These results suggest that a great number of endoplasmic reticulum (ER) gene products are regulated at the post-transcriptional level in the liver of Wrn mutant mice exhibiting an ER stress response.
A mislocalization of the Wrn mutant protein in the liver endoplasmic reticulum fraction increased oxidative stress in that cellular compartment. Vitamin C reversed this oxidative stress.
Studies show that in the context of Myc-associated tumorigenesis loss of Wrn amplifies the DNA damage response both in preneoplastic and neoplastic tissue engaging activation of tumor suppressor pathways.
embryonic fibroblasts lacking a functional Wrn helicase inhibited the immortalization of Safb1-null cells. These results indicate that an intact Wrn protein is required for immortalization and tumorigenesis in Safb1-null mice.
BCR/ABL-mediated stimulation of WRN modulates the efficiency and fidelity of major DSB repair mechanisms to protect leukemia cells from apoptosis and to facilitate genomic instability.
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