Nuclear factor of activated T (NFAT) cells activity within CD4+ T cells is influenced by activation status and tissue localisation

Harris, Nicola L.; Watt, Victoria; MacLenachan, Sam; Diehl, Sean A.; Marsland, Benjamin J.; Rincón, Mercedes; Gros, Graham Le

doi:10.1016/j.micinf.2005.06.020

Cited by 3 publications

(1 citation statement)

References 40 publications

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“…In support of this idea, TFE3 and TFEB have been shown to be mutually redundant transcriptional activators of genes encoding E‐cadherin (Huan et al , ), CD40 ligand (Huan et al , ), PGC1α (Settembre et al , ; Salma et al , ) and ATF4 (Martina et al , ), among others. However, in specific physiological contexts, either TFE3 or TFEB may play a more prominent role, a situation similar to that proposed for the differential regulation of various NFAT subunits (Harris et al , ). This could explain the strikingly different effects observed between Tcfeb KO mice, which die during embryonic development, and Tfe3 KO mice which are viable.…”

Section: Discussionsupporting

confidence: 56%

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

et al. 2017

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TFE3 and TFEB are members of the MiT family of HLH–leucine zipper transcription factors. Recent studies demonstrated that they bind overlapping sets of promoters and are post‐transcriptionally regulated through a similar mechanism. However, while Tcfeb knockout (KO) mice die during early embryonic development, no apparent phenotype was reported in Tfe3 KO mice. Thus raising the need to characterize the physiological role of TFE3 and elucidate its relationship with TFEB. TFE3 deficiency resulted in altered mitochondrial morphology and function both in vitro and in vivo due to compromised mitochondrial dynamics. In addition, Tfe3 KO mice showed significant abnormalities in energy balance and alterations in systemic glucose and lipid metabolism, resulting in enhanced diet‐induced obesity and diabetes. Conversely, viral‐mediated TFE3 overexpression improved the metabolic abnormalities induced by high‐fat diet (HFD). Both TFEB overexpression in Tfe3 KO mice and TFE3 overexpression in Tcfeb liver‐specific KO mice (Tcfeb LiKO) rescued HFD‐induced obesity, indicating that TFEB can compensate for TFE3 deficiency and vice versa. Analysis of Tcfeb LiKO/Tfe3 double KO mice demonstrated that depletion of both TFE3 and TFEB results in additive effects with an exacerbation of the hepatic phenotype. These data indicate that TFE3 and TFEB play a cooperative, rather than redundant, role in the control of the adaptive response of whole‐body metabolism to environmental cues such as diet and physical exercise.

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Section: Discussionsupporting

confidence: 56%

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

et al. 2017

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Transcription factors TFE3 and TFEB are critical for CD40 ligand expression and thymus-dependent humoral immunity

et al. 2006

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TFE3 and TFEB are broadly expressed transcription factors related to the transcription factor Mitf. Although they have been linked to cytokine signaling pathways in nonlymphoid cells, their function in T cells is unknown. TFE3-deficient mice are phenotypically normal, whereas TFEB deficiency causes early embryonic death. We now show that combined inactivation of TFE3 and TFEB in T cells resulted in a hyper-immunoglobulin M syndrome due to impaired expression of CD40 ligand by CD4 + T cells. Native TFE3 and TFEB bound to multiple cognate sites in the promoter of the gene encoding CD40 ligand (Cd40lg), and maximum Cd40lg promoter activity and gene expression required TFE3 or TFEB. Thus, TFE3 and TFEB are direct, physiological and mutually redundant activators of Cd40lg expression in activated CD4 + T cells critical for T cell-dependent antibody responses.Transcription factors TFE3 and TFEB are the most closely related members of a functionally interactive DNA-binding family known as Mitf-TFE (MiT) that includes the microphthalmiaassociated transcription factor Mitf and TFEC 1 . MiT proteins bind to μE3 sites, a subset of Eboxes that match a general CANNTG consensus sequence 2 , with those binding to TFE3 in vitro first identified and characterized in immunoglobulin heavy-chain and T cell receptor (TCR) enhancers 3-5 . DNA binding is mediated by nearly identical basic regions and requires homo-or heterodimer formation mediated by conserved helix-loop-helix and leucine zipper domains 5-7 . Such interactions are restricted in the MiT family.MiT proteins share similar structures and are often expressed together, yet genetic studies have demonstrated both overlapping and nonoverlapping functions for MiT proteins in different cell

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Cinnamic Acid Derivatives as Anticancer Agents-A Review

De¹,

Baltas²,

Bedos‐Belval

2011

CMC

377

227

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Cinnamic acid and its phenolic analogues are natural substances. Chemically, in cinnamic acids the 3-phenyl acrylic acid functionality offers three main reactive sites; substitution at the phenyl ring, addition at the α,β- unsaturation and the reactions of the carboxylic acid functionality. Owing to these chemical aspects cinnamic acid derivatives received much attention in medicinal research as traditional as well as recent synthetic antitumor agents. We observed that in spite of their rich medicinal tradition, cinnamic acid derivatives and their anticancer potentials remained underutilized for several decades since the first published clinical use in 1905. In last two decades, there has been huge attention towards various cinnamoyl derivatives and their antitumor efficacy. This review provides a comprehensive and unprecedented literature compilation concerning the synthesis and biological evaluation of various cinnamoyl acids, esters, amides, hydrazides and related derivatives in anticancer research. We envisage that our effort in this review contributes a much needed and timely addition to the literature of medicinal research.

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Nuclear factor of activated T (NFAT) cells activity within CD4+ T cells is influenced by activation status and tissue localisation

Cited by 3 publications

References 40 publications

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

TFE 3 regulates whole‐body energy metabolism in cooperation with TFEB

Transcription factors TFE3 and TFEB are critical for CD40 ligand expression and thymus-dependent humoral immunity

Cinnamic Acid Derivatives as Anticancer Agents-A Review

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