| + |
NFYA | up-regulates quantity by expression 
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252232 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15496512 |
Coactivator RNF4 is involved in the GCH gene expression. Through serial deletion and mutagenesis studies of the GCH promoter, we defined the RNF4-responsive element on GCH proximal promoter as a CCAAT box. RNF4 did not possess specific DNA binding activity toward this CCAAT box, which suggests that RNF4 may be a coactivator of the CCAAT boxbinding protein nuclear factor Y (NF-Y). RNF4 is a coactivator for nuclear factor Y on GTP cyclohydrolase I proximal promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
GCH1 |
0.247 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252210 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9204951 |
The de novo synthesis of 6-BH4 depends on the induction of GTP-CH-1, e.g., by tumor necrosis factor-alpha (TNF alpha). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CRP | down-regulates quantity by repression 
transcriptional regulation
|
GCH1 |
0.278 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252216 |
|
|
Homo sapiens |
Human Aortic Endothelial Cell |
| pmid |
sentence |
| 17942113 |
The gene expression and enzymatic activity of GTPCH1, the first enzyme in the de novo biosynthesis of BH(4), were significantly inhibited by CRP. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HSPB1 | up-regulates quantity by stabilization 
binding
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252222 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18241680 |
GTP cyclohydrolase I (GCH), an oligomeric protein composed of 10 identical subunits, is required for the synthesis of neurotransmitters; mutations in GCH are associated with dopa-responsive dystonia (DRD) and hyperphenylalaninemia. Mutated GCH proteins are unstable and prone to dominant-negative effect. We show herein that expression of the GCH mutant GCH-201E or the splicing variant GCH-II caused intracellular inclusion bodies. When Hsp27 was expressed together with the GCH mutants, Hsp27 expression decreased the formation of inclusion bodies by GCH (as assessed by immunofluorescence) and decreased the amount of insoluble GCH mutant proteins (as assessed by Western blot). we demonstrated that Hsp27 increases the expression of the wild-type GCH protein, causes the appearance of the soluble GCH-II protein, and decreases the quantities of insoluble mutated GCH protein. Therefore, it is likely that Hsp27 improves the folding of mutated GCH proteins, so they can stay in free cytosolic compartment. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IL6 | down-regulates quantity by repression
transcriptional regulation
|
GCH1 |
0.264 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252220 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12859689 |
CT-1 exerted these effects by decreasing tyrosine hydroxylase, GTP cyclohydrolase (GCH) and NE transporter mRNAs, while IL-6 lowered only GCH mRNA. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IL1B | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.342 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252224 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10435048 |
IL-1 beta induces expression of GTP cyclohydrolase-1 which leads to increased generation of BH4 and activation of eNOS. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Blood Vessel Endothelium |
| + |
NFYB | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252233 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15496512 |
Coactivator RNF4 is involved in the GCH gene expression. Through serial deletion and mutagenesis studies of the GCH promoter, we defined the RNF4-responsive element on GCH proximal promoter as a CCAAT box. RNF4 did not possess specific DNA binding activity toward this CCAAT box, which suggests that RNF4 may be a coactivator of the CCAAT boxbinding protein nuclear factor Y (NF-Y). RNF4 is a coactivator for nuclear factor Y on GTP cyclohydrolase I proximal promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AHSA1 | up-regulates activity
binding
|
GCH1 |
0.298 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252213 |
|
|
Homo sapiens |
Endothelial Cell Line |
| pmid |
sentence |
| 16696853 |
The interaction of GCH1 with Aha1 may recruit GCH1 into the eNOS/Hsp90 complex so as to support local changes in nitric oxide production by endothelial cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NFYC | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252234 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15496512 |
Coactivator RNF4 is involved in the GCH gene expression. Through serial deletion and mutagenesis studies of the GCH promoter, we defined the RNF4-responsive element on GCH proximal promoter as a CCAAT box. RNF4 did not possess specific DNA binding activity toward this CCAAT box, which suggests that RNF4 may be a coactivator of the CCAAT boxbinding protein nuclear factor Y (NF-Y). RNF4 is a coactivator for nuclear factor Y on GTP cyclohydrolase I proximal promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NGF | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.249 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252228 |
