This suggests that the difference in serum stability does not contribute to the enhanced targeting activity of the cyclic form of ApoPep-1 over the linear form of ApoPep-1. An alternative explanation may be that 
the formation of constrained structure by disulfide bonding may lead to more favorable binding to apoptotic cells by the cyclic ApoPep-1 over its linear form. In addition to fluorescence dyes, ApoPep-1 may be labeled with radioisotopes, such as 123I, 18F, and 68Ga, through chemical linkers and be used as a probe for single photon emission computed tomographyor PET imaging. As a future direction, PET imaging of apoptosis using 18F-labeled linear or cyclic ApoPep-1 remains to be investigated for monitoring of tumor response. ApoPep-1-based imaging of apoptosis would be useful in consideration of therapeutic strategies in clinics and contribute to the development of new anti-cancer therapeutics. Numerous studies have shown the Alprostadil deleterious effects of obesity on health, increasing all-cause mortalityand predisposing individuals to cardiovascular disease, diabetes and cancer. Diet plays a crucial role in obesity, specifically those high in fats and sugar that increase body fat. Adipocytes, which increase in size and number during obesity, can dramatically influence a variety of metabolic processes by disturbing normal homeostatic signals. Chief among these disturbances is insulin resistance, leading to hyperglycemia and diabetes. Energy imbalance �C essentially a combination of increased food intake with decreased energy expenditure �C causes obesity. Circulating hormones, such as insulin and leptin, are readouts of the body’s energy state and act at the hypothalamus to affect food intake. Ideally, energy intake is equal to energy expenditure, leading to weight homeostasis. However, if not enough energy is released proportional to calories consumed, the excess energy is stored as lipid in adipocytes and weight gain ensues. For example, dietary fat consumption affects both sides of the energy imbalance equation. Since it releases less satiety Etidronate signals in comparison to protein and carbohydrate, it leads to increased food intake. Conversely, since fats are an efficient form of energy and because they are stored instead of used as an energy source after feeding, dietary lipids also contribute to decreased energy expenditure. Therefore, from both biochemical and physiologic perspectives of energy homeostasis, an excess of food intake over what is expended leads to weight gain. Protein tyrosine phosphatasesmodulate signaling pathways that regulate a variety of metabolic processes through dephosphorylating tyrosine residues on proteins. Increasing evidence suggests that PTPs play a crucial role in obesity and metabolic disease. It has long been known that PTP1B is implicated in obesity, insulin resistance and type-2 diabetes mellitus by regulating insulin signaling. A recent study showed that TCPTP is also involved in obesity through modulating leptin signaling. TCPTP dephosphorylates STAT3 at the tyrosine 705residue. STAT3 Y705 phosphorylation is a key mediator of leptin signaling in the hypothalamus. Leptin-STAT3 signaling suppresses the drive for food intake by increasing the expression of anorectic neuropeptides and repress those favoring orexigenic responses. Because we previously showed that STAT3 is a substrate of protein tyrosine phosphatase receptor T, we investigate here whether PTPRT regulates food intake and obesity in mice.