| + |
CSNK2A1 | down-regulates quantity by destabilization 
phosphorylation
|
ATF4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276425 |
Ser215 |
IKEEDTPsDNDSGIC |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 23123191 |
By using mutants of ATF4 we identified serine 215 as the main CK2 phosphorylation site. The ATF4 S215A mutant turned out to be more stable than the wild-type form. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
CSNK2B | down-regulates quantity by destabilization
phosphorylation
|
ATF4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276424 |
Ser215 |
IKEEDTPsDNDSGIC |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 23123191 |
By using mutants of ATF4 we identified serine 215 as the main CK2 phosphorylation site. The ATF4 S215A mutant turned out to be more stable than the wild-type form. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RPS6KA3 | up-regulates 
phosphorylation
|
ATF4 |
0.634 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124436 |
Ser245 |
TRGSPNRsLPSPGVL |
Homo sapiens |
|
| pmid |
sentence |
| 15109498 |
Here, we show that rsk2 is required for osteoblast differentiation and function. We identify the transcription factor atf4 as a critical substrate of rsk2 that is required for the timely onset of osteoblast differentiation, for terminal differentiation of osteoblasts, and for osteoblast-specific gene expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RET | down-regulates quantity by destabilization
phosphorylation
|
ATF4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276448 |
Thr107 |
LGIDDLEtMPDDLLT |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 25795775 |
We observed that RET physically interacted with and phosphorylated ATF4 at tyrosine and threonine residues. Indeed, RET kinase activity was required to inhibit the ATF4-dependent activation of the NOXA gene because the site-specific substitution mutations that block threonine phosphorylation increased ATF4 stability and activated its targets NOXA and PUMA. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276449 |
Thr114 |
TMPDDLLtTLDDTCD |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 25795775 |
We observed that RET physically interacted with and phosphorylated ATF4 at tyrosine and threonine residues. Indeed, RET kinase activity was required to inhibit the ATF4-dependent activation of the NOXA gene because the site-specific substitution mutations that block threonine phosphorylation increased ATF4 stability and activated its targets NOXA and PUMA. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276447 |
Thr115 |
MPDDLLTtLDDTCDL |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 25795775 |
We observed that RET physically interacted with and phosphorylated ATF4 at tyrosine and threonine residues. Indeed, RET kinase activity was required to inhibit the ATF4-dependent activation of the NOXA gene because the site-specific substitution mutations that block threonine phosphorylation increased ATF4 stability and activated its targets NOXA and PUMA. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276450 |
Thr119 |
LLTTLDDtCDLFAPL |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 25795775 |
We observed that RET physically interacted with and phosphorylated ATF4 at tyrosine and threonine residues. Indeed, RET kinase activity was required to inhibit the ATF4-dependent activation of the NOXA gene because the site-specific substitution mutations that block threonine phosphorylation increased ATF4 stability and activated its targets NOXA and PUMA. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
EPRS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269419 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
SARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269424 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NUPR1 | up-regulates quantity by expression 
transcriptional regulation
|
ATF4 |
0.389 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253731 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 19946894 |
Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIGBOS1 | down-regulates quantity by repression 
transcriptional regulation
|
ATF4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261041 |
|
|
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 |
| + |
ER stress | up-regulates
|
ATF4 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253728 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23205607 |
Reporter gene analyses using the 5'-promoter region of FGF19 revealed that a functional AARE (amino-acid-response element) was localized in this region, and this site was responsible for inducing its transcription through ATF4 (activating transcription factor 4), which is activated in response to ER stress |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
NLRP1 inflammasome |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260354 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26086088 |
Transcription Factor ATF4 Induces NLRP1 Inflammasome Expression During Endoplasmic Reticulum Stress. Here we report that expression of NLRP1, a core inflammasome component, is specifically up-regulated during severe ER stress conditions in human cell lines. Both IRE1α and PERK, but not the ATF6 pathway, modulate NLRP1 gene expression. Furthermore, using mutagenesis, chromatin immunoprecipitation and CRISPR-Cas9-mediated genome editing technology, we demonstrate that ATF4 transcription factor directly binds to NLRP1 promoter during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
TARS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269428 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
NARS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269423 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
CARS2 |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269417 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NCOA3 | up-regulates activity
binding
|
ATF4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275452 |
|
|
Homo sapiens |
Hepatoma Cell Line |
| pmid |
sentence |
| 31066068 |
Mechanistically, Dyrk3 directly phosphorylated NCOA3 at Ser-1330, disrupting its binding to ATF4 and thereby causing the inhibition of ATF4 transcriptional activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
DDIT3 |
0.816 |
| 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 |
| + |
ATF4 | down-regulates quantity by repression
transcriptional regulation
|
HSPA5 |
0.667 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253749 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16205636 |
Suppression of ATF4 expression by small interfering RNA (siRNA) partially inhibited the celecoxib-dependent upregulation of GRP78. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
GARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269426 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
WARS2 |
0.247 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269430 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
ASNS |
0.65 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253747 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11960987 |
Transcription from the asparagine synthetase (A.S.) gene is increased in response to either amino acid (amino acid response) or glucose (endoplasmic reticulum stress response) deprivation. the results provide both in vitro and in vivo evidence for a role of ATF4 in the transcriptional activation of the A.S. gene in response to nutrient deprivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Aspartate and asparagine metabolism |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
AARS2 |
