DDIT3/CHOP Antibody - #AF5280

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Product: DDIT3/CHOP Antibody
Catalog: AF5280
Description: Rabbit polyclonal antibody to DDIT3/CHOP
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog
Mol.Wt.: 19~30kD; 19kD(Calculated).
Uniprot: P35638
RRID: AB_2837766

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 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(90%), Dog(100%)
Clonality:
Polyclonal
Specificity:
DDIT3 Antibody detects endogenous levels of total DDIT3.
RRID:
AB_2837766
Cite Format: Affinity Biosciences Cat# AF5280, RRID:AB_2837766.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

C/EBP homologous protein; C/EBP Homology Protein; C/EBP zeta; C/EBP-homologous protein 10; C/EBP-homologous protein; CCAAT/enhancer binding protein homologous protein; CEBPZ; CHOP 10; CHOP; CHOP-10; CHOP10; DDIT 3; DDIT-3; Ddit3; DDIT3_HUMAN; DNA Damage Inducible Transcript 3; DNA damage-inducible transcript 3 protein; GADD 153; GADD153; Growth Arrest and DNA Damage Inducible Protein 153; Growth arrest and DNA damage inducible protein GADD153; Growth arrest and DNA damage-inducible protein GADD153; MGC4154;

Immunogens

Immunogen:
Uniprot:

P35638(DDIT3_HUMAN) >>Visit HPA database.

Gene(ID):
DDIT3(1649)
Description:
Inhibits the DNA-binding activity of C/EBP and LAP by forming heterodimers that cannot bind DNA.
Sequence:
MAAESLPFSFGTLSSWELEAWYEDLQEVLSSDENGGTYVSPPGNEEEESKIFTTLDPASLAWLTEEEPEPAEVTSTSQSPHSPDSSQSSLAQEEEEEDQGRTRKRKQSGHSPARAGKQRMKEKEQENERKVAQLAEENERLKQEIERLTREVEATRRALIDRMVNLHQA

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Rabbit
90
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P35638 As Substrate

Site PTM Type Enzyme
S14 Phosphorylation P68400 (CSNK2A1)
S15 Phosphorylation P68400 (CSNK2A1)
S30 Phosphorylation P68400 (CSNK2A1)
S31 Phosphorylation P68400 (CSNK2A1)
S49 Phosphorylation
T54 Phosphorylation
T64 Phosphorylation
S79 Phosphorylation Q16539 (MAPK14)
S82 Phosphorylation Q16539 (MAPK14)

Research Backgrounds

Function:

Multifunctional transcription factor in 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). 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.

PTMs:

Ubiquitinated, leading to its degradation by the proteasome.

Phosphorylation at serine residues by MAPK14 enhances its transcriptional activation activity while phosphorylation at serine residues by CK2 inhibits its transcriptional activation activity.

Subcellular Location:

Cytoplasm. Nucleus.
Note: Present in the cytoplasm under non-stressed conditions and ER stress leads to its nuclear accumulation.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

Heterodimer. Interacts with TCF7L2/TCF4, EP300/P300, HDAC1, HDAC5 and HDAC6. Interacts with TRIB3 which blocks its association with EP300/P300. Interacts with FOXO3, CEBPB and ATF4. Interacts with isoform AltDDIT3 of DDIT3.

Family&Domains:

The N-terminal region is necessary for its proteasomal degradation, transcriptional activity and interaction with EP300/P300.

Belongs to the bZIP family.

Research Fields

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Genetic Information Processing > Folding, sorting and degradation > Protein processing in endoplasmic reticulum.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

References

1). Ghrelin ameliorates acute lung injury induced by oleic acid via inhibition of endoplasmic reticulum stress. LIFE SCIENCES, 2018 (PubMed: 28751159) [IF=6.1]

Application: WB    Species: rat    Sample:

2). Lactobacillus acidophilus NX2-6 Improved High-Fat Diet-Induced Glucose Metabolism Disorder Independent of Promotion of Insulin Secretion in Mice. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2021 (PubMed: 34788040) [IF=6.1]
3). Peroxisome Proliferator-Activated Receptor-Gamma Reduces ER Stress and Inflammation via Targeting NGBR Expression. Frontiers in Pharmacology, 2022 (PubMed: 35111067) [IF=5.6]

Application: WB    Species: Human    Sample: HUVEC cells

FIGURE 6 PPARγ reduces tunicamycin-induced ER stress by regulating NGBR. (A–C) HUVEC cells in a six-well plate were transfected with control siRNA (NC siRNA) or NGBR siRNA for 24 h in serum-free medium, followed by switching the cells into complete medium to culture for another 24 h. After treatment with rosiglitazone (10 μM) for 12 h, the cells were treated with tunicamycin (0.5 μg/ml) with or without rosiglitazone for another 12 h. Expression of CHOP, BIP, NGBR p-PERK, p-IRE1α and c-ATF6 protein was determined by Western blot (A, B). Expression of CHOP, BIP and NGBR mRNA was determined by qPCR (C). Values were expressed as means ± SD. *p < 0.05; **p < 0.01; ns, not significant (n = 3). (D) liver total proteins were collected from Figure 4. Expression of BIP and CHOP in mouse liver was determined by Western blot. Values were expressed as means ± SD. *p < 0.05; **p < 0.01; ns, not significant (n = 3).
4). CTRP1 attenuates cerebral ischemia/reperfusion injury via the PERK signaling pathway. Frontiers in Cell and Developmental Biology, 2021 (PubMed: 34422821) [IF=5.5]

