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Human DDIT4 Protein expressed in Escherichia coli (E. coli) - ABIN667871
Regazzetti, Bost, Le Marchand-Brustel, Tanti, Giorgetti-Peraldi: Insulin induces REDD1 expression through hypoxia-inducible factor 1 activation in adipocytes. in The Journal of biological chemistry 2010
Show all 2 references for ABIN667871
C/EBPbeta (show CEBPB Proteins) promotes autophagy in PC3 (show PCSK1 Proteins) 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 Proteins) resistance and may be a target to improve insulin (show INS Proteins) action in insulin (show INS Proteins)-resistant individuals.
REDD1 knockout (KO) mice, all skin compartments, epidermal stem, and progenitor cells were protected from atrophic effects of glucocorticoids.
MiR (show MLXIP Proteins)-630 reduced apoptosis by downregulating several apoptotic modulators, PARP3 (show PARP3 Proteins), DDIT4, and EP300 (show EP300 Proteins).
REDD1 and p-AKT (show AKT1 Proteins) 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 Proteins) 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 Proteins) in response to growth factors and nutrients.
analysis of ubiquitin-mediated proteolysis of DNA damage-inducible transcript 4 (DDIT4) by the E3 ligase HUWE1 (show HUWE1 Proteins)
Translocation to the plasma membrane appears to be an inactivation mechanism of REDD1 by G-protein coupled receptors.
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 Proteins) is physiological rheostat controlling stress-induced autophagy.
LPS (show TLR4 Proteins) induces REDD1 expression by two distinct CREB (show CREB1 Proteins)-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 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