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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).
REDD1 and p-AKT (show AKT1 ELISA Kits) over-expression may serve as a prognostic biomarker in ovarian cancer, but KRAS mutations and REDD1 protein over-expression were not correlated in OC.
Caspase 3 (show CASP3 ELISA Kits) cleaved REDD1 during apoptotic activation.
the results demonstrate that REDD1 acts not only as a repressor of mTORC1 but also as a constant modulator of the phosphorylation of Akt (show AKT1 ELISA Kits) in response to growth factors and nutrients.
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 is necessary for hyperglycemia mediated effects on VEGF expression in the retina of diabetic mice.
These data suggest that epithelial mTORC1 activity plays a protective role against lung injury, and its inhibition by Rtp801 exacerbates alveolar injury caused by endotoxin.
The REDD1 KO mouse muscle displayed blunted mTORC1 signaling responses.
REDD1 is required for glucocorticoid-induced inhibition of protein synthesis via mTORC1 downregulation
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