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A microarray analysis revealed that in A3G-transduced Vero cells, several cellular transcripts were differentially expressed, suggesting that A3G regulates the expression of host factors. One of the most upregulated host cell factors, REDD1 (regulated in development and DNA damage response-1, also called DDIT4), reduced MV replication approximately 10-fold upon overexpression in Vero cells.
This is concurrent with an increase in the expression level of DDIT4, which is an inhibitor of the mammalian target of rapamycin (mTOR (show FRAP1 Proteins)) signaling pathway. these results provided a novel insight on miR1243p involvement in the biological alterations of male patients with major depressive disorder and suggested that this miRNA may also serve as a malespeci fi c target for antidepressant treatment
DDIT4 activity is directly linked to regulation of mTOR (show FRAP1 Proteins) signalling
The HIF-1alpha (show HIF1A Proteins)-REDD1-mTOR (show FRAP1 Proteins) pathway was involved in the response to hypoxia in BeWo cells. Hypoxia-induced REDD1 upregulation is mediated by a HIF-1alpha (show HIF1A Proteins)-dependent pathway. Disruption of REDD1 blocked the effects of hypoxia on suppressing mTOR (show FRAP1 Proteins) and resulted in additional accumulation of HIF-1alpha (show HIF1A Proteins) in BeWo cells.
REDD1 is overexpressed during Familial Mediterranean fever (show MEFV Proteins) inflammatory attacks induced by physical or psychological stress
Expression of key autophagy markers (microtubule-associated protein 1A/1B light chain 3 and autophagy protein 5) was markedly reduced in cultured human chondrocytes with REDD1 depletion.
The production of superoxide anion in nockout-Rtp801 mouse lung fibroblasts (MLF) was lower than that in Rtp801 Wt cells after cigarette smoke extract treatment, and it was inhibited in Wt MLF by silencing nicotinamide adenine dinucleotide phosphate oxidase (show DUOX2 Proteins)-4 (Nox4 (show NOX4 Proteins)) expression with small interfering Nox4 (show NOX4 Proteins) RNA.
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.g., sepsis, alcoholism, diabetes, obesity) suggesting a role for REDD1 in regulating mTORC1-dependent skeletal muscle protein metabolism. [Review]
a novel STAT3 (show STAT3 Proteins)-dependent mechanism of both IL-6 (show IL6 Proteins)-induced activation of mTOR (show FRAP1 Proteins) and IL-6 (show IL6 Proteins)-dependent reversion of stress-induced inhibition of mTOR (show FRAP1 Proteins) activity, is reported.
findings implicate REDD1 as a crucial regulator of mTORC1 activity in iron-depleted cells
RTP801 plays a essential role in the progression of restraint stress induced neurodegenerative disease.
Findings suggest that REDD1 in cacna1c (show CACNA1C Proteins) heterozygous mice may influence depression-related behavior via regulation of the FoxO3a (show FOXO3 Proteins) pathway. Study identified the prefrontal cortex as a key brain region in which cacna1c (show CACNA1C Proteins) mechanisms through previously unidentified, novel molecular pathways contribute to depression-related behavior.
Diabetic wild-type mice exhibited functional deficiencies in visual acuity and contrast sensitivity, whereas diabetic REDD1-deficient mice had no visual dysfunction. The results support a role for REDD1 in diabetes-induced retinal neurodegeneration.
these data show that REDD1 induction regulates the exercise-mediated change in a distinct set of genes within skeletal muscle.
Findings suggest that REDD1 is a key mediator of cartilage homeostasis through regulation of autophagy and mitochondrial biogenesis and that REDD1 deficiency exacerbates the severity of injury-induced osteoarthritis.
These data suggest that loss of REDD1 augments the rate of the OV-induced increase in muscle mass by altering multiple protein balance pathways.
The production of superoxide anion in nockout-Rtp801 mouse lung fibroblasts (MLF) was lower than that in Rtp801 Wt cells after cigarette smoke extract treatment, and it was inhibited in Wt MLF by silencing nicotinamide adenine dinucleotide phosphate oxidase (show DUOX1 Proteins)-4 (Nox4 (show NOX4 Proteins)) expression with small interfering Nox4 (show NOX4 Proteins) RNA.
REDD1 is required for normal insulin (show INS Proteins)-stimulated signaling, and a subtle balance exists between MEK1 (show MAP2K1 Proteins)/2, REDD1, and mTOR (show FRAP1 Proteins)
study suggests that VDR regulates Ddit4 expression during epidermal homeostasis and the wound healing process, while elevated Ddit4 represents an early growth-arresting stress response within VDR(-/-) follicles.
REDD1 knockout T cells exhibit a defect in proliferation and cell survival, although markers of activation appear normal. These findings demonstrate a previously unappreciated role for REDD1 in T cell function.
Redd1 alters dorsoventral patterning by antagonizing the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling pathway.
HIF-1-responsive gene that may protect some types of cells from hypoxia and H(2)O(2)-triggered apoptosis
DNA damage-inducible transcript 4 protein
, DNA-damage-inducible transcript 4 protein
, protein regulated in development and DNA damage response 1
, DNA-damage-inducible transcript 4
, HIF-1 responsive protein RTP801
, HIF-1 responsive RTP801
, dexamethasone-induced gene 2 protein
, regulated in development and DNA damage response 1