0.245 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269415 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | down-regulates quantity by repression
transcriptional regulation
|
ASNS |
0.65 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253838 |
|
|
Homo sapiens |
95D 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 |
| Pathways: | Aspartate and asparagine metabolism |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
LARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269420 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
LARS2 |
0.252 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269421 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EIF2S1 | down-regulates quantity
transcriptional regulation
|
ATF4 |
0.64 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260169 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27629041 |
ER stress, viral infection, and other cellular stress signals activate PERK, PKR, HRI, and GCN2 kinases that converge on phosphorylation of eIF2alpha, the core of ISR. This leads to global attenuation of Cap Âdependent translation while concomitantly initiates the preferential translation of ISR Âspecific mRNAs, such as ATF4. ATF4 is the main effector of the ISR. eIF2alpha phosphorylation causes a reduction in global protein synthesis while allowing the translation of selected genes including activating transcription factor 4 (ATF4), aiding cell survival and recovery |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
FGF21 |
0.433 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253748 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22233381 |
These results add FGF21 gene induction to the transcriptional programme initiated by increased levels of ATF4 and offer a new mechanism for the induction of the FGF21 gene expression under nutrient deprivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
CARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269416 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
IARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269427 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
NARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269422 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
PPP1R15A |
0.658 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260172 |
|
|
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 |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
YARS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269432 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
AARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269414 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
DARS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269418 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
SARS2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269425 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SCF-betaTRCP | down-regulates quantity by destabilization
polyubiquitination
|
ATF4 |
0.329 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272580 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 11238952 |
Here we show that the F-box protein betaTrCP, the receptor component of the SCF E3 ubiquitin ligase responsible for IkappaBalpha and beta-catenin degradation, is colocalized in the nucleus with ATF4, a member of the ATF-CREB bZIP family of transcription factors, and controls its stability. ATF4 ubiquitination in HeLa cells is enhanced in the presence of betaTrCP. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BZW2 | up-regulates quantity by expression
transcriptional regulation
|
ATF4 |
0.416 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261222 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 31643092 |
Subsequent research reveals that BZW2 induces ATF4 translation which is a pro‐oncogenic transcription factor |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EIF2S1 | up-regulates quantity by expression
transcriptional regulation
|
ATF4 |
0.64 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251820 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24714526 |
Reduction of globin inclusions and induction of ATF4 and HbF by the HRI-eIF2αP signaling provide strong bases for targeting this pathway for novel pharmaceutical therapy of hemoglobinopathy. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV ER STRESS |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
SIGMAR1 |
0.386 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253750 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22079628 |
we have demonstrated that Sig-1Rs were transcriptionally upregulated by ATF4 in ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
WARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269429 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ROS | up-regulates
|
ATF4 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253729 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19439225 |
Oxidative and ER stress conditions induce rapid and significant activation of ATF4 downstream of eIF2alpha phosphorylation, which is responsible for Redd1 expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
NUPR1 |
0.389 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253730 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 19946894 |
Nuclear protein 1 induced by ATF4 in response to various stressors acts as a positive regulator on the transcriptional activation of ATF4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
DDIT4 |
0.418 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253726 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19439225 |
We additionally identified Redd1 as a downstream effector of C/EBP-beta stimulated by ATF4 activated under the stress conditions examined. RNA interference studies provided further evidence of the requirement of C/EBP-beta for Redd1 expression. We conclude that the Redd1 gene is transactivated by the ATF4 and C/EBP family of transcription factors, leading to mTOR inhibition in response to oxidative and ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | down-regulates quantity by repression
transcriptional regulation
|
DYRK3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275453 |
|
|
Homo sapiens |
Hepatoma Cell Line |
| pmid |
sentence |
| 31066068 |
Interestingly, the promoter activity of Dyrk3 was negatively regulated by ATF4, indicating a double-negative feedback loop. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
YARS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269431 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33384352 |
QRICH1 promotes the expression of translation-related genes. our combined ChIP-seq and RNA-seq analyses identified that QRICH1 and ATF4 were enriched at the promoters of these specific tRNA synthetases, and that ER stress positively regulated their transcription (Fig. 4I). Together, these findings suggest that QRICH1 and ATF4 modulate tRNA metabolic processes to promote secreted protein synthesis during ER stress. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF4 | up-regulates quantity by expression
transcriptional regulation
|
FGF19 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253727 |
|
|
Homo sapiens |
CACO-2 Cell |
| pmid |
sentence |
| 23205607 |
Reporter gene analyses using the 5'-promoter region of FGF19 revealed that a functional AARE (amino-acid-response element) was localized in this region, and this site was responsible for inducing its transcription through ATF4 (activating transcription factor 4), which is activated in response to ER stress |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
ATF4
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