+ |
CSNK2A1 | down-regulates activity
phosphorylation
|
DDIT3 |
0.35 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250850 |
Ser14 |
PFSFGTLsSWELEAW |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
12876286 |
CHOP transcription factor phosphorylation by casein kinase 2 inhibits transcriptional activation. | The serine to alanine substituted site CHOP mutant was not phosphorylated by CK2, indicating that serines 14–15 and 30–31 of CHOP are the CK2 phosphoacceptor sites |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250851 |
Ser15 |
FSFGTLSsWELEAWY |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
12876286 |
CHOP transcription factor phosphorylation by casein kinase 2 inhibits transcriptional activation. | The serine to alanine substituted site CHOP mutant was not phosphorylated by CK2, indicating that serines 14–15 and 30–31 of CHOP are the CK2 phosphoacceptor sites |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250852 |
Ser30 |
EDLQEVLsSDENGGT |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
12876286 |
CHOP transcription factor phosphorylation by casein kinase 2 inhibits transcriptional activation. | The serine to alanine substituted site CHOP mutant was not phosphorylated by CK2, indicating that serines 14–15 and 30–31 of CHOP are the CK2 phosphoacceptor sites |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250853 |
Ser31 |
DLQEVLSsDENGGTY |
Homo sapiens |
HeLa Cell |
pmid |
sentence |
12876286 |
CHOP transcription factor phosphorylation by casein kinase 2 inhibits transcriptional activation. | The serine to alanine substituted site CHOP mutant was not phosphorylated by CK2, indicating that serines 14–15 and 30–31 of CHOP are the CK2 phosphoacceptor sites |
|
Publications: |
4 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network |
+ |
PRKAA1 | down-regulates activity
phosphorylation
|
DDIT3 |
0.268 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-259864 |
Ser30 |
EDLQEVLsSDENGGT |
Mus musculus |
|
pmid |
sentence |
27650555 |
Here, we report that phosphorylation of CHOP at Ser30 by AMPKα1 triggers CHOP degradation resulting in reduced macrophage apoptosis and subsequent ameliorated plaque vulnerability in vivo. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
MAPK14 | up-regulates activity
phosphorylation
|
DDIT3 |
0.593 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-42200 |
Ser79 |
EVTSTSQsPHSPDSS |
Homo sapiens |
|
pmid |
sentence |
8650547 |
...undergoes inducible phosphorylation on two adjacent serine residues (78 and 81). In vitro, chop is phosphorylated on these residues by p38 mitogen-activated protein kinase (map kinase). phosphorylation of chop on these residues enhanced its ability to function as a transcriptional activator. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250096 |
Ser82 |
STSQSPHsPDSSQSS |
in vitro |
|
pmid |
sentence |
8650547 |
CHOP, a member of the C/EBP family of transcription factors, mediates effects of cellular stress on growth and differentiation. It accumulates under conditions of stress and undergoes inducible phosphorylation on two adjacent serine residues (78 and 81). In vitro, CHOP is phosphorylated on these residues by p38 mitogen-activated protein kinase (MAP kinase). |
|
Publications: |
2 |
Organism: |
Homo Sapiens, In Vitro |
Pathways: | P38 Signaling |
+ |
DDIT3 | down-regulates quantity by repression
transcriptional regulation
|
ASNS |
0.382 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253837 |
|
|
Homo sapiens |
HEK-293T Cell |
pmid |
sentence |
18940792 |
C/EBP homology protein (CHOP) interacts with activating transcription factor 4 (ATF4) and negatively regulates the stress-dependent induction of the asparagine synthetase gene. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
S | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260353 |
|
|
Homo sapiens |
|
pmid |
sentence |
16940539 |
Perturbation of the function of endoplasmic reticulum (ER) causes stress leading to the activation of cell signaling pathways known as the unfolded protein response (UPR). Severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) uses ER as a site for synthesis and processing of viral proteins. In this report, we demonstrate that infection with SARS-CoV induces the UPR in cultured cells. A comparison with M, E, and NSP6 proteins indicates that SARS-CoV spike (S) protein sufficiently induces transcriptional activation of several UPR effectors, including glucose-regulated protein 78 (GRP78), GRP94, and C/EBP homologous protein. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
+ |
DDIT3 | down-regulates quantity
transcriptional regulation
|
CEBPA |
0.533 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255913 |
|
|
Mus musculus |
|
pmid |
sentence |
7588595 |
We find that expression of CHOP, a nuclear protein that dimerizes avidly with C/EBP isoforms alpha and beta and directs the resulting heterodimer away from classic C/EBP-binding sites, markedly inhibits this differentiation process. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
p38 | up-regulates activity
phosphorylation
|
DDIT3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260724 |
|
|
in vitro |
|
pmid |
sentence |
8650547 |
Stress-Induced Phosphorylation and Activation of the Transcription Factor CHOP (GADD153) by p38 MAP Kinase |
|
Publications: |
1 |
Organism: |
In Vitro |
Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
+ |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.809 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260170 |
|
|
Homo sapiens |
|
pmid |
sentence |
31226023 |
