keyword
MENU ▼
Read by QxMD icon Read
search

REDD1

keyword
https://www.readbyqxmd.com/read/28199842/the-mtor-and-pp2a-pathways-regulate-phd2-phosphorylation-to-fine-tune-hif1%C3%AE-levels-and-colorectal-cancer-cell-survival-under-hypoxia
#1
Giusy Di Conza, Sarah Trusso Cafarello, Stefan Loroch, Daniela Mennerich, Sofie Deschoemaeker, Mario Di Matteo, Manuel Ehling, Kris Gevaert, Hans Prenen, Rene Peiman Zahedi, Albert Sickmann, Thomas Kietzmann, Fabiola Moretti, Massimiliano Mazzone
Oxygen-dependent HIF1α hydroxylation and degradation are strictly controlled by PHD2. In hypoxia, HIF1α partly escapes degradation because of low oxygen availability. Here, we show that PHD2 is phosphorylated on serine 125 (S125) by the mechanistic target of rapamycin (mTOR) downstream kinase P70S6K and that this phosphorylation increases its ability to degrade HIF1α. mTOR blockade in hypoxia by REDD1 restrains P70S6K and unleashes PP2A phosphatase activity. Through its regulatory subunit B55α, PP2A directly dephosphorylates PHD2 on S125, resulting in a further reduction of PHD2 activity that ultimately boosts HIF1α accumulation...
February 14, 2017: Cell Reports
https://www.readbyqxmd.com/read/28115701/induction-of-dormancy-in-hypoxic-human-papillomavirus-positive-cancer-cells
#2
Karin Hoppe-Seyler, Felicitas Bossler, Claudia Lohrey, Julia Bulkescher, Frank Rösl, Lars Jansen, Arnulf Mayer, Peter Vaupel, Matthias Dürst, Felix Hoppe-Seyler
Oncogenic human papillomaviruses (HPVs) are closely linked to major human malignancies, including cervical and head and neck cancers. It is widely assumed that HPV-positive cancer cells are under selection pressure to continuously express the viral E6/E7 oncogenes, that their intracellular p53 levels are reconstituted on E6/E7 repression, and that E6/E7 inhibition phenotypically results in cellular senescence. Here we show that hypoxic conditions, as are often found in subregions of cervical and head and neck cancers, enable HPV-positive cancer cells to escape from these regulatory principles: E6/E7 is efficiently repressed, yet, p53 levels do not increase...
February 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27982685/responses-of-skeletal-muscle-hypertrophy-in-wistar-rats-to-different-resistance-exercise-models
#3
T F Luciano, S de Oliveira Marques, B L da Silva Pieri, D Roxo de Souza, L V Araújo, R T Nesi, D da Luz Scheffer, V H Comin, R A Pinho, A P Muller, C T de Souza
This study aimed to compare the effects of three different resistance exercise models on the quadriceps muscle cross-sectional area, as well as on mTOR phosphorylation and other pivotal molecules involved in the upstream regulation of mTOR. Twenty-four male Wistar rats were divided into untrained (control), endurance resistance training, strength resistance training, and hypertrophy resistance training (HRT) groups (n = 6). After 12 weeks of training, the red portion of the quadriceps was removed for histological and western blot analyses...
December 16, 2016: Physiological Research
https://www.readbyqxmd.com/read/27922594/cacna1c-in-the-prefrontal-cortex-regulates-depression-related-behaviors-via-redd1
#4
Zeeba D Kabir, Anni S Lee, Caitlin E Burgdorf, Delaney Fischer, Aditi M Rajadhyaksha, Ethan Mok, Bryant Rizzo, Richard C Rice, Kamalpreet Singh, Kristie T Ota, Danielle M Gerhard, Kathryn C Schierberl, Michael Glass, Ronald S Duman, Anjali M Rajadhyaksha
The CACNA1C gene that encodes the L-type Ca(2+) channel (LTCC) Cav1.2 subunit has emerged as a candidate risk gene for multiple neuropsychiatric disorders including bipolar disorder, major depressive disorder and schizophrenia, all marked with depression-related symptoms. Although cacna1c heterozygous (HET) mice have been previously reported to exhibit an antidepressant-like phenotype, the molecular and circuit-level dysfunction remains unknown. Here we report that viral vector-mediated deletion of cacna1c in the adult prefrontal cortex (PFC) of mice recapitulates the antidepressant-like effect observed in cacna1c HET mice using the sucrose preference test (SPT), the forced swim test (FST), and the tail suspension test (TST)...
