Obesity is pathogenically associated with the occurrence of leptin resistance in human as well as in animal models. Because our results support that leptin exerts its crucial metabolic effects through controlling the expression of lipogenic enzymes, it is conceivable that dysregulated lipogenic pathway may underlie the deleterious effects of defective leptin signaling upon lipid metabolism. Indeed, as we have previously demonstrated in db/db mice, KRX-0401 company hepatic ACL is dysregulated in the absence of functional leptin signaling; furthermore, hepatic ACL suppression leads to marked protection of the obese mice against the development of liver steatosis. It has been proposed that yeast telomeres form fold back loops and that this process is dependent on the Sir proteins. A looping back model have been suggested previously to explain the repression patterns observed at native telomeres. Thus, our results provide physiological evidence that the lipogenic pathway serves as a key component in mediating leptin’s regulatory actions in lipid homeostasis. CaMdr1p is one of the major MDR transporter involved in frequently occurring azole resistance in C. albicans. The efflux pump proteins display promiscuity towards substrate specificity wherein a very large number of structurally diverse compounds can be extruded by the transporter. In-depth knowledge of protein structure and function is essential for any logical approach to block the activity of such protein in MDR isolates of Candida. Many of these are highly conserved and form a large interactive network that associates with genes that impact on numerous cellular processes including mitochondrial function. Genetic defects and/or polymorphisms in these conserved DOX resistance genes may mediate cardiotoxicity in patients undergoing DOX chemotherapy or serve as biomarkers for therapeutic response to DOX chemotherapy in human tumors. MtDNA is essential for mitochondrial energy production through oxidative phosphorylation, and hundreds to thousands of mtDNA molecules may be found per cell depending upon the energy requirements of the tissue. In contrast to nuclear genes, mtDNA is inherited only from the mother ; therefore, mtDNA mutations associated with inherited mitochondrial diseases follow the maternal lineage with no transmission from the father. Along the maternal lineage, different amounts of a pathogenic and normal mtDNAs may be inherited due to a genetic bottle neck during oogenesis and/or by purifying selection of severe mtDNA mutations. Homoplasmy describes the state where only mutant or variant mtDNAs exist; whereas, in heteroplasmy there is a mixture of normal and mutant or variant mtDNAs. This study represents an attempt in that direction wherein a rational approach is applied to predict functionally critical amino acids of this transporter.