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Новая страница: «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...»

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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) [CHOP] [CHOP10] [GADD153]

==Publications==

{{medline-entry
|title=Inhibition of glioma growth by flavokawain B is mediated through endoplasmic reticulum stress induced autophagy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30025493
|abstract=Flavokawain B (FKB), a natural kava chalcone, displays potent antitumor activity in various types of cancer. The mechanism of action, however, remains unclear. Here, we evaluated the efficacy of FKB in the treatment of human glioblastoma multiforme (GBM) as well as the molecular basis for its inhibitory effects in cancer. Approximately 60% of GBM cells became senescent after treatment with FKB as assessed in the senescence-associated (SA)-GLB1/SA-β-galactosidase assay. The cellular process of autophagy potentially contributed to the establishment of senescence. Transmission electron microscopy revealed the formation of autophagic vesicles under FKB treatment, and [[MAP1LC3B]] (microtubule associated protein 1 light chain 3 beta)-II was increased. Transfection of [[ATG5]] or [[ATG7]] small interfering RNAs (siRNAs) inhibited FKB-induced autophagy in U251 cells. Western blot revealed that molecular components of the endoplasmic reticulum stress pathway were activated, including [[ATF4]] (activating transcription factor 4) and [[[[DDIT3]]]] (DNA damage inducible transcript 3), while levels of [[TRIB3]] (tribbles pseudokinase 3) increased. In addition, based on the phosphorylation status, the AKT-[[MTOR]]-[[RPS6KB1]] pathway was inhibited, which induced autophagy in GBM cells. Inhibition of autophagy by autophagy inhibitors 3-methyladenine and chloroquine or knockdown of [[ATG5]] or [[ATG7]] caused FKB-treated U251 cells to switch from senescence to apoptosis. Finally, knockdown of [[ATG5]] or treatment with chloroquine in combination with FKB, significantly inhibited tumor growth in vivo. Our results demonstrated that FKB induced protective autophagy through the [[ATF4]]-[[[[DDIT3]]]]-[[TRIB3]]-AKT-[[MTOR]]-[[RPS6KB1]] signaling pathway in GBM cells, indicating that the combination treatment of FKB with autophagy inhibitors may potentially be an effective therapeutic strategy for GBM. 3-MA: 3-methyladenine; 4-PBA: 4-phenylbutyrate; AKT: AKT serine/threonine kinase; [[ATF4]]: activating transcription factor 4; ATG: autophagy related; CASP3: caspase 3; [[CCK]]-8: cell counting kit-8; CDKN1A: cyclin-dependent kinase inhibitor 1A; CQ: chloroquine; [[[[DDIT3]]]]: DNA damage inducible transcript 3; DMEM: Dulbecco's modified Eagle's medium; EIF2A: eukaryotic translation initiation factor 2A; EIF2AK3: eukaryotic translation initiation factor 2 alpha kinase 3; ER: endoplasmic reticulum; FKB: flavokawain B; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GBM: glioblastoma multiforme; GFP: green fluorescent protein; HSPA5: heat shock protein family A (Hsp70) member 5; [[MAP1LC3B]]: microtubule associated protein 1 light chain 3 beta; [[MTOR]]: mechanistic target of rapamycin kinase; PARP1: poly(ADP-ribose) polymerase; 1[[RPS6KB1]]: ribosomal protein S6 kinase B1; SA-GLB1: senescence-associated galactosidase beta 1; siRNA: short interfering RNA; SQSTM1: sequestosome 1; TEM: transmission electron microscopy; [[TRIB3]]: tribbles pseudokinase 3; TUNEL: deoxynucleotidyl transferase-mediated dUTP nick-end labeling.
|mesh-terms=* Animals
* Antineoplastic Agents, Phytogenic
* Autophagy
* Autophagy-Related Protein 5
* Autophagy-Related Protein 7
* Cell Proliferation
* Cells, Cultured
* Endoplasmic Reticulum Stress
* Flavonoids
* Gene Expression Regulation, Neoplastic
* Glioma
* Humans
* Male
* Mice
* Mice, Nude
* Xenograft Model Antitumor Assays
|keywords=* Apoptosis
* ER stress
* autophagy
* flavokawain B
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6152528
}}
{{medline-entry
|title=Transcriptomic biomarkers of the response of hospitalized geriatric patients admitted with heart failure. Comparison to hospitalized geriatric patients with infectious diseases or hip fracture.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/21335025
|abstract=The abundance of a preselection of transcripts involved in inflammation, immunosenescence and stress response was compared between PBMC of healthy aged donors and aged patients in acute phase of heart failure and at recovery. This study identified 22 transcripts differentially abundant in acute phase of heart failure versus healthy aged subjects. Transcripts involved in inflammation and oxidative stress were more abundant. Those associated with T-cell functions were less abundant. The results were compared to two other major acute geriatric issues: infectious diseases and hip fracture. In acute phase, compared to healthy aged subjects, the abundance of 15/22 transcripts was also altered in both geriatric infectious diseases and hip fracture. Many variations had not vanished at the recovery phase. The abundance of [[CD28]], [[CD69]], [[LCK]], [[HMOX1]], [[TNFRSF1A]] transcripts, known to be altered in healthy aged versus healthy young subjects, was further affected in acute phase of the three geriatric diseases considered. The transcript levels of [[BCL2]], [[CASP8]], [[CCL5]], [[[[DDIT3]]]], [[EGR3]], [[IL10RB]], [[IL1R2]], [[SERPINB2]] and [[TIMP1]] were affected in all three pathological conditions compared to healthy aged, but not versus healthy young subjects. In conclusion, this work provides critical targets for therapeutic research on geriatric heart failure, infectious diseases and hip fracture.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Biomarkers
* Communicable Diseases
* Female
* Heart Failure
* Hip Fractures
* Hospitalization
* Humans
* Male
* Neutrophils
* Transcription, Genetic

|full-text-url=https://sci-hub.do/10.1016/j.mad.2011.02.002
}}

DDIT3 - История изменений

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