degradation.