Department of Bioscience & Bioengineering

&ldquo;IIT Jodhpur is committed to impart quality education to facilitate the creation of qualified, competent and responsible human resources to meet the emerging technological challenges of the world. It is working towards creating an equitable learning platform that is positive, accessible and effective in the face of the modern societal and scientific advancements.

Flexibility in curriculum, in all its academic programs, encompassing elements of teaching, research, creativity, innovation and entrepreneurship is the most unique feature of IIT Jodhpur. The Department of Science and Technology (DST), under the National Mission on Cyber Physical Systems, has identified IIT Jodhpur as a Technology &amp; Innovation Hub in the area of Augmented Reality and Virtual Reality. The institute has also been nominated as the coordinator for the Jodhpur City and Knowledge Cluster by the Office of Principal Scientific Adviser, Government of India.

The sprawling 852-acre IIT Jodhpur campus is a majestic tribute to the deep-rooted diverse cultural heritage of the region. The campus is an architectural masterpiece, which is slated to become an international exemplar of sustainability with net-zero energy, and advanced water and waste management strategies.&rdquo;

IIT Jodhpur

The number and importance of intrinsically disordered proteins (IUP), known to be involved in various human disorders, are growing rapidly. To test for the generalized implications of intrinsic disorders in proteins involved in Neurodegenerative diseases, disorder prediction tools have been applied to three datasets comprising of proteins involved in Huntington Disease (HD), Parkinson's disease (PD), Alzheimer's disease (AD). Results show, in general, proteins in disease datasets possess significantly enhanced intrinsic unstructuredness. Most of these disordered proteins in the disease datasets are found to be involved in neuronal activities, signal transduction, apoptosis, intracellular traffic, cell differentiation etc. Also these proteins are found to have more number of interactors and hence as the proportion of disorderedness (i.e., the length of the unfolded stretch) increased, the size of the interaction network simultaneously increased. All these observations reflect that, "Moonlighting" i.e. the contextual acquisition of different structural conformations (transient), eventually may allow these disordered proteins to act as network "hubs" and thus they may have crucial influences in the pathogenecity of neurodegenerative diseases. {\textcopyright} 2009 Raychaudhuri et al.

World University root node

Fulltext

PLoS ONE

The role of intrinsically unstructured proteins in neurodegenerative diseases

Walking the line: Selective photodestruction of nitrilotriacetic acid moieties on a poly(ethylene glycol) polymer brush by a light-induced Fenton reaction enabled the functional organization of motor proteins into micropatterns (see schematic illustration). Microtubules were selectively captured on the structures, and adenosine triphosphate dependent transport along lines was observed. © 2009 Wiley-VCH Verlag GmbH & Co. KGaA.

Angewandte Chemie - International Edition

Organization of motor proteins into functional micropatterns fabricated by a photoinduced fenton reaction

An image analysis-based method for high throughput screening of an α-amylase mutant library using chromogenic assays was developed. Assays were performed in microplates and high resolution images of the assay plates were read using the Virtual Microplate Reader (VMR) script to quantify the concentration of the chromogen. This method is fast and sensitive in quantifying 0.025-0.3 mg starch/ml as well as 0.05-0.75 mg glucose/ml. It was also an effective screening method for improved α-amylase activity with a coefficient of variance of 18%. © Springer Science+Business Media B.V. 2009.

Biotechnology Letters

Quantitative digital image analysis of chromogenic assays for high throughput screening of α-amylase mutant libraries

Solitary waves in continuum media pass through each other with only a slight phase change. However, in an intrinsically nonlinear many-body system such solitary waves could behave differently. It was predicted and experimentally confirmed that head-on solitary wave collisions in granular alignments are followed by the formation of tiny secondary solitary waves in the vicinity of the collision point. While it remains a challenge to provide an analytical treatment of the local time evolution, we present arguments and associated simulations to address a crucial unknown, namely, why the secondary solitary waves must form. Extensive numerical investigations on solitary wave collisions at a grain center and at an edge show marked differences. The effects of softening the grain repulsion are discussed to validate the arguments. © 2009 The American Physical Society.

Physical Review E - Statistical, Nonlinear, and Soft Matter Physics

How solitary waves collide in discrete granular alignments

Huntington's disease is a hereditary neurodegenerative disorder caused by an aberrant polyglutamine expansion in the amino terminus of the huntingtin protein. The resultant mutant huntingtin form aggregates in neurons and causes neuronal dysfunction and degeneration in many ways including transcriptional dysregulation. Here, we report that the expression of mutant huntingtin in the mouse neuroblastoma cell results in massive transcriptional induction of several chemokines including monocyte chemoattractant protein-1 (MCP-1) and murine chemokine (KC). The mutant huntingtin expressing cells also exhibit proteasomal dysfunction and down-regulation of NF-κB activity in a time-dependent manner and both these phenomena regulate the expression of MCP-1 and KC. The expression of MCP-1 and KC are increased in the mutant huntingtin expressing cells in response to mild proteasome inhibition. However, the expression of MCP-1 and KC and proteasome activity are not altered and inflammation is rarely observed in the brain of 12-week-old Huntington's disease transgenic mice in comparison with their age-matched controls. Our result suggests that the mutant huntingtin-induced proteasomal dysfunction can up-regulate the expression of MCP-1 and KC in the neuronal cells and therefore might trigger the inflammation process. © 2008 The Authors.

