Study findings reveal an indispensable role of ZFP36L1 as a posttranscriptional safeguard against aberrant hypoxic signaling and abnormal cell-cycle progression. ZFP36L1 is significantly mutated and underexpressed in bladder cancer and reduction of ZFP36L1 expression was associated with worse survival in patients with breast cancer.
Study shows that the ZFP36 family member ZFP36L1 is specifically upregulated in osteoarthritis (OA) chondrocytes and OA cartilage of humans and mice. ZFP36L1 regulates the mRNAs encoding two members of the HSP70 family that appear to exert protective effects on OA pathogenesis by inhibiting chondrocyte apoptosis.
The results indicated that ZFP36L1 and ZFP36L2 play a negative role in cell proliferation; the underlying mechanisms might be mediated through a cyclin D-dependent and p53-independent pathway.
Gene expression analysis revealed that three gene BACH2 PTGER4 and ZFP36L1 are down-regulated in MS patients' blood cells compared to healthy subjects.
Von Hippel-Lindau gene product modulates TIS11B expression in renal cell carcinoma and has a role in vascular endothelial growth factor expression in hypoxia
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