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抗Human DDIT4 抗体:
抗Mouse (Murine) DDIT4 抗体:
抗Rat (Rattus) DDIT4 抗体:
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
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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 - 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
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
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 (显示 DUOX2 抗体)-4 (Nox4 (显示 NOX4 抗体)) expression with small interfering Nox4 (显示 NOX4 抗体) 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 (显示 STAT3 抗体)-dependent mechanism of both IL-6 (显示 IL6 抗体)-induced activation of mTOR (显示 FRAP1 抗体) and IL-6 (显示 IL6 抗体)-dependent reversion of stress-induced inhibition of mTOR (显示 FRAP1 抗体) activity, is reported.
findings implicate REDD1 as a crucial regulator of mTORC1 activity in iron-depleted cells
C/EBPbeta (显示 CEBPB 抗体) promotes autophagy in PC3 (显示 PCSK1 抗体) 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 (显示 INS 抗体) resistance and may be a target to improve insulin (显示 INS 抗体) action in insulin (显示 INS 抗体)-resistant individuals.
REDD1 knockout (KO) mice, all skin compartments, epidermal stem, and progenitor cells were protected from atrophic effects of glucocorticoids.
MiR (显示 MLXIP 抗体)-630 reduced apoptosis by downregulating several apoptotic modulators, PARP3 (显示 PARP3 抗体), DDIT4, and EP300 (显示 EP300 抗体).
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 (显示 DUOX1 抗体)-4 (Nox4 (显示 NOX4 抗体)) expression with small interfering Nox4 (显示 NOX4 抗体) RNA.
REDD1 is required for normal insulin (显示 INS 抗体)-stimulated signaling, and a subtle balance exists between MEK1 (显示 MAP2K1 抗体)/2, REDD1, and mTOR (显示 FRAP1 抗体)
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 (显示 TXNIP 抗体) is physiological rheostat controlling stress-induced autophagy.
LPS (显示 TLR4 抗体) induces REDD1 expression by two distinct CREB (显示 CREB1 抗体)-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 (显示 WNT2 抗体)/beta-catenin (显示 CTNNB1 抗体) 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