<?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%">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%">Singh, Archana</style></author><author><style face="normal" font="default" size="100%">Gotherwal, Vishvabandhu</style></author><author><style face="normal" font="default" size="100%">Junni, Paivi</style></author><author><style face="normal" font="default" size="100%">Vijayan, Vinaya</style></author><author><style face="normal" font="default" size="100%">Tiwari, Manisha</style></author><author><style face="normal" font="default" size="100%">Ganju, Parul</style></author><author><style face="normal" font="default" size="100%">Kumar, Avinash</style></author><author><style face="normal" font="default" size="100%">Sharma, Pankaj</style></author><author><style face="normal" font="default" size="100%">Fatima, Tanveer</style></author><author><style face="normal" font="default" size="100%">Gupta, Aayush</style></author><author><style face="normal" font="default" size="100%">Holla, Ananthaprasad</style></author><author><style face="normal" font="default" size="100%">Kar, Hemanta K.</style></author><author><style face="normal" font="default" size="100%">Khanna, Sangeeta</style></author><author><style face="normal" font="default" size="100%">Thukral, Lipi</style></author><author><style face="normal" font="default" size="100%">Malik, Garima</style></author><author><style face="normal" font="default" size="100%">Natarajan, Krishnamurthy</style></author><author><style face="normal" font="default" size="100%">Gadgil, Chetan J.</style></author><author><style face="normal" font="default" size="100%">Lahesmaa, Riitta</style></author><author><style face="normal" font="default" size="100%">Natarajan, Vivek T.</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%">Mapping architectural and transcriptional alterations in non-lesional and lesional epidermis in vitiligo</style></title><secondary-title><style face="normal" font="default" size="100%">Scientific Reports</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">AUG</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">In vitiligo, chronic loss of melanocytes and consequent absence of melanin from the epidermis presents a challenge for long-term tissue maintenance. The stable vitiligo patches are known to attain an irreversible depigmented state. However, the molecular and cellular processes resulting in this remodeled tissue homeostasis is unclear. To investigate the complex interplay of inductive signals and cell intrinsic factors that support the new acquired state, we compared the matched lesional and non-lesional epidermis obtained from stable non-segmental vitiligo subjects. Hierarchical clustering of genome-wide expression of transcripts surprisingly segregated lesional and non-lesional samples in two distinct clades, despite the apparent heterogeneity in the lesions of different vitiligo subjects. Pathway enrichment showed the expected downregulation of melanogenic pathway and a significant downregulation of cornification and keratinocyte differentiation processes. These perturbations could indeed be recapitulated in the lesional epidermal tissue, including blunting of rete-ridges, thickening of stratum corneum and increase in the size of corneocytes. In addition, we identify marked increase in the putrescine levels due to the elevated expression of spermine/spermidine acetyl transferase. Our study provides insights into the intrinsic self-renewing ability of damaged lesional tissue to restore epidermal functionality in vitiligo.</style></abstract><issue><style face="normal" font="default" size="100%">Article Number: 9860</style></issue><work-type><style face="normal" font="default" size="100%">Article</style></work-type><custom3><style face="normal" font="default" size="100%">Foreign</style></custom3><custom4><style face="normal" font="default" size="100%">5.228</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%">Mehdiratta, Kritee</style></author><author><style face="normal" font="default" size="100%">Singh, Shubham</style></author><author><style face="normal" font="default" size="100%">Sharma, Sachin</style></author><author><style face="normal" font="default" size="100%">Bhosale, Rashmi S.</style></author><author><style face="normal" font="default" size="100%">Choudhury, Rahul</style></author><author><style face="normal" font="default" size="100%">Masal, Dattatraya P.</style></author><author><style face="normal" font="default" size="100%">Manocha, Alzu</style></author><author><style face="normal" font="default" size="100%">Dhamale, Bhushan Dilip</style></author><author><style face="normal" font="default" size="100%">Khan, Naseem</style></author><author><style face="normal" font="default" size="100%">Asokachandran, Vivekanand</style></author><author><style face="normal" font="default" size="100%">Sharma, Pooja</style></author><author><style face="normal" font="default" size="100%">Ikeh, Melanie</style></author><author><style face="normal" font="default" size="100%">Brown, Amanda C.</style></author><author><style face="normal" font="default" size="100%">Parish, Tanya</style></author><author><style face="normal" font="default" size="100%">Ojha, Anil K.</style></author><author><style face="normal" font="default" size="100%">Michael, Joy Sarojini</style></author><author><style face="normal" font="default" size="100%">Faruq, Mohammed</style></author><author><style face="normal" font="default" size="100%">Medigeshi, Guruprasad R.</style></author><author><style face="normal" font="default" size="100%">Mohanty, Debasisa</style></author><author><style face="normal" font="default" size="100%">Reddy, D. Srinivasa</style></author><author><style face="normal" font="default" size="100%">Natarajan, Vivek T.</style></author><author><style face="normal" font="default" size="100%">Kamat, Siddhesh S.