J
Jyothi Rengarajan
Researcher at Emory University
Publications - 51
Citations - 3929
Jyothi Rengarajan is an academic researcher from Emory University. The author has contributed to research in topics: Tuberculosis & Mycobacterium tuberculosis. The author has an hindex of 23, co-authored 45 publications receiving 3422 citations. Previous affiliations of Jyothi Rengarajan include Harvard University & Yerkes National Primate Research Center.
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Genome-wide requirements for Mycobacterium tuberculosis adaptation and survival in macrophages
TL;DR: The majority of Mycobacterium tuberculosis genes found by this analysis to be required for survival are constitutively expressed rather than regulated by macrophages, revealing the host-adapted lifestyle of an evolutionarily selected intracellular pathogen.
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Transcriptional regulation of Th1/Th2 polarization.
TL;DR: This work proposes a model of Th1/Th2 polarization based on the balance between Th1- and Th2-specific transcription factors, which is critical for elucidating the process of Th cell differentiation.
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Inhibitory Function of Two NFAT Family Members in Lymphoid Homeostasis and Th2 Development
TL;DR: It is shown that mice lacking both NFATp and NFAT4 develop a profound lymphoproliferative disorder likely due to a lowered threshold for TCR signaling coupled with increased resistance to apoptosis secondary to defective FasL expression.
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Interferon Regulatory Factor 4 (IRF4) Interacts with NFATc2 to Modulate Interleukin 4 Gene Expression
Jyothi Rengarajan,Kerri A. Mowen,Kathryn D. McBride,Erica D. Smith,Harinder Singh,Laurie H. Glimcher +5 more
TL;DR: It is demonstrated that IRF4 potently synergizes with NFATc2 to specifically enhance NFAT c2-driven transcriptional activation of the IL-4 promoter, providing an important molecular function for IRF 4 in T helper cell differentiation.
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Sequential Involvement of NFAT and Egr Transcription Factors in FasL Regulation
Jyothi Rengarajan,Paul R. Mittelstadt,Hans W. Mages,Andrea J. Gerth,Richard A. Kroczek,Jonathan D. Ashwell,Laurie H. Glimcher +6 more
TL;DR: It is found that Egr2 and Egr3 are NFAT target genes, and activation of FasL occurs via the NFAT-dependent induction of EGr3, as demonstrated by the ability of exogenously provided NFATp to restore Egr-dependent FasL promoter activity in DKO lymph node cells.