<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Chougale, Ashok D.</style></author><author><style face="normal" font="default" size="100%">Bhat, Shweta P.</style></author><author><style face="normal" font="default" size="100%">Bhujbal, Swapnil V.</style></author><author><style face="normal" font="default" size="100%">Zambare, Mandar R.</style></author><author><style face="normal" font="default" size="100%">Puntambekar, Shraddha</style></author><author><style face="normal" font="default" size="100%">Somani, Rahul S.</style></author><author><style face="normal" font="default" size="100%">Boppana, Ramanamurthy</style></author><author><style face="normal" font="default" size="100%">Giri, Ashok P.</style></author><author><style face="normal" font="default" size="100%">Kulkarni, Mahesh J.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Proteomic analysis of glycated proteins from streptozotocin-induced diabetic rat kidney</style></title><secondary-title><style face="normal" font="default" size="100%">Molecular Biotechnology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">AGE</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes</style></keyword><keyword><style  face="normal" font="default" size="100%">Glucose toxicity</style></keyword><keyword><style  face="normal" font="default" size="100%">Nephropathy</style></keyword><keyword><style  face="normal" font="default" size="100%">Post-translation modification</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">JAN</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">1</style></number><publisher><style face="normal" font="default" size="100%">HUMANA PRESS INC</style></publisher><pub-location><style face="normal" font="default" size="100%">999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA</style></pub-location><volume><style face="normal" font="default" size="100%">50</style></volume><pages><style face="normal" font="default" size="100%">28-38</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Glycation of proteins leading to formation of advanced glycation end products (AGEs) has been considered as one of the important causes of diabetic nephropathy. Therefore, in this study, glycated proteins were detected by anti-AGE antibodies from kidney of streptozotocin-induced diabetic rat showing nephropathic symptoms, by using two dimensional electrophoresis and western blot analysis. These glycated proteins were identified and characterized by using combination of peptide mass finger printing and tandem mass spectrometric approaches. Glycated proteins identified included proteins from metabolic pathways, oxidative stress, cell signaling, and transport. Several of the proteins modified by glycation were involved in glucose metabolism. The extent of glycation was higher in diabetes compared to control, in the glycated proteins that were common to both control and diabetic kidney. Two dimensional electrophoresis proteins profiling of glycated proteins suggest that four of the glycated proteins were significantly up regulated in diabetes.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom3><style face="normal" font="default" size="100%">Foreign</style></custom3><custom4><style face="normal" font="default" size="100%">2.262
</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Natarajan, Vivek T.</style></author><author><style face="normal" font="default" size="100%">Ganju, Parul</style></author><author><style face="normal" font="default" size="100%">Singh, Archana</style></author><author><style face="normal" font="default" size="100%">Vijayan, Vinaya</style></author><author><style face="normal" font="default" size="100%">Kirty, Kritika</style></author><author><style face="normal" font="default" size="100%">Yadav, Shalini</style></author><author><style face="normal" font="default" size="100%">Puntambekar, Shraddha</style></author><author><style face="normal" font="default" size="100%">Bajaj, Sonali</style></author><author><style face="normal" font="default" size="100%">Dani, Prachi P.</style></author><author><style face="normal" font="default" size="100%">Kar, Hemanta K.</style></author><author><style face="normal" font="default" size="100%">Gadgil, Chetan J.</style></author><author><style face="normal" font="default" size="100%">Natarajan, Krishnamurthy</style></author><author><style face="normal" font="default" size="100%">Rani, Rajni</style></author><author><style face="normal" font="default" size="100%">Gokhale, Rajesh S.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">IFN-gamma signaling maintains skin pigmentation homeostasis through regulation of melanosome maturation</style></title><secondary-title><style face="normal" font="default" size="100%">Proceedings of the National Academy of Sciences of the United States of America</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">detanning</style></keyword><keyword><style  face="normal" font="default" size="100%">gene regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">interferon</style></keyword><keyword><style  face="normal" font="default" size="100%">melanin</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">FEB</style></date></pub-dates></dates><number><style face="normal" font="default" size="100%">6</style></number><publisher><style face="normal" font="default" size="100%">NATL ACAD SCIENCES</style></publisher><pub-location><style