Institute of Microbial Technology (सूक्ष्मजीव प्रौद्योगिकी संस्थान)
A Council of Scientific & Industrial Research (वैज्ञानिक औद्योगिक अनुसंधान परिषद)
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  About AutophagySMDB and Autophagy  
  AutophagySMDB (Autophagy Small Molecule Database) is an interactive, comprehensive manually curated database of small molecules and their protein targets which modulates autophagy. All small molecule entries includes 2D & 3D structure files along with information such as molecular formula, canonical smile, IUPAC name, function, PubMed ID, FDA approval status, quantitative structure activity relationship (QSAR) properties, experimental values such as Ki, Kd, IC50 and EC50 from published literature. This database can be searched by different options like text search, structure search and advanced search. We also implemented different advanced tools like clustering, cataloguing and tree functionality through which user can perform advanced structural analysis for drug discovery. All living organisms undergo continuous repair. Cells and other cellular components are invariably remodeled and recycled. This is, in part, in order to replace the unwanted old components with healthier ones. The term autophagy or “self-eating” signifies a well conserved catabolic process vital for cell viability and homeostasis. Since long it has been considered as a housekeeping pathway responsible for maintaining equilibrium between biosynthesis and intracellular degradation. Autophagy maneuvers major self-degradative mechanism by which a cell recycles its macromolecules and organelles thereby renovating the cells and tissues. Autophagy is a multistep process, subsequent to a stress signal first step is sequestration of damaged organelles, malformed proteins and other dysfunctional cellular components inside a membraned phagophore. Phagophore expands by surrounding a portion of cytoplasm into a double membraned autophagosome. Loaded autophagosome then fuses with the lysosomes oftenly described as “cellular garbage can” where lysosomal hydrolases digest the stockpiled cellular components. Monomeric units or byproducts from lysosomal degradation are exported back to cytoplasm through lysosomal permeases and transporters. As autophagosomes engulf a small portion of cytoplasm along with the cytoplasmic components to be degraded, autophagy is generally thought to be a non-selective degradation system. Autophagy is broadly classified into three major types- macroautophagy, microautophagy and chaperone mediated autophagy – and the term autophagy generally indicates macroautophagy unless specified. Macroautophagy can further be subclassified into basal and induced autophagy. Former comes into play during starvation while latter is important for constitutive turnover of cellular constituents. Recent reports indicate autophagy regulates various cellular processes to maintain metabolic turnover and homeostasis. It plays a variety of roles, such as cellular stress, embryonic development, anti-aging, elimination of microorganisms and intracellular proteins, organelle clearance, apoptosis, tumor suppression, and antigen presentation. Tissue-specific impairment of autophagy in central nervous system results in massive neurodegeneration, while in liver it causes accumulation of waste and damaged organelles, leading to hepatomegaly. The deficiency of LAMP2 in humans has been shown to cause Danon’s disease that is associated with the accumulation of autophagic material in striated myocytes revealing autophagy mediated role in disease. In cancer cells defects in autophagy can result in reduced removal of ROS and NOS from damaged mitochondria and other organelles which could lead to cancer progression. Moreover, it leads to activated autophagy subsequent to chemotherapy which promotes the cancer cell survival. Also, when autophagy is activated beyond basal levels during a stress signal it can damage the cardiomyocytes leading to cardiac failure. A massive network of signaling proteins and transcription factors regulate this process of autophagy. Various pathophysiological evidences demand a more detailed understanding of this network and the small molecules regulating them in modulating autophagy. Recent reports indicate the amenability of these targets to be modulated by enormous number of small molecule modulators which would be critical for pharmacological interventions. Unfortunately, there isn’t any platform available on which all the information regarding these would be accessible. AutophagySMDB is designed as one of the dias gathering significant information regarding each one of these small molecules and their associated drug targets.


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