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Facts about DDIT3 upstream open reading frame protein.
Acts as a dominant-negative regulator of C/EBP-induced transcription: dimerizes with members of their C/EBP family, impairs their affiliation 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.
Human | |
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Gene Name: | DDIT3 |
Uniprot: | P0DPQ6 |
Entrez: | 1649 |
Belongs to: |
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No superfamily |
C/EBP-homologous protein 10; C/EBP-homologous protein; CCAAT/enhancer-binding protein homologous protein; CEBP zeta; CHOP; CHOP10 CEBPZ; CHOP10; CHOP-10; CHOPC/EBP zeta; DDIT3; DDIT-3; DNA damage-inducible transcript 3 protein; DNA-damage-inducible transcript 3; GADD153; Growth arrest and DNA damage-inducible protein GADD153
Mass (kDA):
4.284 kDA
Human | |
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Location: | 12q13.3 |
Sequence: | 12; NC_000012.12 (57516588..57520517, complement) |
Nucleus. Cytoplasm.
Boster scientists now have the option to submit their research results for species as well as special samples and applications. They can also request product credits. Every scientist, all over the world are able to benefit from these results. The Boster bio: The Best Uses of The DDIT3Marker can be used in a variety of ways for biologists. Here are a few of them:
The DDIT3 marker is a key component of the apoptosis process. The NDRG4 protein is responsible for the expression of DDIT3. The tumor-suppressive capability of NDRG4 is linked to ER stress. Zhang et. al. found that patients suffering from advanced gastric cancer had a poor prognosis if DDIT3 expression was low. Therefore, a low DDIT3 level might serve as a prognostic indicator. This study has demonstrated that NDRG4 is a key player in regulating DDIT3 expression in gastric cancer.
As seen in overexpressing NDRG4 SW480 cells, NDRG4 enhanced the sensitivity of CRC cells to 5-FU. These findings suggest that NDRG4 could contribute to the increase in DDIT3 expression in CRC cells. Further research is required to determine if the overexpression of NDRG4 can increase DDIT3 expression. This study was supported by the National Natural Science Foundation of China (grant no. 82072655). The data used in this study are available from the author upon reasonable request.
Incredibly enough, administration of FUS-DDIT3 resulted in significantly higher expressions of DDIT3 in this study. Additionally, DDIT3 was upregulated in more than 54% of instances where FUS-DDIT3 was utilized as a positive control. These findings are also crucial for understanding the molecular signaling pathway that control neurodegeneration in various types of neurons.
We have developed new biomarkers that detect DDIT3 and other genes associated with diabetes which is a common affliction of type 2 diabetes. These new biomarkers include HSPA5, DDIT3 and DNAJC3. We also tested BCL2-associated proteinX expression and insulin. The primary antibodies were visualized using EnVision+System HRP DAB (Dako). Islet immunostaining was graded as moderate or low.
DDIT3 is a nuclear cytoplasmic protein that is found in nearly every tissue. It is found in neutrophils, which form the immune system. It is frequently fusioned to the genes FUS or EWSR1 on chromosomes 16, 22, and 24. Mutations in this protein have been linked to fat-liver disease, as well as many skin diseases. St John's Laboratory offers trial-sized antibodies against DDIT3 in small amounts.
The results of the study suggest that the production of DDIT3 protein is increased by palmitate as well as Oleate, in a timing-dependent manner. It is involved in cell metabolism and ageing. However, it also interacts with other proteins such as TCF7L2/TCF and EP300/P300.
In a ongoing research, the use of immunostaining to determine the expression of the DDIT3 gene in thyroid tumors was carried out on 30 cases that were in-house. We identified tumor cells that expressed the DDIT3 gene, FAM129A and ARG2 with a monoclonal antibody to DDIT3. All three tumor types showed positive staining using anti-ARG2, anti -STT3A and anti FAM129A antibodies, however only in a minority of cases. Additionally, we identified follicular adenomas with an antibody that is polyclonal to FAM129A.
The pGEX VAMP7 plasmid was deposited by the Jeremy Luban Lab at Addgene, a non-profit repository for plasmids. This plasmid allows researchers to make use of it for research. Jeremy Luban thanks Thierry Galli for supplying the plasmid. The materials deposited by Jeremy Luban Lab can be accessed through Addgene
This study demonstrated that pGEX's Grb2 SH2-Sh3 could be an effective inhibitor of the growth of tumors. Grb2 is involved in embryonic stem cell fate as well as proliferation and normal development. It functions in close reliance on Sos1. Noonan syndrome and cancer are caused by an abnormal the phosphorylation Grb2 in tumor cells. Grb2 is targeted by anti-cancer strategies which block the interaction between Grb2 and Sos1.
We evaluated the Grb2SH2-SH3 protein with AblW99R, which is a mutant that lacks specific binding to proline-rich sequences. This was done in the first study. As as a positive control, we utilized pGEX Grb2SH2-SH3 the same manner. Grb2 SH3C was bound to HPK1's P2 site during this study. The results support our hypothesis that the SH3-N domain is bound to the P2 site.
Changes in Grb2 SH2-SH3 domain reduced CD28 binding. The Sh2-Sh3 interaction between Grb2 and CD28 was inhibited when the PXXPXR receptor site was damaged. Additionally, the impact of pGEX Grb2 SH2-SH3 on CD28 expression was observed in the Gln193 mutant.
The carboxyl-truncated hSos1 mutant contains the two first copies of Grb2-BM and is not different from the full-length protein. The myristoylated carboxyl truncated HeSos1 is not different from HeLa cells. Additionally, hSos1 carboxyl mutants lack the p90 RSK-2 phosphorylation sites and show no difference when compared to pGEX Grb2-SH3 as a positive control.
The DDIT3 marker is a fusion of two cDNAs. It is highly expressed and requires factorXa cleavage order to express. The DDIT3 marker can be expressed in many cell types. This plasmid can be located on the EcoliWiki. You can help by writing about the history of the plasmid and managing it with Help:References.
A DDIT3 marker is a biomarker used to identify the gene that encodes the cell cycle protein PIK3CA. The gene encodes the homologous C/EBP protein. A variety of strategies have been devised to target this gene in various cancers. One strategy is the inhibition of PERK, which has been shown to phosphorylate eIF2a.
PMID: 29083303 by Samandi S., et al. Deep transcriptome annotation enables the discovery and functional characterization of cryptic small proteins.
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