December 6, 2016: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/27913296/regulation-of-skeletal-muscle-insulin-stimulated-signaling-through-the-mek-redd1-mtor-axis
#5
Cory M Dungan, David L Williamson
Recent findings in adipocytes suggest that mitogen-activated protein kinase (MAPK)/extracellular-regulated signaling kinase (ERK) kinase 1/2 (MEK1/2) signaling regulates regulated in development and DNA damage 1 (REDD1) protein expression. Similarly, our previous work show that a lack of REDD1 protein expression, and associated hyperactive basal mechanistic target of rapamycin (mTOR) signaling, limits skeletal muscle's response to insulin. Therefore, we sought to determine: 1) if MEK1/2 inhibition is sufficient to reduce REDD1 protein expression and subsequently insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation via negative feedback of hyperactive mTOR in REDD1 wild-type (WT) mice and 2) if rapamycin-mediated mTOR inhibition is sufficient to improve IRS-1 tyrosine phosphorylation in REDD1 knockout (KO) mice...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27909227/castration-alters-protein-balance-following-high-frequency-muscle-contraction
#6
Jennifer L Steiner, David H Fukuda, Michael L Rossetti, Jay R Hoffman, Bradley S Gordon
Resistance exercise increases muscle mass by shifting protein balance in favor of protein accretion. Androgens independently alter protein balance, but it is unknown whether androgens alter this measure following resistance exercise. To answer this, male mice were subjected to sham or castration surgery 7-8 weeks prior to undergoing a bout of unilateral, high frequency, electrically induced muscle contractions in the fasted or refed state. Puromycin was injected 30 min prior to sacrifice to measure protein synthesis...
December 1, 2016: Journal of Applied Physiology
https://www.readbyqxmd.com/read/27829135/macrophage-metabolism-shapes-angiogenesis-in-tumors
#7
Alberto Mantovani, Massimo Locati
In this issue, Wenes et al. (2016) show that REDD1, an mTOR inhibitor induced by hypoxia, enhances glycolysis in tumor-associated macrophages (TAMs). Metabolic competition for glucose between TAMs and endothelial cells leads to an abnormal, leaky vascular network. Targeting REDD1 normalizes glycolysis in TAMs, stabilizes the vascular network, and inhibits metastasis.
November 8, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27787518/glioblastoma-hypoxia-and-autophagy-a-survival-prone-m%C3%A3-nage-%C3%A3-trois
#8
REVIEW
Soha Jawhari, Marie-Hélène Ratinaud, Mireille Verdier
Glioblastoma multiforme is the most common and the most aggressive primary brain tumor. It is characterized by a high degree of hypoxia and also by a remarkable resistance to therapy because of its adaptation capabilities that include autophagy. This degradation process allows the recycling of cellular components, leading to the formation of metabolic precursors and production of adenosine triphosphate. Hypoxia can induce autophagy through the activation of several autophagy-related proteins such as BNIP3, AMPK, REDD1, PML, and the unfolded protein response-related transcription factors ATF4 and CHOP...
October 27, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27773694/macrophage-metabolism-controls-tumor-blood-vessel-morphogenesis-and-metastasis
#9
Mathias Wenes, Min Shang, Mario Di Matteo, Jermaine Goveia, Rosa Martín-Pérez, Jens Serneels, Hans Prenen, Bart Ghesquière, Peter Carmeliet, Massimiliano Mazzone
Hypoxic tumor-associated macrophages (TAMs) acquire angiogenic and immunosuppressive properties. Yet it remains unknown if metabolic changes influence these functions. Here, we argue that hypoxic TAMs strongly upregulate the expression of REDD1, a negative regulator of mTOR. REDD1-mediated mTOR inhibition hinders glycolysis in TAMs and curtails their excessive angiogenic response, with consequent formation of abnormal blood vessels. Accordingly, REDD1 deficiency in TAMs leads to the formation of smoothly aligned, pericyte-covered, functional vessels, which prevents vessel leakiness, hypoxia, and metastases...
November 8, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27749759/restorative-mechanisms-regulating-protein-balance-in-skeletal-muscle-during-recovery-from-sepsis
#10
Kristen T Crowell, David I Soybel, Charles H Lang
Muscle deconditioning is commonly observed in patients surviving sepsis. Little is known regarding the molecular mechanisms regulating muscle protein homeostasis during the recovery or convalescence phase. We adapted a sepsis-recovery mouse model that uses cecal ligation and puncture (CLP), followed 24 h later by cecal resection and antibiotic treatment, to identify putative cellular pathways regulating protein synthesis and breakdown in skeletal muscle. Ten days after CLP, body weight and food consumption did not differ between control and sepsis-recovery mice, but gastrocnemius weight was reduced...
