We used our vectors to demonstrate that a protein of interest can be overexpressed or depleted in mitotically-arrested cells, generate stable cell lines where the senescence secretory associated phenotype can be induced, and show that the chromo BMN673 domain of the AT-Rich Interacting Domain 4B protein is not required for the G1 arrest upon overexpression. Leptin is an adipocyte-secreted hormone that plays a critical role in energy homeostasis. Primarily acting through activation of leptin receptor-expressing neurons in the hypothalamus, leptin functions to control energy balance and the fat mass via reducing food intake and increasing energy expenditure. On the other hand, leptin can also exert crucial metabolic effects upon lipid metabolism, preventing triglyceride accumulation in peripheral tissues. For instance, it has been shown that leptin is able to stimulate fatty acid oxidation through activation of AMPactivated protein kinase, subsequently inhibiting acetylCoA carboxylase activity, in the skeletal muscle. Increased circulating levels of leptin have been found to be associated with obesity induced by overnutrition, as in the case of chronic intake of high-fat diet. However, whether hyperleptinemia exerts its metabolic liporegulatory actions and represents an adaptive response to chronic overnutrition has yet to be completely understood. Nucleolin is a ubiquitous expressed acidic phosphoprotein of exponentially growing cells. It is involved mainly in the synthesis and maturation of ribosomes. Nucleolin is a nonhistone nucleolar phosphoprotein, present mainly at the dense fibrillar and granular regions of the nucleolus. In nondividing cells, degraded forms of various molecular sizes are predominantly expressed due to auto degradation. Hence, the protein appears to be involved in essential aspects of transcriptional regulation, cell proliferation, and growth. Recently, it was demonstrated that nucleolin is a multifunctional shuttling protein present in nucleus, cytoplasm, and on the surface of some types of cells. It was also demonstrated that inhibition of cellsurface nucleolin suppresses tumor growth and angiogenesis. Inhibition of nucleolin activity results in cell growth inhibition. In addition, it was demonstrated in several studies that AS1411, a quadruplex-forming oligonucleotide aptamer, targets nucleolin and inhibits cancer cells growth. The WRN gene encodes for a RecQ-DNA helicase, which has been shown to resolve DNA structures that form during S-phase, such as those generated at stalled of replication forks. Loss of function mutations in WRN cause progeroid features in humans, a condition known as Werner Syndrome. Fibroblasts isolated from WS patients exhibit genomic instability, increased sensitivity to specific DNA damaging agents, slow proliferation, lengthened S-phase, and accelerated replicative senescence.