Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human DDIT4 Anticorps:
anti-Mouse (Murine) DDIT4 Anticorps:
anti-Rat (Rattus) DDIT4 Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal DDIT4 Primary Antibody pour ELISA, WB - ABIN1003102
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. dans Molecular cell 2002
Show all 4 Pubmed References
Human Polyclonal DDIT4 Primary Antibody pour IHC, ELISA - ABIN1003101
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. dans Molecular and cellular biology 2002
Show all 4 Pubmed References
Human Polyclonal DDIT4 Primary Antibody pour 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. dans Nature chemical biology 2015
Show all 2 Pubmed References
Human Polyclonal DDIT4 Primary Antibody pour 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. dans Nature methods 2013
these findings uncover a novel mechanism by which PML (Montrer PML Anticorps) loss may contribute to mTOR (Montrer FRAP1 Anticorps) activation and cancer progression via dysregulation of basal DDIT4 gene expression.
A microarray analysis revealed that in A3G-transduced Vero cells, several cellular transcripts were differentially expressed, suggesting that A3G regulates the expression of host factors. One of the most upregulated host cell factors, REDD1 (regulated in development and DNA damage response-1, also called DDIT4), reduced MV replication approximately 10-fold upon overexpression in Vero cells.
This is concurrent with an increase in the expression level of DDIT4, which is an inhibitor of the mammalian target of rapamycin (mTOR (Montrer FRAP1 Anticorps)) signaling pathway. these results provided a novel insight on miR1243p involvement in the biological alterations of male patients with major depressive disorder and suggested that this miRNA may also serve as a malespeci fi c target for antidepressant treatment
DDIT4 activity is directly linked to regulation of mTOR (Montrer FRAP1 Anticorps) signalling
The HIF-1alpha (Montrer HIF1A Anticorps)-REDD1-mTOR (Montrer FRAP1 Anticorps) pathway was involved in the response to hypoxia in BeWo cells. Hypoxia-induced REDD1 upregulation is mediated by a HIF-1alpha (Montrer HIF1A Anticorps)-dependent pathway. Disruption of REDD1 blocked the effects of hypoxia on suppressing mTOR (Montrer FRAP1 Anticorps) and resulted in additional accumulation of HIF-1alpha (Montrer HIF1A Anticorps) in BeWo cells.
REDD1 is overexpressed during Familial Mediterranean fever (Montrer MEFV Anticorps) 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 (Montrer DUOX2 Anticorps)-4 (Nox4 (Montrer NOX4 Anticorps)) expression with small interfering Nox4 (Montrer NOX4 Anticorps) 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 (Montrer STAT3 Anticorps)-dependent mechanism of both IL-6 (Montrer IL6 Anticorps)-induced activation of mTOR (Montrer FRAP1 Anticorps) and IL-6 (Montrer IL6 Anticorps)-dependent reversion of stress-induced inhibition of mTOR (Montrer FRAP1 Anticorps) activity, is reported.
RTP801 plays a essential role in the progression of restraint stress induced neurodegenerative disease.
Findings suggest that REDD1 in cacna1c (Montrer CACNA1C Anticorps) heterozygous mice may influence depression-related behavior via regulation of the FoxO3a (Montrer FOXO3 Anticorps) pathway. Study identified the prefrontal cortex as a key brain region in which cacna1c (Montrer CACNA1C Anticorps) mechanisms through previously unidentified, novel molecular pathways contribute to depression-related behavior.
Diabetic wild-type mice exhibited functional deficiencies in visual acuity and contrast sensitivity, whereas diabetic REDD1-deficient mice had no visual dysfunction. The results support a role for REDD1 in diabetes-induced retinal neurodegeneration.
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 (Montrer DUOX1 Anticorps)-4 (Nox4 (Montrer NOX4 Anticorps)) expression with small interfering Nox4 (Montrer NOX4 Anticorps) RNA.
REDD1 is required for normal insulin (Montrer INS Anticorps)-stimulated signaling, and a subtle balance exists between MEK1 (Montrer MAP2K1 Anticorps)/2, REDD1, and mTOR (Montrer FRAP1 Anticorps)
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.
Redd1 alters dorsoventral patterning by antagonizing the Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) 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