DDIT3 Recombinant Monoclonal Antibody

Code: CSB-RA918842A0HU

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Size:

50μl100μl

US$210

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Species Reactivity: Human

Application: ELISA, FC

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Target Background

Product Details

Uniprot NO.

P35638

Target Names

DDIT3

Alternative Names

DNA damage-inducible transcript 3 protein (DDIT-3) (C/EBP zeta) (C/EBP-homologous protein) (CHOP) (C/EBP-homologous protein 10) (CHOP-10) (CCAAT/enhancer-binding protein homologous protein) (Growth arrest and DNA damage-inducible protein GADD153), DDIT3, CHOP CHOP10 GADD153

Species Reactivity

Human

Immunogen

A synthesized peptide derived from Human DDIT3

Conjugate

Non-conjugated

Clonality

Monoclonal

Isotype

Rabbit IgG

Clone No.

17A10

Purification Method

Affinity-chromatography

Concentration

It differs from different batches. Please contact us to confirm it.

Buffer

Rabbit IgG in 10mM phosphate buffered saline , pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.

Form

Liquid
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.

Scope Application

ELISA Protocol Flow Cytometry (FC) Protocol

Recommended Dilution

Application	Recommended Dilution
FC	1:50-1:200

Storage

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

Lead Time

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.

Usage

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

Datasheet & COA

Antibody FAQs

Images

Overlay Peak curve showing Hela cells stained with CSB-RA918842A0HU (red line) at 1:50. The cells were fixed in 4% formaldehyde and permeated by 0.2% TritonX-100. Then 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (1µg/1*10⁶cells) for 45min at 4℃. The secondary antibody used was FITC-conjugated Goat Anti-rabbit IgG(H+L) at 1:200 dilution for 35min at 4℃.Control antibody (green line) was rabbit IgG (1µg/1*10⁶cells) used under the same conditions. Acquisition of >10,000 events was performed.

Description

DDIT3, also known as CHOP or GADD153, serves as a critical transcription factor in the cellular stress response, particularly during endoplasmic reticulum stress and the unfolded protein response. This protein functions as a key mediator linking metabolic stress to apoptotic pathways, making it an essential marker for researchers investigating cellular adaptation mechanisms, metabolic disorders, and stress-induced cell death. Its role in growth arrest and DNA damage response positions DDIT3 at the intersection of multiple signaling cascades relevant to disease pathology and developmental processes.

This recombinant monoclonal antibody, clone 17A10, offers the consistency and reliability that demanding experimental workflows require. Produced using recombinant technology with a defined sequence, this antibody eliminates the lot-to-lot variability that can compromise longitudinal studies or multi-site collaborations. The rabbit IgG format, raised against a synthetic peptide derived from human DDIT3, provides high specificity for your target while the affinity-chromatography purification ensures minimal background interference.

Validation studies using flow cytometry demonstrate clear detection of DDIT3 in HeLa cells, with recommended dilutions ranging from 1:50 to 1:200. The intracellular staining protocol, employing formaldehyde fixation and Triton X-100 permeabilization, yielded distinct signal separation from isotype control, confirming specific detection of this nuclear transcription factor. This antibody is also validated for ELISA applications, providing flexibility across different experimental platforms.

Researchers studying epigenetics and nuclear signaling, developmental biology, metabolism, or stem cell biology will find this antibody particularly valuable for investigating stress response pathways and their downstream consequences in human cell models.

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Target Background

Function(From Uniprot)

Multifunctional transcription factor in endoplasmic reticulum (ER) stress response. Plays an essential role in the response to a wide variety of cell stresses and induces cell cycle arrest and apoptosis in response to ER stress. Plays a dual role both as an inhibitor of CCAAT/enhancer-binding protein (C/EBP) function and as an activator of other genes. Acts as a dominant-negative regulator of C/EBP-induced transcription: dimerizes with members of the C/EBP family, impairs their association with C/EBP binding sites in the promoter regions, and inhibits the expression of C/EBP regulated genes. Positively regulates the transcription of TRIB3, IL6, IL8, IL23, TNFRSF10B/DR5, PPP1R15A/GADD34, BBC3/PUMA, BCL2L11/BIM and ERO1L. Negatively regulates; expression of BCL2 and MYOD1, ATF4-dependent transcriptional activation of asparagine synthetase (ASNS), CEBPA-dependent transcriptional activation of hepcidin (HAMP) and CEBPB-mediated expression of peroxisome proliferator-activated receptor gamma (PPARG). Together with ATF4, mediates ER-mediated cell death by promoting expression of genes involved in cellular amino acid metabolic processes, mRNA translation and the unfolded protein response (UPR) in response to ER stress. Inhibits the canonical Wnt signaling pathway by binding to TCF7L2/TCF4, impairing its DNA-binding properties and repressing its transcriptional activity. Plays a regulatory role in the inflammatory response through the induction of caspase-11 (CASP4/CASP11) which induces the activation of caspase-1 (CASP1) and both these caspases increase the activation of pro-IL1B to mature IL1B which is involved in the inflammatory response. Acts as a major regulator of postnatal neovascularization through regulation of endothelial nitric oxide synthase (NOS3)-related signaling.

