titled “A CLOCK-binding small molecule disrupts the interaction between CLOCK and BMAL1 and enhances circadian rhythm amplitude” is Accepted to be published in paper . Journal of Biological Chemistry
This paper describe the discovery of the small molecules has potential to be used as drug to eliminate circadian clock related diseases in ageing.
titled “Identification and characterization of a new class of (6-4) photolyase from paper Vibrio cholerae” is accepted to be published in Biochemistry.
Our laboratory is interested in understanding how clock works at cellular level. For more information please visit our research interest section.
Almost every day, we wake up, get hungry, feel ourselves energetic or tired or succumb to sleep at the same hours. Although people may have different cycles, at certain hours of the day our bodies show the same responses. The circadian clock regulates the timing of sleep and wakefulness and, therefore, all dependent behavioural and physiological processes. In humans, a defect in the clock gene PER2 produces familial advanced sleep phase syndrome (FASPS); an analogous mutation causes the same phenotype in mice. People with a causal mutation in casein kinase CSNK1D and an associated variant in CSNK1E display ASPS and delayed sleep phase syndrome (DSPS), respectively. Finally, a human CLOCK variant is associated with diurnal sleep preference. Circadian clock genes are also associated with a host of neurological disorders including schizophrenia, unipolar major depression, and bipolar disorder. Although it was widely believed that circadian clock disruption predisposes humans to cancer based largely on epidemiologic data, studies with Cry mutant mice revealed a more complex pattern of interactions among the clock, apoptosis, and oncogenic transformation.