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anti-Human DDIT4 Antibodies:
anti-Mouse (Murine) DDIT4 Antibodies:
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Human Polyclonal DDIT4 Primary Antibody for IHC, ELISA - ABIN1003101
Ellisen, Ramsayer, Johannessen, Yang, Beppu, Minda, Oliner, McKeon, Haber: REDD1, a developmentally regulated transcriptional target of p63 and p53, links p63 to regulation of reactive oxygen species. in Molecular cell 2002
Show all 4 Pubmed References
Human Polyclonal DDIT4 Primary Antibody for ELISA, WB - ABIN1003102
Shoshani, Faerman, Mett, Zelin, Tenne, Gorodin, Moshel, Elbaz, Budanov, Chajut, Kalinski, Kamer, Rozen, Mor, Keshet, Leshkowitz, Einat, Skaliter, Feinstein: Identification of a novel hypoxia-inducible factor 1-responsive gene, RTP801, involved in apoptosis. in Molecular and cellular biology 2002
Show all 4 Pubmed References
Human Polyclonal DDIT4 Primary Antibody for ICC, IF - ABIN439647
Potts, McMillan, Rosales, Kim, Ou, Toombs, Brekken, Minden, MacMillan, White: Mode of action and pharmacogenomic biomarkers for exceptional responders to didemnin B. in Nature chemical biology 2015
Human Polyclonal DDIT4 Primary Antibody for ICC, IF - ABIN4304577
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
The HIF-1alpha (show HIF1A Antibodies)-REDD1-mTOR (show FRAP1 Antibodies) pathway was involved in the response to hypoxia in BeWo cells. Hypoxia-induced REDD1 upregulation is mediated by a HIF-1alpha (show HIF1A Antibodies)-dependent pathway. Disruption of REDD1 blocked the effects of hypoxia on suppressing mTOR (show FRAP1 Antibodies) and resulted in additional accumulation of HIF-1alpha (show HIF1A Antibodies) in BeWo cells.
REDD1 is overexpressed during Familial Mediterranean fever (show MEFV Antibodies) 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 Antibodies)-4 (Nox4 (show NOX4 Antibodies)) expression with small interfering Nox4 (show NOX4 Antibodies) 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 Antibodies)-dependent mechanism of both IL-6 (show IL6 Antibodies)-induced activation of mTOR (show FRAP1 Antibodies) and IL-6 (show IL6 Antibodies)-dependent reversion of stress-induced inhibition of mTOR (show FRAP1 Antibodies) activity, is reported.
findings implicate REDD1 as a crucial regulator of mTORC1 activity in iron-depleted cells
C/EBPbeta (show CEBPB Antibodies) promotes autophagy in PC3 (show PCSK1 Antibodies) 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 Antibodies) resistance and may be a target to improve insulin (show INS Antibodies) action in insulin (show INS Antibodies)-resistant individuals.
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 Antibodies)-4 (Nox4 (show NOX4 Antibodies)) expression with small interfering Nox4 (show NOX4 Antibodies) RNA.
REDD1 is required for normal insulin (show INS Antibodies)-stimulated signaling, and a subtle balance exists between MEK1 (show MAP2K1 Antibodies)/2, REDD1, and mTOR (show FRAP1 Antibodies)
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 Antibodies) is physiological rheostat controlling stress-induced autophagy.
LPS (show TLR4 Antibodies) induces REDD1 expression by two distinct CREB (show CREB1 Antibodies)-mediated mechanisms
Glucocorticoids induce skin atrophy and activate REDD1 expression.
Redd1 alters dorsoventral patterning by antagonizing the Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) 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