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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 ELISA Kits)-4 (Nox4 (show NOX4 ELISA Kits)) expression with small interfering Nox4 (show NOX4 ELISA Kits) 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 ELISA Kits)-dependent mechanism of both IL-6 (show IL6 ELISA Kits)-induced activation of mTOR (show FRAP1 ELISA Kits) and IL-6 (show IL6 ELISA Kits)-dependent reversion of stress-induced inhibition of mTOR (show FRAP1 ELISA Kits) activity, is reported.
findings implicate REDD1 as a crucial regulator of mTORC1 activity in iron-depleted cells
C/EBPbeta (show CEBPB ELISA Kits) promotes autophagy in PC3 (show PCSK1 ELISA Kits) 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 (show INS ELISA Kits) resistance and may be a target to improve insulin (show INS ELISA Kits) action in insulin (show INS ELISA Kits)-resistant individuals.
REDD1 knockout (KO) mice, all skin compartments, epidermal stem, and progenitor cells were protected from atrophic effects of glucocorticoids.
MiR (show MLXIP ELISA Kits)-630 reduced apoptosis by downregulating several apoptotic modulators, PARP3 (show PARP3 ELISA Kits), DDIT4, and EP300 (show EP300 ELISA Kits).
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 ELISA Kits)-4 (Nox4 (show NOX4 ELISA Kits)) expression with small interfering Nox4 (show NOX4 ELISA Kits) RNA.
REDD1 is required for normal insulin (show INS ELISA Kits)-stimulated signaling, and a subtle balance exists between MEK1 (show MAP2K1 ELISA Kits)/2, REDD1, and mTOR (show FRAP1 ELISA Kits)
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 (show TXNIP ELISA Kits) is physiological rheostat controlling stress-induced autophagy.
LPS (show TLR4 ELISA Kits) induces REDD1 expression by two distinct CREB (show CREB1 ELISA Kits)-mediated mechanisms
Glucocorticoids induce skin atrophy and activate REDD1 expression.
REDD1 expression limits the nutrient-induced stimulation of protein synthesis and activation of mTORC1 signaling during periods of feed deprivation.
Redd1 alters dorsoventral patterning by antagonizing the Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) 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