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The HIF-1alpha (Montrer HIF1A Kits ELISA)-REDD1-mTOR (Montrer FRAP1 Kits ELISA) pathway was involved in the response to hypoxia in BeWo cells. Hypoxia-induced REDD1 upregulation is mediated by a HIF-1alpha (Montrer HIF1A Kits ELISA)-dependent pathway. Disruption of REDD1 blocked the effects of hypoxia on suppressing mTOR (Montrer FRAP1 Kits ELISA) and resulted in additional accumulation of HIF-1alpha (Montrer HIF1A Kits ELISA) in BeWo cells.
REDD1 is overexpressed during Familial Mediterranean fever (Montrer MEFV Kits ELISA) 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 (Montrer DUOX2 Kits ELISA)-4 (Nox4 (Montrer NOX4 Kits ELISA)) expression with small interfering Nox4 (Montrer NOX4 Kits ELISA) 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 (Montrer STAT3 Kits ELISA)-dependent mechanism of both IL-6 (Montrer IL6 Kits ELISA)-induced activation of mTOR (Montrer FRAP1 Kits ELISA) and IL-6 (Montrer IL6 Kits ELISA)-dependent reversion of stress-induced inhibition of mTOR (Montrer FRAP1 Kits ELISA) activity, is reported.
findings implicate REDD1 as a crucial regulator of mTORC1 activity in iron-depleted cells
C/EBPbeta (Montrer CEBPB Kits ELISA) promotes autophagy in PC3 (Montrer PCSK1 Kits ELISA) cells by augmenting REDD1 expression.
These data highlight the central role of REDD1 in regulating both protein synthesis and autophagy in skeletal muscle during sepsis.
Findings from this study propose a REDD1-regulated mechanism in T2D skeletal muscle that may contribute to whole body insulin (Montrer INS Kits ELISA) resistance and may be a target to improve insulin (Montrer INS Kits ELISA) action in insulin (Montrer INS Kits ELISA)-resistant individuals.
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 (Montrer DUOX1 Kits ELISA)-4 (Nox4 (Montrer NOX4 Kits ELISA)) expression with small interfering Nox4 (Montrer NOX4 Kits ELISA) RNA.
REDD1 is required for normal insulin (Montrer INS Kits ELISA)-stimulated signaling, and a subtle balance exists between MEK1 (Montrer MAP2K1 Kits ELISA)/2, REDD1, and mTOR (Montrer FRAP1 Kits ELISA)
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.
Reactive oxygen species regulation through REDD1/TXNIP (Montrer TXNIP Kits ELISA) is physiological rheostat controlling stress-induced autophagy.
LPS (Montrer TLR4 Kits ELISA) induces REDD1 expression by two distinct CREB (Montrer CREB1 Kits ELISA)-mediated mechanisms
Redd1 alters dorsoventral patterning by antagonizing the Wnt (Montrer WNT2 Kits ELISA)/beta-catenin (Montrer CTNNB1 Kits ELISA) 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