October 5, 2016: Shock
https://www.readbyqxmd.com/read/27649272/heat-stress-modulates-both-anabolic-and-catabolic-signaling-pathways-preventing-dexamethasone-induced-muscle-atrophy-in-vitro
#11
Wakako Tsuchida, Masahiro Iwata, Takayuki Akimoto, Shingo Matsuo, Yuji Asai, Shigeyuki Suzuki
It is generally recognized that synthetic glucocorticoids induce skeletal muscle weakness, and endogenous glucocorticoid levels increase in patients with muscle atrophy. It is reported that heat stress attenuates glucocorticoid-induced muscle atrophy; however, the mechanisms involved are unknown. Therefore, we examined the mechanisms underlying the effects of heat stress against glucocorticoid-induced muscle atrophy using C2C12 myotubes in vitro, focusing on expression of key molecules and signaling pathways involved in regulating protein synthesis and degradation...
March 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27613400/is-redd1-a-metabolic-%C3%A3-minence-grise
#12
REVIEW
Christopher Lipina, Harinder S Hundal
Regulated in development and DNA damage response 1 (REDD1) has been functionally linked to the control of diverse cellular processes due, at least in part, to its ability to repress mammalian or mechanistic Target of Rapamycin (mTOR) Complex-1 (mTORC1), a key protein complex controlled by hormonal and nutrient cues. Notably, emerging evidence suggests that REDD1 also regulates several pathways involved in modulating energy balance and metabolism. Herein, we discuss evidence implicating REDD1 as a key modulator of insulin action and metabolic function, including its potential contribution to mitochondrial biology and pancreatic islet function...
December 2016: Trends in Endocrinology and Metabolism: TEM
https://www.readbyqxmd.com/read/27577706/regulation-of-hypoxia-inducible-factor-1%C3%AE-regulated-in-development-and-dna-damage-response-1-and-mammalian-target-of-rapamycin-in-human-placental-bewo-cells-under-hypoxia
#13
F Zhou, L B Guan, P Yu, X D Wang, Y Y Hu
INTRODUCTION: Hypoxia-inducible factor-1 (HIF-1), regulated in development and DNA damage response-1 (REDD1) and mammalian target of rapamycin (mTOR) are crucial mediators of many metabolic processes in various cell types under hypoxia. The involvement and regulation of these three factors underlying trophoblasts' response to hypoxia remains to be determined. METHODS: Specific siRNAs were applied to inhibit the expression of the corresponding genes and to investigate the roles of HIF-1α in modulating REDD1/mTOR and REDD1 in regulating mTOR/HIF-1α in the human choriocarcinoma cell line BeWo under normoxia and hypoxia...
September 2016: Placenta
https://www.readbyqxmd.com/read/27549090/hypoxia-induced-regulation-of-placental-redd1-and-mtor-was-impaired-in-a-rat-model-of-estrogen-induced-cholestasis
#14
Fan Zhou, Huafang Chen, Xiaodong Wang, Pin Yu, Yayi Hu
PURPOSE: Hypoxia inducible factor-1α (HIF-1α), regulated in development and DNA damage response-1 (REDD1), and mammalian target of rapamycin (mTOR) play distinct roles in response to hypoxia. The aim of this study was to evaluate whether the HIF-1α-REDD1-mTOR-mediated hypoxic stress response also operates normally in estrogen-induced cholestasis. METHODS: Pregnant rats were administered with ethinylestradiol (EE) to induce cholestasis and then were subjected to feto-placental ischemia reperfusion (IR); as controls, one group received neither EE nor IR, and another two groups received only EE or IR...
August 22, 2016: Archives of Gynecology and Obstetrics
https://www.readbyqxmd.com/read/27536856/fat1-is-a-novel-upstream-regulator-of-hif1%C3%AE-and-invasion-of-high-grade-glioma
#15
Evanka Madan, Bhawana Dikshit, Srinivas H Gowda, Chitrangda Srivastava, Chitra Sarkar, Parthaprasad Chattopadhyay, Subrata Sinha, Kunzang Chosdol
The hypoxic microenvironment is an important contributor of glioblastoma (GBM) aggressiveness via HIF1α, while tumour inflammation is profoundly influenced by FAT Atypical Cadherin (FAT1). This study was designed to explore the functional interaction and significance of FAT1 and HIF1α under severe hypoxia-mimicking tumour microenvironment in primary human tumours. We first identified a positive correlation of FAT1 with HIF1α and its target genes in GBM tumour specimens, revealing the significance of the FAT1-HIF1α axis in glioma cells...