ATF4 also induces another bZIP protein C/EBP-homologous protein (CHOP), which is responsible for triggering apoptosis in cells under prolonged ER stress. ATF4 and CHOP further induce growth arrest and DNA damage–inducible protein 34 (GADD34),a regulatory subunit of protein phosphatase 1 (PP1) that dephosphorylates eIF2α. This negative feedback mechanism enables protein synthesis to resume after resolution of ER stress. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
+ |
DDIT3 | down-regulates quantity
transcriptional regulation
|
CEBPB |
0.669 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-255914 |
|
|
Mus musculus |
|
pmid |
sentence |
7588595 |
We find that expression of CHOP, a nuclear protein that dimerizes avidly with C/EBP isoforms alpha and beta and directs the resulting heterodimer away from classic C/EBP-binding sites, markedly inhibits this differentiation process. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
ATF6 | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.646 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260180 |
|
|
Homo sapiens |
|
pmid |
sentence |
31226023 |
Apart from ER protein chaperones, ATF6 also induces the expression of CHOP and XBP1, thereby connecting the three UPR branches into an integrated signaling network |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
+ |
DDIT3 | up-regulates
|
Apoptosis |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260171 |
|
|
Homo sapiens |
|
pmid |
sentence |
31226023 |
ATF4 also induces another bZIP protein C/EBP-homologous protein (CHOP), which is responsible for triggering apoptosis in cells under prolonged ER stress. ATF4 and CHOP further induce growth arrest and DNA damage–inducible protein 34 (GADD34),a regulatory subunit of protein phosphatase 1 (PP1) that dephosphorylates eIF2α. This negative feedback mechanism enables protein synthesis to resume after resolution of ER stress. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, P38 Signaling, SARS-CoV MAPK PERTURBATION, SARS-CoV ER STRESS |
+ |
DDIT3 | down-regulates quantity by repression
transcriptional regulation
|
ANKRD1 |
0.277 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254122 |
|
|
Rattus norvegicus |
Cardiomyocyte Cell Line |
pmid |
sentence |
19299913 |
Promoter deletion and reporter analysis revealed that hypoxia transcriptionally activates a GADD153 promoter through the AP-1 element in neonatal cardiomyocytes. Ectopic overexpression of GADD153 resulted in the downregulation of CARP expression. |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
JUN | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.596 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254123 |
|
|
Rattus norvegicus |
|
pmid |
sentence |
19299913 |
Promoter deletion and reporter analysis revealed that hypoxia transcriptionally activates a GADD153 promoter through the AP-1 element in neonatal cardiomyocytes. Ectopic overexpression of GADD153 resulted in the downregulation of CARP expression. |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
DDIT3 | up-regulates quantity by expression
transcriptional regulation
|
PPP1R15A |
0.468 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-260173 |
|
|
Homo sapiens |
|
pmid |
sentence |
31226023 |
ATF4 also induces another bZIP protein C/EBP-homologous protein (CHOP), which is responsible for triggering apoptosis in cells under prolonged ER stress. ATF4 and CHOP further induce growth arrest and DNA damage–inducible protein 34 (GADD34),a regulatory subunit of protein phosphatase 1 (PP1) that dephosphorylates eIF2α. This negative feedback mechanism enables protein synthesis to resume after resolution of ER stress. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
+ |
DDIT3 | up-regulates quantity by expression
transcriptional regulation
|
TRIB3 |
0.591 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253839 |
|
|
Homo sapiens |
95C Cell |
pmid |
sentence |
18940792 |
Exogenous CHOP expression enhanced the TRB3 gene induction by amino acid deprivation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
ZNF804A | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-269464 |
|
|
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
23434502 |
ZNF804A has been implicated in susceptibility to schizophrenia by several genome-wide association studies (GWAS), follow-up association studies and meta-analyses. ZNF804A was identified as a schizophrenia-associated gene by GWAS and was predicted to play a role in DNA binding and transcription To identify the genes that are affected by ZNF804A, we manipulated the expression of the ZNF804A protein in HEK293 human embryonic kidney cell lines and performed a cDNA microarray analysis followed by qPCR. We found that ZNF804A-overexpression up-regulated four genes (ANKRD1, INHBE, PIK3AP1, and DDIT3) and down-regulated three genes (CLIC2, MGAM, and BIRC3). |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
PIGBOS1 | down-regulates quantity by repression
transcriptional regulation
|
DDIT3 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-261043 |
|
|
Homo sapiens |
|
pmid |
sentence |
31653868 |
We then confirmed via Western blot that TM treatment of PIGBOS-KD cells led to higher ATF4 and CHOP protein levels (Supplementary Fig. 13h). These data identified PIGBOS as a heretofore unknown mitochondrial regulator of UPR, and the only known microprotein linked to the regulation of cell stress or inter-organelle signaling. Upon UPR induction with TM, the loss of PIGBOS led to dramatic increases in the levels of all UPR target genes measured, indicating increased UPR signaling across all the branches (IRE1, PERK, and ATF6) (Fig. 6d and Supplementary Fig. 14a). Meanwhile, PIGBOS overexpressing cells showed the opposite effect, in which the UPR target genes showed less UPR activation, indicating a tunable modulation of ER stress by PIGBOS microprotein levels |
|
Publications: |
1 |
Organism: |
Homo Sapiens |