Browse our anti-DDIT4 (DDIT4) Antibodies

Human DNA-Damage-Inducible Transcript 4 (DDIT4) interaction partners

1. these findings uncover a novel mechanism by which PML (show PML Antibodies) loss may contribute to mTOR (show FRAP1 Antibodies) activation and cancer progression via dysregulation of basal DDIT4 gene expression.

2. 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.

3. This is concurrent with an increase in the expression level of DDIT4, which is an inhibitor of the mammalian target of rapamycin (mTOR (show FRAP1 Antibodies)) 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

4. DDIT4 activity is directly linked to regulation of mTOR (show FRAP1 Antibodies) signalling

5. 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.

6. REDD1 is overexpressed during Familial Mediterranean fever (show MEFV Antibodies) inflammatory attacks induced by physical or psychological stress

7. 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.

8. 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.

9. 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]

10. 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.

Mouse (Murine) DNA-Damage-Inducible Transcript 4 (DDIT4) interaction partners

1. RTP801 plays a essential role in the progression of restraint stress induced neurodegenerative disease.

2. Findings suggest that REDD1 in cacna1c (show CACNA1C Antibodies) heterozygous mice may influence depression-related behavior via regulation of the FoxO3a (show FOXO3 Antibodies) pathway. Study identified the prefrontal cortex as a key brain region in which cacna1c (show CACNA1C Antibodies) mechanisms through previously unidentified, novel molecular pathways contribute to depression-related behavior.

3. 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.

4. these data show that REDD1 induction regulates the exercise-mediated change in a distinct set of genes within skeletal muscle.

5. 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.

6. These data suggest that loss of REDD1 augments the rate of the OV-induced increase in muscle mass by altering multiple protein balance pathways.

7. 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.

8. 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)

9. 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.

10. 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.

Zebrafish DNA-Damage-Inducible Transcript 4 (DDIT4) interaction partners

1. Redd1 alters dorsoventral patterning by antagonizing the Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling pathway.