|
|
Rattus norvegicus |
PC-12D Cell |
| pmid |
sentence |
| 16190874 |
We examined intracellular signals required for NGF-induced expression of the GCH gene in PC12D cells. The activity of GCH was increased up to 5-fold after the NGF treatment. The human GCH promoter activity was significantly enhanced by NGF treatment. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
CREB1 | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252227 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16149046 |
Constitutively active mutants of activating transcription factor 2 (ATF2) and c-Jun additionally stimulated GTP cyclohydrolase I promoter activity, but to a lesser extent than the constitutively active CREB mutant. Enzymatic reactions that require tetrahydrobiopterin as cofactor are therefore indirectly controlled by signaling cascades involving the signal-responsive transcription factors CREB, c-Jun, and ATF2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CTF1 | down-regulates quantity by repression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252218 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12859689 |
CT-1 exerted these effects by decreasing tyrosine hydroxylase, GTP cyclohydrolase (GCH) and NE transporter mRNAs, while IL-6 lowered only GCH mRNA. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GCHFR | down-regulates activity 
binding
|
GCH1 |
0.864 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252203 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11361142 |
The enzyme activity of GTP cyclohydrolase I is controlled by a regulatory protein for this enzyme, GFRP, which is a pentamer of identical subunits. GFRP mediates feedback inhibition of GTP cyclohydrolase I activity by BH4, and the inhibition by BH4 is reversed by phenylalanine |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
UVB radiation | up-regulates
|
GCH1 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252206 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9204951 |
UVB light induces GTP-CH.-1 to increase the de novo synthesis of 6-BH4 in association with a concomitant increase in PAH activities, thus providing more L-tyrosine. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IFNG | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.251 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252223 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20525234 |
Pro-inflammatory cytokines like interferon-γ (IFN-γ) induce expression of GTP-cyclohydrolase I in various brain cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
JUN | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252225 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16149046 |
Constitutively active mutants of activating transcription factor 2 (ATF2) and c-Jun additionally stimulated GTP cyclohydrolase I promoter activity, but to a lesser extent than the constitutively active CREB mutant. Enzymatic reactions that require tetrahydrobiopterin as cofactor are therefore indirectly controlled by signaling cascades involving the signal-responsive transcription factors CREB, c-Jun, and ATF2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF2 | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252226 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16149046 |
Constitutively active mutants of activating transcription factor 2 (ATF2) and c-Jun additionally stimulated GTP cyclohydrolase I promoter activity, but to a lesser extent than the constitutively active CREB mutant. Enzymatic reactions that require tetrahydrobiopterin as cofactor are therefore indirectly controlled by signaling cascades involving the signal-responsive transcription factors CREB, c-Jun, and ATF2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CRP | down-regulates activity
|
GCH1 |
0.278 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252215 |
|
|
Homo sapiens |
Human Aortic Endothelial Cell |
| pmid |
sentence |
| 17942113 |
The gene expression and enzymatic activity of GTPCH1, the first enzyme in the de novo biosynthesis of BH(4), were significantly inhibited by CRP. Importantly, GTPCH1 is known to be regulated by cAMP-mediated pathway. In the present study, CRP-mediated inhibition of GTPCH1 activity was reversed by pretreatment with cAMP analogues. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GDNF | up-regulates activity
|
GCH1 |
0.277 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252221 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12358777 |
GDNF can support the function of primary dopaminergic neurones by triggering activation of GTP-cyclohydrolase I (GTPCH I), a key enzyme in catecholamine biosynthesis. GTPCH I mRNA levels in primary dopaminergic neurones were not altered by GDNF treatment, suggesting that the mode of action for that up-regulation is not directly connected to the regulation of GTPCH I transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
GCH1
- 
- 