Gene References into Functions

The herein presented data uncover a novel mechanism by which the fusion oncogene FUS-CHOP actively promotes invasion in myxoid and round cell liposarcoma through the activation of a SRC/FAK/RHO/ROCK signaling axis. PMID:29190494
Low expression of CHOP predicts the poor prognosis of advanced gastric cancer patients, and CHOP may be a prognostic biomarker for patients with advanced gastric cancer. PMID:29910063
This study demonstrates increased placental expression of HIF-1alpha and CHOP in preeclampsia compared to normotensive pregnancies which correlate to their increased syncytiotrophoblast microvesicles concentration in maternal circulation. PMID:29127866
CHOP/GADD153-dependent apoptosis reflects expression of micro-RNA, miR-216b. PMID:27173017
These results indicated activation of Unfolded Protein Response (UPR) in different cell types derived from Gaucher disease patients, highlighting the generality of this process in this disease. They also showed that the UPR-regulated CHOP transcription factor induces transcription of the GBA1 gene. PMID:27856178
Study indicates that CHOP deficiency protects against Western diet-induced AoV calcification in Apoe(-/-) mice. CHOP deficiency prevents oxLDL-induced VIC osteoblastic differentiation via preventing VIC-derived ABs releasing. PMID:28891115
activation of the IGF-IR/PI3K/Akt signaling system is a common pattern in MLS which appears to be transcriptionally controlled, at least in part by induction of IGF2 gene transcription in a FUS-DDIT3-dependent manner. PMID:28637688
GRP78 silencing promoted lung epithelial cell apoptosis during hyperoxia, via regulation of the CHOP pathway. PMID:28586043
siRNA silencing of CHOP significantly reduced cyproterone acetate-induced DR5 up-regulation and TRAIL sensitivity in prostate cancer cells. Our study shows a novel effect of cyproterone acetate on apoptosis pathways in prostate cancer cells and raises the possibility that a combination of TRAIL with cyproterone acetate could be a promising strategy for treating castration-resistant prostate cancer PMID:28270124
asthmatic patients exhibited aberrant Chop expression along with endoplasmic reticulum stress PMID:28238747
GPR4 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression. PMID:29089376
Endoplasmic reticulum stress-induced CHOP activation in the brain is a mechanistic link in the palmitate-induced negative regulation of leptin and IGF1. PMID:27555288
CHOP negatively regulates Polo-like kinase 2 expression via recruiting C/EBPalpha to the upstream-promoter in human osteosarcoma cell line during ER stress PMID:28652211
VEGF is an important angiogenic signal required for tissue expansion. We show that VEGFA variation giving allele-specific response to transcription factors with overlapping binding sites associate closely with circulating TSH levels. Because CHOP is induced by several types of intracellular stress, this indicates that cellular stress could be involved in the normal or pathophysiological response of the thyroid to TSH PMID:27627987
GRP78 inhibition enhances ATF4-induced cell death by the deubiquitination and stabilization of CHOP in human osteosarcoma cells. PMID:28947141
a significant protein-protein interaction between GR and CHOP, (GR-CHOP heterocomplex formation) under endoplasmic reticulum stress conditions, is reported. PMID:27496643
These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK, AP-1, and CHOP may interfere with complete autophagy. PMID:28694294
The role of neutrophil elastase in the activation of unfolded protein response effector molecules via PERK and CHOP is reported. PMID:28507169
The PERK-eIF2alpha-ATF4-CHOP signaling pathway has a critical role in tumor progression during endoplasmic reticulum stress. (Review) PMID:27211800
HDL isolated from patients with metabolic syndrome induced macrophage apoptosis, oxidative stress, and CHOP upregulation, which were blocked by PBA and DPI. These data indicate that ox-HDL may activate ER stress-CHOP-induced apoptotic pathway in macrophages via enhanced oxidative stress and that this pathway may be mediated by TLR4. PMID:27895089
We found that 25-epi Ritterostatin GN1N induced cell death in melanoma cells at nanomolar concentrations, and this cell death was characterized by inhibition of GRP78 expression, increased expression of the ER stress marker CHOP, loss of mitochondrial membrane potential, and lipidation of the autophagy marker protein LC3B. PMID:28393217
Western blot analysis of subcutaneously implanted AsPC-1 and BxPC-3 tumors as well as orthotopically implanted Panc-1 tumors demonstrated upregulation of BIP, CHOP, and IRE1alpha expression in the tumor lysates from penfluridol-treated mice as compared to tumors from control mice PMID:28618969
