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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

DNA-damage-inducible transcript 4

HIF-1-responsive gene that may protect some types of cells from hypoxia and H(2)O(2)-triggered apoptosis [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: mTOR, mTORC1, V1a, Akt, CAN
Papers on REDD1
Quinolinic acid induces cell apoptosis in PC12 cells through HIF-1-dependent RTP801 activation.
Li et al., Zhenjiang, China. In Metab Brain Dis, Feb 2016
In this study, we investigated the role of HIF-1α (hypoxia inducible factor-1α) and RTP801 in cell apoptosis induced by quinolinic acid (QUIN), a glutamatergic agonist, in PC12 cells.
Disruption of REDD1 gene ameliorates sepsis-induced decrease in mTORC1 signaling but has divergent effects on proteolytic signaling in skeletal muscle.
Lang et al., State College, United States. In Am J Physiol Endocrinol Metab, Jan 2016
The REDD1 (regulated in development and DNA damage-1) protein is increased in sepsis and can negatively regulate mTORC1 activity.
Aging Reduces the Activation of the mTORC1 Pathway after Resistance Exercise and Protein Intake in Human Skeletal Muscle: Potential Role of REDD1 and Impaired Anabolic Sensitivity.
Deldicque et al., Louvain-la-Neuve, Belgium. In Nutrients, Dec 2015
After Pro+ex, REDD1 expression tended to be higher (p = 0.087) in the older group while AMPK phosphorylation was not modified by any condition.
Selective Activator of the Glucocorticoid Receptor Compound A Dissociates Therapeutic and Atrophogenic Effects of Glucocorticoid Receptor Signaling in Skin.
Budunova et al., Chicago, United States. In J Cancer Prev, Dec 2015
Unlike glucocorticoids, CpdA itself did not induce skin atrophy which correlated with lack of induction of atrophogene regulated in development and DNA damage response 1 (REDD1) causatively involved in skin and muscle steroid-induced atrophy.
Melatonin enhances arsenic trioxide-induced cell death via sustained upregulation of Redd1 expression in breast cancer cells.
Park et al., Seoul, South Korea. In Mol Cell Endocrinol, Dec 2015
Interestingly, we found that the cell death induced by co-treatment with melatonin and ATO was mediated by sustained upregulation of Redd1, which was associated with increased production of reactive oxygen species (ROS).
Metformin and cancer: Between the bioenergetic disturbances and the antifolate activity.
López-Muñoz et al., Santiago, Chile. In Pharmacol Res, Nov 2015
It has also been reported that cell cycle arrest, autophagy, apoptosis and cell death induction is mediated by the activation of AMPK and Redd1 proteins, thus inhibiting the mTOR pathway.
Time course of the response to ACTH in pig: biological and transcriptomic study.
Mormède et al., France. In Bmc Genomics, 2014
In particular, DDIT4, DUSP1, FKBP5, IL7R, NFKBIA, PER1, RGS2 and RHOB were shown to be connected to each other by the glucocorticoid receptor NR3C1.
Emerging therapies for Parkinson's disease: from bench to bedside.
Mousa et al., Belmont, United States. In Pharmacol Ther, 2014
Other emerging non-pharmacotherapies include viral vector gene therapy, microRNAs, transglutaminases, RTP801, stem cells and glial derived neurotrophic factor (GDNF).
Targeting mitochondrial dysfunction as in aging and glaucoma.
del Olmo Aguado et al., Oviedo, Spain. In Drug Discov Today, 2014
A substance worthy of mention is rapamycin, which affects regulated in development and DNA damage 1 (REDD1), and is known to enhance mitochondrial function.
REDD1 is essential for stress-induced synaptic loss and depressive behavior.
Duman et al., New Haven, United States. In Nat Med, 2014
Here, we show that stress increases levels of REDD1 (regulated in development and DNA damage responses-1), an inhibitor of mTORC1 (mammalian target of rapamycin complex-1; ref. 10), in rat prefrontal cortex (PFC).
RTP801/REDD1: a stress coping regulator that turns into a troublemaker in neurodegenerative disorders.
Malagelada et al., Barcelona, Spain. In Front Cell Neurosci, 2013
RTP801/REDD1/Dig2 has become one of the most puzzling regulators of mTOR.
mTOR: on target for novel therapeutic strategies in the nervous system.
Wang et al., Newark, United States. In Trends Mol Med, 2013
Recent studies highlight the importance of both traditional and newly recognized interactors of mTOR, such as p70S6K, 4EBP1, GSK-3β, REDD1/RTP801, TSC1/TSC2, growth factors, wingless, and forkhead transcription factors, that influence Alzheimer's disease, Parkinson's disease, Huntington's disease, tuberous sclerosis, and epilepsy.
Feedback control of p53 translation by REDD1 and mTORC1 limits the p53-dependent DNA damage response.
Ellisen et al., Boston, United States. In Mol Cell Biol, 2011
REDD1-mediated suppression of mTORC1 activity exerts feedback control on p53, thereby limiting the apoptotic response and contributing to cellular survival following DNA damage.
Chemical inhibition of RNA viruses reveals REDD1 as a host defense factor.
Fontoura et al., Dallas, United States. In Nat Chem Biol, 2011
REDD1 is a new host defense factor, and chemical activation of REDD1 expression represents a potent antiviral intervention strategy
Interplay between pVHL and mTORC1 pathways in clear-cell renal cell carcinoma.
Brugarolas et al., Dallas, United States. In Mol Cancer Res, 2011
mechanisms have evolved in tumors to escape growth suppressive signals resulting from VHL loss and REDD1 upregulation
Glucocorticoid elevation of dexamethasone-induced gene 2 (Dig2/RTP801/REDD1) protein mediates autophagy in lymphocytes.
Distelhorst et al., Cleveland, United States. In J Biol Chem, 2011
elevation of Dig2/RTP801/REDD1 contributes to the induction of autophagy.
Metformin, independent of AMPK, induces mTOR inhibition and cell-cycle arrest through REDD1.
Bost et al., Nice, France. In Cancer Res, 2011
Metformin increases REDD1 expression in a p53-dependent manner. REDD1 invalidation, using siRNA or REDD1(-/-) cells, abrogates metformin inhibition of mTOR.
Crosstalk between glucocorticoid receptor and nutritional sensor mTOR in skeletal muscle.
Tanaka et al., Tokyo, Japan. In Cell Metab, 2011
We identified direct target genes of the glucocorticoid receptor (GR) in skeletal muscle, i.e., REDD1 and KLF15.
Plzf regulates germline progenitor self-renewal by opposing mTORC1.
Pandolfi et al., Boston, United States. In Cell, 2010
Plzf opposes mTORC1 activity by inducing expression of the mTORC1 inhibitor Redd1.
Rtp801, a suppressor of mTOR signaling, is an essential mediator of cigarette smoke-induced pulmonary injury and emphysema.
Tuder et al., Baltimore, United States. In Nat Med, 2010
Our data support the notion that Rtp801 may represent a major molecular sensor and mediator of cigarette smoke-induced lung injury.
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