|
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 DDIT3(NM_001195056.1) Search again
Product ID:
HQP062710
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AltDDIT3, C/EBPzeta, CEBPZ, CHOP, CHOP-10, CHOP10, GADD153
Gene Description:
DNA damage inducible transcript 3
Target Gene Accession:
NM_001195056.1(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:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Gene References into function
- Nitric oxide-induced apoptosis in RAW 264.7 macrophages is mediated by endoplasmic reticulum stress pathway involving ATF6 and CHOP
- Activation of peroxisome proliferator-activated receptor-gamma stimulates the growth arrest and DNA-damage inducible 153 gene in non-small cell lung carcinoma cells
- expression mediated by AP-1 and C-EBP is involved in deoxycholic acid-induced apoptosis
- HRG stimulation of mammary epithelial cells induces the expression of GADD153 mRNA and protein and transcription of GADD153 promoter.
- Genomic sequences necessary for transcriptional activation by amino acid deprivation of mammalian cells. chop expression is associated with cell stress and apoptosis.
- These results suggest that GADD153 overexpression induced by N-(4-hydroxyphenyl)retinamide(4HPR) may contribute to the anticancer effects (induction of apoptosis and growth arrest) of 4HPR on cancer cells.
- GADD 153 may play an important role in melanoma progression
- This nuclear transcription factor triggers down-regulation of TFF expression in human stomach neoplasm cells cultivated in vitro.
- CHOP (C/EBPzeta)is constitutively multiubiquitinated & degraded by the proteasome. Ubiquitination and degradation are suppressed by forming dimers through the leucine zipper domains.
- CHOP up-regulates IL-6 transcription by trapping negative regulating NF-IL6 isoform.
- CK2-mediated phosphorylation of CHOP inhibits its transcriptional activity
- Transferrin and other target genes identified may play a functional role in the downstream pathway of GADD153.
- CHOP expression induction by amino acid limitation requires both ATF4 expression and ATF2 phosphorylation
- These findings suggest that phenethylisothiocyanate creates an oxidative cellular environment that induces DNA damage and GADD153, 34 and 45 gene activation, which in turn helps trigger apoptosis
- Oil A induces apoptosis of pancreatic cancer cells via activating caspase cascade, modifying cell cycle progress and changing cell cycle-regulating proteins and GADD expression.
- One of the components of the Endoplasmic reticulum stress-mediated apoptosis pathway is C/EBP homologous protein (CHOP), also known as growth arrest- and DNA damage-inducible gene 153 (GADD153).
- AP1 and CHOP are induced by MEKK3 and have roles in TRAF7-related apoptosis
- Depriving cells of iron increased mRNA expression of GADD153 at the level of transcription rather than mRNA stability; neither reactive oxygen species nor DNA damage was involved in triggering GADD153 gene activation
- GADD153 protein was detected before the appearance of apoptotic features in colon cancer cells, which raises the possibility that GADD153 protein might be important for curcumin-induced apoptosis.
- CRP induced an increase of GADD153 mRNA expression. CRP regulation of GADD153 in VSMCs occurs at the posttranscriptional level by mRNA stabilization. GADD153 colocalized to apoptotic VSMCs in coronary lesions, supporting a role in CRP-induced cell death.
- data suggest that different FUS/CHOP variants cause transformation of mesenchymal cells via the same pathways with comparable efficacy
- Retinoic acid signaling in granulocytic differentiation involves regulated expression of CHOP and C/EBPepsilon in a coordinated fashion.
- deoxycholate-induced upregulation of GADD153 mRNA expression occurred at the level of transcription without involving reactive oxygen species and MAPK signaling
- Results indicate that PKC, especially PKCdelta, plays an important role in the induction of GADD153 mRNA following oxidative stress.
- Prostaglandin E2 induces interleukin-8 gene transcription by activating C/EBP homologous protein in human T lymphocytes
- Effect of FUS-DDIT3 fusion on IL6 expression is C/EBP beta dependent in myxoid lipoxarcoma.
