| + |
PRKG1 | up-regulates 
phosphorylation
|
GTF2I |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-89849 |
Ser412 |
GIPFRRPsTYGIPRL |
Homo sapiens |
|
| pmid |
sentence |
| 12082086 |
G-kinase phosphorylated tfii-i in vitro and in vivo on ser(371) and ser(743) outside of the interaction domain. G-kinase strongly enhanced tfii-i transactivation of a serum-response element-containing promoter in cos7 cells |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-89853 |
Ser784 |
GVPFRRPsTFGIPRL |
Homo sapiens |
|
| pmid |
sentence |
| 12082086 |
G-kinase phosphorylated tfii-i in vitro and in vivo on ser(371) and ser(743) outside of the interaction domain. G-kinase strongly enhanced tfii-i transactivation of a serum-response element-containing promoter in cos7 cells |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Kidney |
| + |
MAPK1 | up-regulates
phosphorylation
|
GTF2I |
0.372 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74296 |
Ser668 |
INTKALQsPKRPRSP |
Homo sapiens |
|
| pmid |
sentence |
| 10648599 |
Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74300 |
Ser674 |
QSPKRPRsPGSNSKV |
Homo sapiens |
|
| pmid |
sentence |
| 10648599 |
Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | up-regulates
phosphorylation
|
GTF2I |
0.382 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74304 |
Ser668 |
INTKALQsPKRPRSP |
Homo sapiens |
|
| pmid |
sentence |
| 10648599 |
Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-74308 |
Ser674 |
QSPKRPRsPGSNSKV |
Homo sapiens |
|
| pmid |
sentence |
| 10648599 |
Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
BTK | up-regulates activity
phosphorylation
|
GTF2I |
0.532 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-108338 |
Tyr248 |
EESEDPDyYQYNIQA |
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 11373296 |
These residues, tyr248, tyr357, and tyr462, were also found to be the major sites for btk-dependent phosphorylation of bap/tfii-i in vivo. Residues tyr357 and tyr462 are contained within the loop regions of adjacent helix-loop-helix-like repeats within bap/tfii-i. Mutation of either tyr248, tyr357, or tyr462 to phenylalanine reduced transcription from a c-fos promoter relative to wild-type bap/tfii-i in transfected cos-7 cells, consistent with the interpretation that phosphorylation at these sites contributes to transcriptional activation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-108342 |
Tyr398 |
QSHVEDLyVEGLPEG |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 11373296 |
These residues, tyr248, tyr357, and tyr462, were also found to be the major sites for btk-dependent phosphorylation of bap/tfii-i in vivo. Residues tyr357 and tyr462 are contained within the loop regions of adjacent helix-loop-helix-like repeats within bap/tfii-i. Mutation of either tyr248, tyr357, or tyr462 to phenylalanine reduced transcription from a c-fos promoter relative to wild-type bap/tfii-i in transfected cos-7 cells, consistent with the interpretation that phosphorylation at these sites contributes to transcriptional activation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-108346 |
Tyr503 |
EAHPNDLyVEGLPEN |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 11373296 |
These residues, tyr248, tyr357, and tyr462, were also found to be the major sites for btk-dependent phosphorylation of bap/tfii-i in vivo. Residues tyr357 and tyr462 are contained within the loop regions of adjacent helix-loop-helix-like repeats within bap/tfii-i. Mutation of either tyr248, tyr357, or tyr462 to phenylalanine reduced transcription from a c-fos promoter relative to wild-type bap/tfii-i in transfected cos-7 cells, consistent with the interpretation that phosphorylation at these sites contributes to transcriptional activation. |
|
| Publications: |
3 |
Organism: |
Chlorocebus Aethiops |
| + |
JAK2 | up-regulates activity
phosphorylation
|
GTF2I |
0.333 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235313 |
Tyr248 |
EESEDPDyYQYNIQA |
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 11313464 |
Jak2 activates tfii-i and regulates its interaction with extracellular signal-regulated kinase the interaction between tfii-i and erk, which is essential for its activity, can be regulated by jak2 through phosphorylation of tfii-i at tyrosine 248 |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SRC | up-regulates activity
phosphorylation
|
GTF2I |
0.466 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-247185 |
Tyr248 |
EESEDPDyYQYNIQA |
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 11934902 |
c-Src-dependent transcriptional activation of TFII-ITFII-I is a multifunctional transcription factor that is also involved in signal transduction. Here we show that TFII-I undergoes a c-Src-dependent tyrosine phosphorylation on tyrosine residues 248 and 611 and translocates to the nucleus in response to growth factor signaling |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-247189 |
Tyr652 |
KPELVISyLPPGMAS |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 11934902 |
C-Src-dependent transcriptional activation of TFII-ITFII-I is a multifunctional transcription factor that is also involved in signal transduction. Here we show that TFII-I undergoes a c-Src-dependent tyrosine phosphorylation on tyrosine residues 248 and 611 and translocates to the nucleus in response to growth factor signaling |
|
| Publications: |
2 |
Organism: |
Chlorocebus Aethiops |
| + |
GTF2I | up-regulates activity
binding
|
USF1 |
0.503 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268538 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21282467 |
TFII-I has been shown to interact with USF and to associate with either E-box elements or initiator sequences to activate gene transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ERK1/2 | up-regulates
phosphorylation
|