CHOP protects hepatocytes from a diet high in fat, fructose, and cholesterol (HFCD) and its induced ER stress, and has a significant role in the mechanism of liraglutide-mediated protection against non-alcoholic steatohepatitis (NASH) pathogenesis. PMID:27239734
Study showed that Chop is involved in the pathogenesis of pulmonary fibrosis by regulating the generation of M2 macrophages and TGF-beta signaling. PMID:26883801
Downregulation of CHOP by small interfering RNA somewhat restored expression of AR suggesting that AR degradation is dependent on ER stress pathway. Future studies will need to evaluate other aspects of the unfolded protein response pathway to characterize the regulation of AR degradation PMID:27267997
Herein, the authors extend their previous research and provide evidence that ORF57 of human herpesvirus-8 interacts with CHTOP and CIP29, in contrast to POLDIP3. PMID:27189710
NAG-1 expression was transcriptionally upregulated by CHOP, which promoted chemokine production through sustained NF-kappaB activation. PMID:27771295
plasma exposure resulted in expression of unfolded protein response (UPR) proteins such as glucoserelated protein 78 (GRP78), protein kinase R (PKR)like ER kinase (PERK), and inositolrequiring enzyme 1 (IRE1). Elevated expression of spliced Xbox binding protein 1 (XBP1) and CCAAT/enhancerbinding protein homologous protein (CHOP) further confirmed that ROS generatedby NTGP induces apoptosis through the ER stress PMID:27573888
High DDIT3 expression is associated with non-small-cell lung cancer. PMID:27599983
CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5. Moreover, expression of transcription factor C/EBP homologous protein (CHOP) markedly increased in response to CAPE and transient knockdown of CHOP abolished CAPE/TRAIL-mediated apoptosis. PMID:27260301
the C/EBPD binding site is required for RU486-mediated activation of the CHOP promoter. PMID:26174226
Data show CGK733 induced microtubule associated protein LC3B formation upstream of AMP-activated protein kinase and protein kinase RNA-like endoplasmic reticulum kinase/CCAAT-enhancer-binding protein homologous protein pathways and p21 Cip1 expression. PMID:26486079
Data suggest that HOXA-AS2 could be an oncogene for GC partly through suppressing P21, PLK3, and DDIT3 expression. PMID:26384350
FUS-DDIT3 is uniquely regulated at the transcriptional as well as the post-translational level and that its expression level is important for myxoid liposarcoma tumour development. PMID:26865464
CGK733-induced intracellular calcium sequestration in pancreatic tumor cells is correlated with the PERK/CHOP signaling pathway and may also be involved in the dysregulations of calcium-binding proteins. PMID:26259235
Combined administration inhibited the cells most potently and time-dependently, decreased the expression of HO-1, and significantly increased the expression of ATF4, CHOP, and Ire-1 proteins expression levels PMID:26125799
Blockage of PERK signaling expression by siRNA not only significantly reduced the expression of CHOP. PMID:26090483
Up-regulation of CHOP is associated with Pancreatic Neuroendocrine Tumors. PMID:26504039
knockdown of a proton-sensing G protein-coupled receptor GPR4 markedly reduced CHOP expression and endothelial cell apoptosis after hypoxia exposure. PMID:25343248
These data show that altered/impaired expression of mtDNA induces CHOP-10 expression in a signaling pathway that depends on the eIF2alpha/ATF4 axis of the integrated stress response rather than on the mitochondrial unfolded protein response. PMID:25643991
In a GRP78-positive breast cancer subset, CHOP overexpression correlated with a lower risk of recurrence. PMID:24781973
Letter/Case Report: DDIT3 gene amplification in primary gallbladder myxoid liposarcoma. PMID:25532011
Data indicate that Tanshinone IIA (Tan-IIA)T upregulated the protein expression of CHOP and Bax, but downregulated the protein expression of BiP, TCTP, Mcl-1 and Bcl-xL. PMID:25270224
DDIT3 and KAT2A cooperatively up-regulate TNFRSF10A and TNFRSF10B. PMID:25770212
CHOP is critical for mediating ASPP2-induced autophagic apoptosis by decreasing Bcl-2 expression and maintaining nuclear ASPP2-Bcl-2 complexes. PMID:25032846
This study reveals novel molecular events underlying the regulation of DDIT3 protein homeostasis and provides insight in understanding the relationship between SPOP mutations and ER stress dysregulation in prostate cancer. PMID:24990631
Data suggest that expression of CHOP (c/EBP-homologous protein) and ERO1alpha (oxidoreductin-1-L-alpha) is up-regulated in liver of patients with acute liver failure. PMID:25387528
TLR7 played an important role in macrophage apoptosis and cytokine secretion through the CHOP-dependent pathway. PMID:24994112
a role for CHOP as a positive regulator of carcinogen-induced HCC progression PMID:24339898
crucial role in pathogenesis of chronic kidney disease-dependent vascular calcification PMID:24963104