@article { ISI:000307814000728,
	title = {Novel mechanism involved in temporal regulation of skin pigmentation homeostasis},
	journal = {Journal of Investigative Dermatology},
	volume = {132},
	number = {2},
	year = {2012},
	note = {42nd Annual Meeting of the European-Society-for-Dermatological-Research (ESDR), Venice, ITALY, SEP 07-10, 2012},
	month = {SEP},
	pages = {S128},
	publisher = {European Soc Dermatol Res (ESDR)},
	address = {75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA},
	issn = {0022-202X},
	author = {Ganju, Parul and Natarajan, V. T. and Singh, A. and Vijayan, V. and Dani, Prachi P. and Kar, H. K. and Natarajan, K. and Gadgil, Chetan J. and Rani, R. and Gokhale, R. S.}
}
@article { ISI:000330999600057,
	title = {IFN-gamma signaling maintains skin pigmentation homeostasis through regulation of melanosome maturation},
	journal = {Proceedings of the National Academy of Sciences of the United States of America},
	volume = {111},
	number = {6},
	year = {2014},
	month = {FEB},
	pages = {2301-2306},
	publisher = {NATL ACAD SCIENCES},
	address = {2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA},
	abstract = {<p>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.</p>},
	keywords = {detanning, gene regulation, interferon, melanin},
	issn = {0027-8424},
	doi = {10.1073/pnas.1304988111},
	author = {Natarajan, Vivek T. and Ganju, Parul and Singh, Archana and Vijayan, Vinaya and Kirty, Kritika and Yadav, Shalini and Puntambekar, Shraddha and Bajaj, Sonali and Dani, Prachi P. and Kar, Hemanta K. and Gadgil, Chetan J. and Natarajan, Krishnamurthy and Rani, Rajni and Gokhale, Rajesh S.}
}
@article {43790,
	title = {Mapping architectural and transcriptional alterations in non-lesional and lesional epidermis in vitiligo},
	journal = {Scientific Reports},
	volume = {7},
	year = {2017},
	month = {AUG},
	type = {Article},
	abstract = {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.},
	doi = {10.1038/s41598-017-10253-w},
	author = {Singh, Archana and Gotherwal, Vishvabandhu and Junni, Paivi and Vijayan, Vinaya and Tiwari, Manisha and Ganju, Parul and Kumar, Avinash and Sharma, Pankaj and Fatima, Tanveer and Gupta, Aayush and Holla, Ananthaprasad and Kar, Hemanta K. and Khanna, Sangeeta and Thukral, Lipi and Malik, Garima and Natarajan, Krishnamurthy and Gadgil, Chetan J. and Lahesmaa, Riitta and Natarajan, Vivek T. and Rani, Rajni and Gokhale, Rajesh S.}
}