</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%">Kupyaphores are zinc homeostatic metallophores required for colonization of Mycobacterium tuberculosis</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%">metallophore</style></keyword><keyword><style  face="normal" font="default" size="100%">nutritional immunity</style></keyword><keyword><style  face="normal" font="default" size="100%">tuberculosis</style></keyword><keyword><style  face="normal" font="default" size="100%">zinc</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2022</style></year><pub-dates><date><style  face="normal" font="default" size="100%">FEB</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">119</style></volume><pages><style face="normal" font="default" size="100%">e2110293119</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	Mycobacterium tuberculosis (Mtb) endures a combination of metal scarcity and toxicity throughout the human infection cycle, contributing to complex clinical manifestations. Pathogens counteract this paradoxical dysmetallostasis by producing specialized metal trafficking systems. Capture of extracellular metal by siderophores is a widely accepted mode of iron acquisition, and Mtb iron-chelating siderophores, mycobactin, have been known since 1965. Currently, it is not known whether Mtb produces zinc scavenging molecules. Here, we characterize low-molecular-weight zinc-binding compounds secreted and imported by Mtb for zinc acquisition. These molecules, termed kupyaphores, are produced by a 10.8 kbp biosynthetic cluster and consists of a dipeptide core of ornithine and phenylalaninol, where amino groups are acylated with isonitrilecontaining fatty acyl chains. Kupyaphores are stringently regulated and support Mtb survival under both nutritional deprivation and intoxication conditions. A kupyaphore-deficient Mtb strain is unable to mobilize sufficient zinc and shows reduced fitness upon infection. We observed early induction of kupyaphores in Mtb-infected mice lungs after infection, and these metabolites disappeared after 2 wk. Furthermore, we identify an Mtb-encoded isonitrile hydratase, which can possibly mediate intracellular zinc release through covalent modification of the isonitrile group of kupyaphores. Mtb clinical strains also produce kupyaphores during early passages. Our study thus uncovers a previously unknown zinc acquisition strategy of Mtb that could modulate host-pathogen interactions and disease outcome.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><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;
	12.779&lt;/p&gt;
</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%">Sultan, Farina</style></author><author><style face="normal" font="default" size="100%">Basu, Reelina</style></author><author><style face="normal" font="default" size="100%">Murthy, Divya</style></author><author><style face="normal" font="default" size="100%">Kochar, Manisha</style></author><author><style face="normal" font="default" size="100%">Attri, Kuldeep S.</style></author><author><style face="normal" font="default" size="100%">Aggarwal, Ayush</style></author><author><style face="normal" font="default" size="100%">Kumari, Pooja</style></author><author><style face="normal" font="default" size="100%">Dnyane, Pooja</style></author><author><style face="normal" font="default" size="100%">Tanwar, Jyoti</style></author><author><style face="normal" font="default" size="100%">Motiani, Rajender K.</style></author><author><style face="normal" font="default" size="100%">Singh, Archana</style></author><author><style face="normal" font="default" size="100%">Gadgil, Chetan</style></author><author><style face="normal" font="default" size="100%">Bhavesh, Neel Sarovar</style></author><author><style face="normal" font="default" size="100%">Singh, Pankaj K.</style></author><author><style face="normal" font="default" size="100%">Natarajan, Vivek T.</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%">Temporal analysis of melanogenesis identifies fatty acid metabolism as key skin pigment regulator</style></title><secondary-title><style face="normal" font="default" size="100%">Plos Biology</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2022</style></year><pub-dates><date><style  face="normal" font="default" size="100%">MAY</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">20</style></volume><pages><style face="normal" font="default" size="100%">e3001634</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;
	Therapeutic methods to modulate skin pigmentation has important implications for skin cancer prevention and for treating cutaneous hyperpigmentary conditions. Towards defining new potential targets, we followed temporal dynamics of melanogenesis using a cell-autonomous pigmentation model. Our study elucidates 3 dominant phases of synchronized metabolic and transcriptional reprogramming. The melanogenic trigger is associated with high MITF levels along with rapid uptake of glucose. The transition to pigmented state is accompanied by increased glucose channelisation to anabolic pathways that support melanosome biogenesis. SREBF1-mediated up-regulation of fatty acid synthesis results in a transient accumulation of lipid droplets and enhancement of fatty acids oxidation through mitochondrial respiration. While this heightened bioenergetic activity is important to sustain melanogenesis, it impairs mitochondria lately, shifting the metabolism towards glycolysis. This recovery phase is accompanied by activation of the NRF2 detoxication pathway. Finally, we show that inhibitors of lipid metabolism can resolve hyperpigmentary conditions in a guinea pig UV-tanning model. Our study reveals rewiring of the metabolic circuit during melanogenesis, and fatty acid metabolism as a potential therapeutic target in a variety of cutaneous diseases manifesting hyperpigmentary phenotype.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><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;
	9.593&lt;/p&gt;
</style></custom4></record></records></xml>