|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for DDIT4(NM_019058.3) Search again
Product ID:
HQP013557
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
Dig2, REDD-1, REDD1
Gene Description:
DNA damage inducible transcript 4
Target Gene Accession:
NM_019058.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- RTP801 might play important roles in Abeta toxicity and the pathogenesis of Alzheimer's disease
- co-transfection with antisense Sp1 oligonucleotide suggests that hypoxia induction of the RTP801 promoter is mediated by Sp1
- REDD1 (RTP801) can act as a transcriptional downstream target of PI 3-kinase signaling in human prostate cancer cells.
- RTP801 and RTP801L work downstream of AKT and upstream of TSC2 to inhibit mTOR functions
- REDD1 as a critical transducer of the cellular response to energy depletion through the TSC-mTOR pathway.
- Stress response gene REDD1 is identified in this review as an essential regulator of checkpoint kinase mTOR activity through the tuberous sclerosis tumor suppressors TSC1/2 complex.
- The elevation of RTP801 we detect in PD substantia nigral neurons may mediate their degeneration.
- These results demonstrate that hypoxic condition-and high cell density-induced expression of Redd1 is mediated by coactivation of Sp1 and HIF-1alpha downstream of the PI3K/Akt signaling pathway.
- unique effect of inhibition of fatty-acid synthase results from negative regulation of the mTOR pathway via DDIT4
- results suggest a novel mechanism by which AMPK activation after hypoxia-induced energy stress may be crucial in regulating REDD1 expression to control the mTOR pathway in head and neck squamous cell carcinoma
- The results suggest that REDD1 expression is upregulated during ER stress through a mechanism involving activation of PERK, phosphorylation of eIF2alpha, and increased ATF4 expression.