- oncogenic Ras-mediated cellular transformation also involves downmodulation of important molecules such as Gadd153 that negatively regulate cell growth and survival
- data provide the first evidence that the posttranscriptional expression of the Gadd153 gene can be regulated by ROS produced by All-trans-N-(4-hydroxyphenyl)retinamide
- insufficient dosage of C/EBPzeta might be involved in the development of leukemia
- CHOP participates in adaptive responses of the epidermis following UVB/UVA exposure in vivo
- Upregulation of GADD153 is a key requirement for cancer prevention in combination with EGCG.
- The fusion oncogene FUS-DDIT3 and the normal DDIT3 induce a liposarcoma phenotype when expressed in a primitive sarcoma cell line.
- hypoglycaemia-induced necrotic cell death of neuroblastoma cells is an active process mediated via the induction of the transcription factor CHOP
- Findings suggest that a regulatory thiol redox-sensitive signaling cascade exists in the molecular pathway leading to induction of GADD153 expression by curcumin.
- DR5/TRAIL-R2 expression is upregulated by fenretinide via the induction of the transcription factor CHOP
- results suggest that the presence of MELAS and NARP mtDNA mutations elicits upregulation of CHOP and ASNS genes through the elevation of ATF4 expression and its binding to the amino acid regulatory element and nutrient-sensing response element-1
- FUS-DDIT3 is a chimeric oncogene generated by the most common chromosomal translocation t(12;16)(q13;p11) associated to liposarcomas.
- A switch between C/enhancer-binding protein (CEBP) zeta and CEBP beta operates at the CEBP site on the C-reactive protein (CRP)promoter to regulate CRP transcription.
- GADD153 (CHOP) and Bcl-2-binding component 3 (PUMA) and apoptosis are induced by 4-hydroxybenzylretinone in a process that is caspase- dependent and independent of the retinoic acid receptor
- Results identify in Italians a suggestive linkage of early-onset type 2 diabetes (T2D) to chromosome 12q15, in the region of the CHOP gene, but no link to C/EBPbeta.
- A single tumor carrying a t(12;22) translocation expressed a hitherto unknown EWSR1-DDIT3 fusion transcript (13-3) linking the complete RNA-binding domain of EWSR1 with a short piece of the 5'-UTR
- GADD153 plays a role in asoprisnil-induced apoptosis.
- expression of WNV nonstructural proteins alone was sufficient to induce CHOP expression
- PGE-2 stimulates IL-8 production through the CHOP transcription factor in cystic fibrosis cells
- the N-terminal portion of CHOP plays a crucial role in its functional regulation and enable us to identify a novel function of TRB3 as an intracellular antagonist of the p300-binding domain of CHOP.
- Celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 expression via GADD153/CHOP
- tert-butyl hydroperoxide (tBH)increases oxidative stress, increases accumulation of ROS in the ER, and upregulates expression of GRP-78 and GADD153.
- oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP
- CHOP transcription by JDP2 following amino acid starvation was investigated.
- Data report a novel mechanistic role of CHOP in the inhibition of Wnt/TCF signaling and stimulation of c-Jun and sucrase-isomaltase reporter activity in intestinal colon cancer cells.
- These results suggest that Stx2-induced apoptosis is mediated by CHOP in human brain microvascular endothelial cells (HBMEC) and involves activation of both the intrinsic and extrinsic pathways of apoptosis.
- CHOP-dependent DR5 up-regulation is a key event mediating SHetA2-induced apoptosis.
- Cnclude that the CHOP T/C and C/T haplotype contributes to our diabetes mellitus type 2 linkage signal on chromosome 12q13.1.
- the increased expression of CHOP in response to PGE(2) exerts a positive transcriptional regulation of the IL-8 promoter mediated by direct binding to a novel consensus site