Application: WB    Species: Rat    Sample: cortex

FIGURE 4 CTRP1 protected against cerebral ischemia reperfusion injury via alleviating neuron injury and apoptosis. (A) Neuron injury was analyzed by double labeling immunofluorescence staining. n = 3 per group. The representative images were acquired under × 400 magnification, scale bars = 50 μm. (B) Apoptosis in the cortex was analyzed by TUNEL, n = 3 per group. The representative images were acquired under × 200 magnification, scale bars = 100 μm. (C) Western blot analyzed the expression of CTRP1, BAX, Bcl-2, and CHOP in cortex. n = 4 per group. ****p < 0.0001, ***p < 0.01, **p < 0.01, *p < 0.05 vs. sham group; ####p < 0.0001, ##p < 0.01, #p < 0.05 vs. MCAO/R + LV-NC group.
5). PTH 1-34 reduced apoptosis of MLO-Y4 osteocyte-like cells by activating autophagy and inhibiting ER stress under RPM conditions. European journal of pharmacology, 2024 (PubMed: 38316249) [IF=5.0]
6). Iron overload induces apoptosis of osteoblast cells via eliciting ER stress-mediated mitochondrial dysfunction and p-eIF2α/ATF4/CHOP pathway in vitro. CELLULAR SIGNALLING, 2021 (PubMed: 33901579) [IF=4.8]

Application: WB    Species: Mice    Sample: MC3T3-E1 osteoblast cells

Fig. 5. Iron overload activated ER stress-mediated apoptosis pathway. (a) and (b) protein expression levels of Bip, ATF4 and CHOP and the phosphorylation level of eIF2α in MC3T3-E1 osteoblast cells treated by indicated concentrations of FAC for 48 h. The data were presented as mean ± SEM, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001 vs. control group. (c) Immunofluorescence analysis of CRT in MC3T3-E1 osteoblast cells using the anti-calreticulin antibody. Cytolemma were counterstained with Dil and nuclei were counterstained with DAPI. (d) Protein expression levels of CRT in MC3T3-E1 osteoblast cells treated by indicated concentrations of FAC for 48 h. The data were presented as mean ± SEM, n = 3. **p < 0.05, **p < 0.01, ***p < 0.001vs. control group.
7). Anti-polycystic ovary syndrome effect of electroacupuncture: IMD inhibits ER stress-mediated apoptosis and autophagy in granulosa cells. Biochemical and Biophysical Research Communications, 2022 (PubMed: 36244114) [IF=3.1]
8). Regulation of endoplasmic reticulum stress on autophagy and apoptosis of nucleus pulposus cells in intervertebral disc degeneration and its related mechanisms. PeerJ, 2024 (PubMed: 38666076) [IF=2.7]

Application: WB    Species: Human    Sample:

Figure 3 The expressions of ERS-, apoptosis- and autophagy-related proteins. (A) Apoptosis- (B) and autophagy-related proteins (C) The quantitative values are expressed as mean ± SD from at least three independent experiments, *p < 0.05, **p < 0.01, ***p < 0.001.
9). Targeting the Ferroptosis and Endoplasmic Reticulum Stress Signaling Pathways by CBX7 in Myocardial Ischemia/reperfusion Injury. Cell biochemistry and biophysics, 2024 (PubMed: 38809351) [IF=2.6]
10). Hydrogen sulfide alleviates ischemia induced liver injury by repressing the SPHK1/S1P pathway. Annals of Translational Medicine, 2023 (PubMed: 36819566)

Application: IF/ICC    Species: Rat    Sample: BRL-3A cells

Figure 1 NaHS decreases endoplasmic reticulum stress and hepatic cell viability under hypoxic conditions. (A) MTT analysis of BRL-3A cell viability after sham, hypoxia, and NaHS treatment. (B) Hoechst staining analysis of BRL-3A cells after sham, hypoxia, and NaHS treatment (magnification, ×200). (C) Left: representative Western blot analysis of the protein expression of CHOP, SPHK1, and S1P. Right: corresponding quantification of the band densities of CHOP, SPHK1, and S1P. (D) Immunofluorescence analysis of CHOP and SPHK1 levels in BRL-3A cells after sham, hypoxia, and NaHS treatment (magnification, ×400). **, P

Application: WB    Species: Rat    Sample: BRL-3A cells

Figure 1 NaHS decreases endoplasmic reticulum stress and hepatic cell viability under hypoxic conditions. (A) MTT analysis of BRL-3A cell viability after sham, hypoxia, and NaHS treatment. (B) Hoechst staining analysis of BRL-3A cells after sham, hypoxia, and NaHS treatment (magnification, ×200). (C) Left: representative Western blot analysis of the protein expression of CHOP, SPHK1, and S1P. Right: corresponding quantification of the band densities of CHOP, SPHK1, and S1P. (D) Immunofluorescence analysis of CHOP and SPHK1 levels in BRL-3A cells after sham, hypoxia, and NaHS treatment (magnification, ×400). **, P

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