face="normal" font="default" size="100%">2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA</style></pub-location><volume><style face="normal" font="default" size="100%">111</style></volume><pages><style face="normal" font="default" size="100%">2301-2306</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Cellular homeostasis is an outcome of complex interacting processes with nonlinear feedbacks that can span distinct spatial and temporal dimensions. Skin tanning is one such dynamic response that maintains genome integrity of epidermal cells. Although pathways underlying hyperpigmentation cascade are recognized, negative feedback regulatory loops that can dampen the activated melanogenesis process are not completely understood. In this study, we delineate a regulatory role of IFN-gamma in skin pigmentation biology. We show that IFN-gamma signaling impedes maturation of the key organelle melanosome by concerted regulation of several pigmentation genes. Withdrawal of IFN-gamma signal spontaneously restores normal cellular programming. This effect in melanocytes is mediated by IFN regulatory factor-1 and is not dependent on the central regulator microphthalmia-associated transcription factor. Chronic IFN-gamma signaling shows a clear hypopigmentation phenotype in both mouse and human skin. Interestingly, IFN-gamma KO mice display a delayed recovery response to restore basal state of epidermal pigmentation after UV-induced tanning. Together, our studies delineate a new spatiotemporal role of the IFN-gamma signaling network in skin pigmentation homeostasis, which could have implications in various cutaneous depigmentary and malignant disorders.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom3><style face="normal" font="default" size="100%">Foreign</style></custom3><custom4><style face="normal" font="default" size="100%">10.29</style></custom4></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gharui, Sowmomita</style></author><author><style face="normal" font="default" size="100%">Puntambekar, Shraddha</style></author><author><style face="normal" font="default" size="100%">Sarkar, Ram Rup</style></author><author><style face="normal" font="default" size="100%">Narlikar, Leelavati</style></author><author><style face="normal" font="default" size="100%">Sengupta, Durba</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Recognition of diverse GATA motifs necessitates multimodal GATA3-DNA binding</style></title><secondary-title><style face="normal" font="default" size="100%">Biochemical and Biophysical Research Communications</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">GATA</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutations</style></keyword><keyword><style  face="normal" font="default" size="100%">Nucleosome</style></keyword><keyword><style  face="normal" font="default" size="100%">Palindrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Reverse palindrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Spacers</style></keyword><keyword><style  face="normal" font="default" size="100%">Tandem</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2026</style></year><pub-dates><date><style  face="normal" font="default" size="100%">JUN</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">817</style></volume><pages><style face="normal" font="default" size="100%">153718</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	GATA3 is a pioneer transcription factor that plays a central role in the formation, proliferation, and sustenance of various immune cell types, notably serving as the ``master regulator'' of T helper 2 (Th2) cell differentiation. It regulates gene expression by recognizing the canonical DNA consensus motif (A/T)GATA(A/G) through its highly conserved zinc finger domains. However, beyond this classical binding motif, emerging evidence indicates that GATA3 also recognizes a varied array of noncanonical and palindromic sequence motifs, but the underlying molecular mechanisms are unclear. In this review, we discuss an emerging aspect of GATA3 function that links these diverse DNA sequence motifs to varying structural binding modes and finally to differential chromatin outcomes. We discuss how the alternative sequence motifs may engage the two zinc finger domains differently, leading towards a multitude of binding modes underlying this diverse motif recognition. The spacer length between the GATA motifs has been shown to modulate DNA binding and the geometric constraints imposed may help determine the binding mode. We reanalyzed previous data and show that these diverse motifs, as well as the spacers, modulate nucleosomal outcomes, highlighting the importance of these motifs in GATA3 function. Several disease-associated mutations, such as those implicated in autoimmune diseases and cancer, have been reported for GATA3, and we discuss how these mutations alter the binding of the zinc finger domains. This link between sequence recognition and DNA binding modes represents an underexplored aspect of GATA3 function that is necessary for understanding its multifaceted regulatory role in human health and disease.&lt;/p&gt;
</style></abstract><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">&lt;p&gt;
	Foreign&lt;/p&gt;
</style></custom3><custom4><style face="normal" font="default" size="100%">&lt;p&gt;
	2.5&lt;/p&gt;
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