In the method developed here, proteins with different affinity of LZs localized to IBs were quantitatively analyzed in living cells using flow cytometry, while the E, K coil proteins in IB fractions was detected by electrophoretic methods after cell disruption in previous study. Therefore, the current method can be applied usefully for high throughput screening of PPI inhibitors, comparisons of interacting protein partners, and engineering binding affinities in bacterial cells. The mammalian retina is a highly metabolically active tissue and one of the most energy-consuming ones. It requires constant supply of blood glucose to sustain its function and its energy demand is normally met through the uptake of glucose and oxygen. Glucose movement across the blood�Cretinal barrier occurs mainly through the glucose transporter 1 and the need for glucose is evidenced by alterations in electroretinogramresponses and altered neurotransmitter release observed in hypoglycemic conditions. It has been shown that acute hypoglycemia decreases rod and cone vision, blurs central vision, and produces temporary central scotomas in humans. The consequence of sustained hypoglycemia on retinal function is less clear. Among many neuronal cellular events, action potential-mediated neuronal communication is believed to be a major process of energy consumption where energy cost comes mainly from postsynaptic receptor 
activation. In the brain, most of the synaptic activity is mediated by glutamate, thus, the excitatory glutamatergic system represents the single largest energy user, consuming 50% of ATP in the brain. Photoreceptors convert light stimuli to electric impulses. Retinal ON bipolar cells receive direct glutamatergic input from photoreceptor cells. These cells exclusively express the class III G0-coupled type 6 metabotropic glutamate receptoras their primary postsynaptic glutamate receptor. Activation of mGluR6 initiates an intracellular signaling cascade ultimately leading to closure of cGMP gated cation channels and cell hyperpolarization. Thus, energy requirement and consumption in the retina changes greatly according to neuronal activity. Sirtuins are an evolutionarily conserved family of NAD + dependent deacylases that have been involved in many cellular responses to stress, including Evodiamine chromatin modifications, genomic stability, metabolism, inflammation, cellular senescence and organismal lifespan. In mammals, 7 sirtuin isoforms have been described that differ in their Kaempferide subcellular localization and substrates. It is currently accepted that sirtuins are crucial regulators of energy metabolism, likely through sensing changes in levels of intracellular NAD+. Among the members of this family of proteins, SIRT6 appears to have particular significance in regulating metabolism, DNA repair and lifespan. SIRT6 knockout mice appear normal at birth, but they rapidly develop a degenerative process that includes loss of subcutaneous fat, lymphopenia, osteopenia, and acute onset of hypoglycemia, leading to death in less than one month of age. Recently, Zhong et al. demonstrated that the lethal hypoglycemia exhibited by SIRT6 deficient mice is caused by an increased in glucose uptake in muscle and brown adipose tissue. At a molecular level, SIRT6 functions as a histone H3K9 and H3K56 deacetylase to control glucose homeostasis by inhibiting multiple glycolytic genes, including GLUT1, and by co-repressing Hif1a, a critical regulator of nutrient stress responses.