GTF2I |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270169 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10648599 |
Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates activity
binding
|
ARID3A |
0.358 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268533 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 16738337 |
In this work, we show that TFII-I directly interacts with human Bright through amino acids in Bright's protein interaction domain and that specific tyrosine residues of TFII-I are essential for Bright-induced activity of an immunoglobulin reporter gene. Moreover, inhibition of TFII-I function in a B-cell line resulted in decreased heavy-chain transcript levels. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates activity
binding, relocalization
|
KDM1A |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268539 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 12493763 |
We identify a new family of HDAC1,2-associated complexes containing BHC110. Moreover, we define the polypeptide composition of a novel member of this family containing the candidate gene for X-linked mental retardation XFIM and the initiator-binding protein TFII-I. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268540 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21282467 |
Moreover, the inhibitory effect of TFII-I on transcription is mediated by its ability to recruit corepressor complexes, including histone deacetylase 3 (HDAC3) (25, 133), histone H3K4-specific demethylase LSD1 (48), and components of the polycomb repressor complex |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates activity
binding
|
USF2 |
0.355 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268537 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21282467 |
TFII-I has been shown to interact with USF and to associate with either E-box elements or initiator sequences to activate gene transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates activity
relocalization
|
Polycomb repressive complex 2 |
0.369 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268543 |
|
|
|
|
| pmid |
sentence |
| 17970752 |
We demonstrate that Suz12, a component of the polycomb repressor complex 2, is recruited to the beta-globin gene.| Our data suggest that TFII-I contributes to the recruitment of the polycomb repressor complex 2 complex to the beta-globin gene. |
|
| Publications: |
1 |
| + |
Gbeta | up-regulates
phosphorylation
|
GTF2I |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270057 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10648599 |
Tfii-i can be phosphorylated in vitro by erk and mutation of consensus map kinase substrate sites at serines 627 and 633 impairs the phosphorylation of tfii-i by erk and its activity on the c-fos promoter. These results suggest that erk regulates the activity of tfii-i by direct phosphorylation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates
binding
|
PRRX1 |
0.351 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-52654 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9334314 |
Spin binds specifically to multiple sequences in the c-fos promoter and interacts cooperatively withphox1to promote serum-inducible transcription of a reporter gene driven by the c-fos serum response element (sre). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates quantity by expression 
transcriptional regulation
|
HSPA5 |
0.381 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254221 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19097122 |
Transcription factor TFII-I causes transcriptional upregulation of GRP78 synthesis in prostate cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GTF2I | up-regulates quantity by expression
transcriptional regulation
|
GSC |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268536 |
|
|
|
|
| pmid |
sentence |
| 16611241 |
For example, TFII-I binds to the Inr element of the T cell receptor Vbeta gene and activates its transcription in reporter gene assays (Cheriyath et al. 1998). TFII-I also activates transcription of c-fos and Goosecoid through binding to the serum response element and the distal element, respectively (Grueneberg et al. 1997; Ku et al. 2005). |
|
| Publications: |
1 |
| + |
GTF2I | up-regulates quantity by expression
transcriptional regulation
|
FOS |
0.328 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268535 |
|
|
|
|
| pmid |
sentence |
| 16611241 |
For example, TFII-I binds to the Inr element of the T cell receptor Vbeta gene and activates its transcription in reporter gene assays (Cheriyath et al. 1998). TFII-I also activates transcription of c-fos and Goosecoid through binding to the serum response element and the distal element, respectively (Grueneberg et al. 1997; Ku et al. 2005). |
|
| Publications: |
1 |
| + |
GTF2IRD1 | down-regulates 
|
GTF2I |
0.426 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268534 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 11438732 |
Here we describe a repressor (MusTRD1/BEN) that appears to specifically regulate the nucleocytoplasmic shuttling of TFII-I. Nuclear exclusion of TFII-I results in a repression of its target reporter gene, and such repression can be alleviated when MusTRD1/BEN is retained in the cytoplasm through targeted mutation. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
BTK | up-regulates
phosphorylation
|
GTF2I |
0.532 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-46060 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 9012831 |
We now describe a protein, bap-135, that is associated with btk in b cells and is a substrate for phosphorylation by btk.Taken together, these observations suggest that bap-135 may reside downstream of btk in a signaling pathway originating at the bcr. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
GTF2I
- 
- 