| + |
P-TEFb | down-regulates quantity by destabilization 
phosphorylation
|
AFF2 |
0.398 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266798 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17135274 |
P-TEFb phosphorylates Af4 and down-regulates its transactivation activity. P-TEFb also phosphorylates AF4 which down-regulates its transactivation activity, providing a negative feedback mechanism for the control of P-TEFb elongation activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CDK9 | form complex 
binding
|
P-TEFb |
0.964 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267740 |
|
|
in vitro |
|
| pmid |
sentence |
| 34955012 |
Cyclin-dependent-kinases (CDKs) are members of the serine/threonine kinase family and are highly regulated by cyclins, a family of regulatory subunits that bind to CDKs. CDK9 represents one of the most studied examples of these transcriptional CDKs. CDK9 forms a heterodimeric complex with its regulatory subunit cyclins T1, T2 and K to form the positive transcription elongation factor b (P-TEFb). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
P-TEFb | up-regulates activity 
phosphorylation
|
POLR2A |
0.745 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261039 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32048991 |
Phosphorylation of Pol II CTD by positive transcription elongation factor b (P-TEFb) is a necessary precursor event that enables productive transcription elongation. To perform this task, Pol II needs to be activated by a complex of proteins called P-TEFb; however, P-TEFb is usually found in an inactive form held by another group of proteins. Yet, it is unclear how P-TEFb is released and allowed to activate Pol II. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
P-TEFb | down-regulates 
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260137 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
| pmid |
sentence |
| 19516275 |
Hexamethylene bis-acetamide inducible protein 1 (HEXIM1) inhibits the positive transcription elongation factor b (P-TEFb), which is a key RNA polymerase II (Pol II) transcriptional regulator. In transfected cells, mutated NPM1 associated with, and sequestered, HEXIM1 in cytoplasm, resulting in higher transcription of RNA pol II target genes, among which were some positive regulators of cell-cycle progression such as cyclin D1 and anti-apoptotic proteins such as Mcl-1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CCNT1 | form complex
binding
|
P-TEFb |
0.964 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267739 |
|
|
in vitro |
|
| pmid |
sentence |
| 34955012 |
Cyclin-dependent-kinases (CDKs) are members of the serine/threonine kinase family and are highly regulated by cyclins, a family of regulatory subunits that bind to CDKs. CDK9 represents one of the most studied examples of these transcriptional CDKs. CDK9 forms a heterodimeric complex with its regulatory subunit cyclins T1, T2 and K to form the positive transcription elongation factor b (P-TEFb). |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
P-TEFb | up-regulates 
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260136 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
| pmid |
sentence |
| 19516275 |
Hexamethylene bis-acetamide inducible protein 1 (HEXIM1) inhibits the positive transcription elongation factor b (P-TEFb), which is a key RNA polymerase II (Pol II) transcriptional regulator. In transfected cells, mutated NPM1 associated with, and sequestered, HEXIM1 in cytoplasm, resulting in higher transcription of RNA pol II target genes, among which were some positive regulators of cell-cycle progression such as cyclin D1 and anti-apoptotic proteins such as Mcl-1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RBM7 | up-regulates activity
relocalization
|
P-TEFb |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261182 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 30824372 |
Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by activating the positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7SK small nuclear ribonucleoprotein (7SK snRNP). these findings establish that RBM7 binds 7SK snRNP and that genotoxic stress activates P-TEFb by relocating it from 7SK snRNP to the CTD of Pol II. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
P-TEFb | down-regulates quantity by destabilization
phosphorylation
|
MLLT3 |
0.687 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266800 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17135274 |
Phosphorylation of Af9 and Enl by P-TEFb promotes their proteolysis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BRD4 | up-regulates activity
binding
|
P-TEFb |
0.62 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266411 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16109377 |
Binding of Brd4 to Core P-TEFb Is Essential for Transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AFF2 | up-regulates activity
binding
|
P-TEFb |
0.398 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266801 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17135274 |
Af4 associates with P-TEFb and stimulates its kinase activity. P-TEFb also phosphorylates AF4 which down-regulates its transactivation activity, providing a negative feedback mechanism for the control of P-TEFb elongation activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
P-TEFb | form complex
binding
|
AEP complex |
0.755 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-239237 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20153263 |
These data demonstrate that AF4, AF5q31 and ENL associate in an endogenous higher-order complex (hereafter referred to as AEP for the AF4 family/ENL family/P-TEFb complex) containing P-TEFb in hematopoietic lineage cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LARP7 | down-regulates activity
binding
|
P-TEFb |
0.604 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261184 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 30824372 |
To investigate whether LARP7 is part of the known 7SK RNP implicated in the regulation of transcription, co‐immunoprecipitation studies were performed using the nuclear extracts of HeLa cells (Fig 3A, lanes 1–4). Antibodies against LARP7, CDK9 and HEXIM1 efficiently precipitated 7SK RNA, whereas no RNA was found in the control (Fig 3A, lower panel, lanes 1–4). Interestingly, HEXIM1, CDK9, CYCT1 and LARP7 were present in all immunopurifications, as determined by mass spectrometry of silver‐stained gels (Fig 3A; data not shown) and western blotting. In conclusion, these experiments show that LARP7 negatively regulates not only viral but also cellular POLII class genes through the 7SK P‐TEFb system. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HEXIM1 | down-regulates activity
binding
|
P-TEFb |
0.743 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260135 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18371977 |
Studies show that more than half of P-TEFb in cells is associated with HEXIM1, which results in the inactivation of P-TEFb. The mislocalization of HEXIM1 and the increased P-TEFb-dependent transcription caused by NPMc+ suggests that the misregulated activity of PTEFb may contribute to the tumorigenesis of NPMc+ AML. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
P-TEFb | down-regulates quantity by destabilization
phosphorylation
|
MLLT1 |
0.708 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266799 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 17135274 |
Phosphorylation of Af9 and Enl by P-TEFb promotes their proteolysis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEPCE | down-regulates activity
binding
|
P-TEFb |
0.565 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261038 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 32048991 |
JMJD6 cleaves MePCE. we propose that JMJD6 is the cognate protease of MePCE and cleaves at the R171 site within MePCE. Experiments using purified JMJD6 showed that it could make a cut in an enzyme called MePCE, which belongs to the group of proteins that hold P-TEFb in its inactive form. The levels of activated Pol II were lower in cells without JMJD6 and higher in those without MePCE. Together, the results suggest that JMJD6 cuts MePCE to release P-TEFb, which then activates Pol II. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
3.0
P-TEFb
CPX-222