Journal of Neurochemistry

Induction of chemokines, MCP-1, and KC in the mutant huntingtin expressing neuronal cells because of proteasomal dysfunction

The UBE3A/E6-AP is known to function both as an E3 ubiquitin ligase of the ubiquitin proteasome system and as a transcriptional coactivator. E6-AP shows brain-specific imprinting and loss of function of maternally inherited E6-AP causes Angelman syndrome. However, how the loss of function of E6-AP causes disease pathogenesis is poorly understood. Here, we show that E6-AP interacts with and promotes proteasome-mediated degradation of cyclin-dependent kinase inhibitor p27. E6-AP also directly ubiquitinates p27 in an in vitro ubiquitination assay. Partial knockdown of E6-AP increases the level of p27 leading to cell cycle arrest. Interestingly, partial knockdown also increases the transcription of p27. Finally, we have demonstrated the increased levels of p27 in E6-AP-maternal-deficient and null mice brain. Our result suggests that E6-AP not only enhances the degradation but also regulates the expression of p27 and its loss of function in Angelman syndrome might cause cell cycle alteration leading to disease pathogenesis. © 2009 Elsevier Inc. All rights reserved.

Neurobiology of Disease

UBE3A/E6-AP regulates cell proliferation by promoting proteasomal degradation of p27

SGPGIMS

STUDY OF CYTOKINE GENES POLYMORPHISM AND RISK ASSOCIATED WITH SUSCEPTIBILITY TO BLADDER CANCER IN CONTEXT TO BCG IMMUNOTHERAPY RESPONSE

Background: Episodes of acute rejection represent an important risk factor for the development of chronic allograft nephropathy. We explored whether certain cytokine gene polymorphisms in renal transplant recipients may be useful markers for susceptibility to allograft rejection. Interleukin 8 (IL8) -251 T>A and interferon gamma (IFNG) +874A>T gene polymorphisms were correlated with allograft outcome in renal transplant recipients. Methods: Genotyping was done by amplification refractory mutational system-polymerase chain reaction (ARMS-PCR) in 264 healthy controls and 296 renal transplant recipients categorized into 235 non-rejecters and 61 rejecters. Results: IL8 -251AA genotype was associated with 2.7-folds increased risk for allograft rejection in recipients experiencing rejection episodes as compared to non-rejecters (OR = 2.70, P = 0.032). Cox proportional analysis revealed > 2-folds increased susceptibility for allograft rejection (HR = 2.38, P = 0.010) in IL8 -251AA recipients. Kaplan-Meier analysis also demonstrated lower mean time to first rejection episode for IL8 -251AA recipients (23 months) as compared to TT recipients (30 months) (log rank P = 0.022). No association of IFNG +874A>T was observed with allograft rejection, however, an increasing trend towards immunosuppressant toxicity was observed in patients with +874TT genotype at one month post transplantation. Conclusion: Thus, IL8 -251AA genotype may serve as potential predictor of allograft outcome in our North Indian cohort of renal transplant recipients. © 2009.

Transplant immunology

Interleukin 8− 251T&gt; A and Interferon gamma+ 874A&gt; T polymorphism: Potential predictors of allograft outcome in renal transplant recipients from north India

Glutathione S-transferases (GSTs) play an important role in detoxification of various toxic compounds like carcinogens in cigarette smoke and tobacco by conjugating to toxic compounds and inactivating their hazardous effect. Variation in Glutathione S-Transferases (GSTs) genes may alter the catalytic efficiency of GST isoenzymes leading to potential increase in cancer susceptibility due to various carcinogens. We therefore, investigated association of GSTM1, GSTM3 and GSTT1 variants with susceptibility to benign prostate hyperplasia (BPH) and cigarette, tobacco chewing and alcohol consumption as confounding factors in 141 BPH and 184 healthy controls. Results showed increased risk for BPH susceptibility in patients with GSTM1 null genotype (OR-2.03, p = 0.013) and smoking (OR-3.12, p = 0.028), tobacco chewing (OR-2.54, p = 0.039) and alcohol habits (OR-3.39, p = 0.010). Null genotype of GSTM1 with cigarette, tobacco and alcohol habits predisposed increased risk for BPH. © 2009 IOS Press and the authors. All rights reserved.

Disease markers

GSTM1, GSTM3 and GSTT1 gene variants and risk of benign prostate hyperplasia in North India

Simultaneous recordings of spike trains from multiple single neurons are becoming commonplace. Understanding the interaction patterns among these spike trains remains a key research area. A question of interest is the evaluation of information flow between neurons through the analysis of whether one spike train exerts causal influence on another. For continuous-valued time series data, Granger causality has proven an effective method for this purpose. However, the basis for Granger causality estimation is autoregressive data modeling, which is not directly applicable to spike trains. Various filtering options distort the properties of spike trains as point processes. Here we propose a new nonparametric approach to estimate Granger causality directly from the Fourier transforms of spike train data. We validate the method on synthetic spike trains generated by model networks of neurons with known connectivity patterns and then apply it to neurons simultaneously recorded from the thalamus and the primary somatosensory cortex of a squirrel monkey undergoing tactile stimulation. © Springer Science+Business Media, LLC 2008.