December 1, 2016: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/27465734/loss-of-redd1-augments-the-rate-of-the-overload-induced-increase-in-muscle-mass
#16
Bradley S Gordon, Chang Liu, Jennifer L Steiner, Gustavo A Nader, Leonard S Jefferson, Scot R Kimball
The overload-induced increase in muscle mass is accompanied by protein accretion; however, the initiating events are poorly understood. Regulated in Development and DNA Damage 1 (REDD1), a repressor of the mechanistic target of rapamycin in complex 1 (mTORC1), blunts the elevation in protein synthesis induced by acute muscle contractions. Therefore, this study was designed to determine whether REDD1 alters the rate of the overload-induced increase in muscle mass. Wild-type (WT) and REDD1-null mice underwent unilateral functional overload (OV) of the plantaris, while the contralateral sham leg served as a control...
September 1, 2016: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/27335637/validation-of-a-commercially-available-anti-redd1-antibody-using-rna-interference-and-redd1-mouse-embryonic-fibroblasts
#17
Deborah L Grainger, Lydia Kutzler, Sharon L Rannels, Scot R Kimball
REDD1 is a transcriptional target gene of p53 and HIF-1, and an inhibitor of mTOR (mechanistic target of rapamycin) complex 1 (mTORC1)-signaling through PP2A-dependent interaction, making it an important convergence point of both tumor suppression and cell growth pathways. In accordance with this positioning, REDD1 levels are transcriptionally upregulated in response to a variety of cellular stress factors such as nutrient deprivation, hypoxia and DNA damage. In the absence of such conditions, and in particular where growth factor signaling is activated, REDD1 expression is typically negligible; therefore, it is necessary to induce REDD1 prior to experimentation or detection in model systems...
2016: F1000Research
https://www.readbyqxmd.com/read/27289530/caloric-restriction-normalizes-obesity-induced-alterations-on-regulators-of-skeletal-muscle-growth-signaling
#18
Cory M Dungan, Ji Li, David L Williamson
The objective of this study was to establish the impact of caloric restriction on high fat diet-induced alterations on regulators of skeletal muscle growth. We hypothesized that caloric restriction would reverse the negative effects of high fat diet-induced obesity on REDD1 and mTOR-related signaling. Following an initial 8 week period of HF diet-induced obesity, caloric restriction (CR ~30 %) was employed while mice continued to consume either a low (LF) or high fat (HF) diet for 8 weeks. Western analysis of skeletal muscle showed that CR reduced (p < 0...
August 2016: Lipids
https://www.readbyqxmd.com/read/27233899/time-course-change-of-redd1-expressions-in-the-hippocampal-ca1-region-following-chronic-cerebral-hypoperfusion
#19
Jin-A Park, Choong-Hyun Lee
Redd1, also known as RTP801/Dig2/DDIT4, is a stress-induced protein and marked changes of Redd1 expression occurs in response to hypoxia or cerebral ischemia. In the present study, we examined the time-course changes in Redd1 protein expressions in the rat hippocampal CA1 region following chronic cerebral hypoperfusion (CCH) induced by permanent bilateral common carotid arteries occlusion (2VO). Redd1 immunoreactivity in the pyramidal neurons of the hippocampal CA1 region was increased at 7 days after 2VO surgery, and then the immunoreactivity was decreased with time...
May 27, 2016: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/27189933/emerging-role-for-regulated-in-development-and-dna-damage-1-redd1-in-the-regulation-of-skeletal-muscle-metabolism
#20
REVIEW
Bradley S Gordon, Jennifer L Steiner, David L Williamson, Charles H Lang, Scot R Kimball
Since its discovery, the protein regulated in development and DNA damage 1 (REDD1) has been implicated in the cellular response to various stressors. Most notably, its role as a repressor of signaling through the central metabolic regulator, the mechanistic target of rapamycin in complex 1 (mTORC1) has gained considerable attention. Not surprisingly, changes in REDD1 mRNA and protein have been observed in skeletal muscle under various physiological conditions (e.g., nutrient consumption and resistance exercise) and pathological conditions (e...
July 1, 2016: American Journal of Physiology. Endocrinology and Metabolism
keyword
keyword
116913
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"