Gene interactions and pathways from curated databases and text-mining

◀ Back to CCNT1

CCNT1 — CCNT2

Pathways - manually collected, often from reviews:

  • Reactome Reaction: CCNT2 → CCNT1 (direct_complex)
  • Reactome Reaction: CCNT2 → CCNT1 (reaction)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

O'Keeffe et al., J Biol Chem 2000 : Requirement for a kinase-specific chaperone pathway in the production of a Cdk9/cyclin T1 heterodimer responsible for P-TEFb mediated tat stimulation of HIV-1 transcription ... Requirement for a kinase-specific chaperone pathway in the production of a Cdk9/cyclin T1 heterodimer responsible for P-TEFb mediated tat stimulation of HIV-1 transcription ... Our data suggest a previously unrecognized chaperone dependent pathway involving the sequential actions of Hsp70 and Hsp90/Cdc37 in the stabilization/folding of Cdk9 as well as the assembly of an active Cdk9/cyclin T1 complex responsible for P-TEFb mediated Tat transactivation
Lis et al., Genes Dev 2000 : Yet, HSF binding to DNA is not sufficient to recruit P-TEFb in vivo, and HSF and P-TEFb immunostainings within a heat shock locus are not coincident ... Analyses of point mutants show this P-TEFb stimulation is dependent on Cdk9 kinase activity and on Cdk9 's interaction with cyclin T
Ping et al., J Biol Chem 2001 : DSIF and NELF interact with RNA polymerase II elongation complex and HIV-1 Tat stimulates P-TEFb mediated phosphorylation of RNA polymerase II and DSIF during transcription elongation ... DSIF and NELF interact with RNA polymerase II elongation complex and HIV-1 Tat stimulates P-TEFb mediated phosphorylation of RNA polymerase II and DSIF during transcription elongation
Yang et al., Nature 2001 : As a Tat cofactor, P-TEFb stimulates HIV-1 transcription by interacting with Tat and the transactivating responsive ( TAR ) RNA structure located at the 5 ' end of the nascent viral transcript
Yedavalli et al., J Biol Chem 2003 : Why P-TEFb requires Tat/TAR for LTRs but not for cellular promoters remains unknown
Shore et al., Gene 2003 : Positive transcription factor b (P-TEFb) is required for RNA polymerase II to make the transition from abortive to productive elongation
Tian et al., J Biol Chem 2003 : Inhibition of P-TEFb kinase activity by 5,6-dichloro-1-beta-d-ribofuranosyl-benzimidazole ( DRB ) suppressed CTD phosphorylation ( especially serine 2 phosphorylation ) and abolished processive elongation without disrupting the assembly of the preinitiation complex at the cyp1a1 promoter
Young et al., Mol Cell Biol 2003 : Activation of the HIV-1 LTR by HIC in NIH 3T3 cells occurs at the RNA level and is mediated by direct interactions with P-TEFb
Garriga et al., Gene 2004 : P-TEFb positively regulates transcriptional elongation by phosphorylating the C-terminal domain (CTD) of RNA polymerase II (RNA pol II), as well as negative elongation factors, which block elongation by RNA pol II shortly after the initiation of transcription
Zhou et al., J Virol 2004 : Second, the stable association of SPT5 with the TECs is dependent upon P-TEFb kinase activity
Schulte et al., J Biol Chem 2005 : Functional assays in HeLa cells showed that this cyclin T-binding domain (TBD) is required for the binding of Hexim1 to P-TEFb and inhibition of transcriptional activity in vivo
Fraldi et al., Retrovirology 2005 : The activity of P-TEFb is regulated in vivo and in vitro by the HEXIM1/7SK snRNA ribonucleic-protein complex ... Enhanced expression of HEXIM1 protein modestly affects P-TEFb activity, suggesting that HEXIM1 mediated repression of Tat activity is not due to a global inhibition of cellular transcription
Jang et al., Mol Cell 2005 : An increase in Brd4 expression led to increased P-TEFb dependent phosphorylation of RNA polymerase II (RNAPII) CTD and stimulation of transcription from promoters in vivo
Haaland et al., J Cell Physiol 2005 : Here we report that 7SK and HEXIM1 levels are induced in activated lymphocytes concomitantly with increased P-TEFb activity and global transcription
Blazek et al., Nucleic Acids Res 2005 : Oligomerization of HEXIM1 via 7SK snRNA and coiled-coil region directs the inhibition of P-TEFb ... Importantly, mutations of the N-terminal part of the coiled-coil region abrogate the ability of HEXIM1 to bind and inhibit P-TEFb
Moisan et al., J Biol Chem 2006 : Here, we investigate the effect of BRCA1 on serine 2 phosphorylation and UV-activated P-TEFb kinase activity ... We now show that BRCA1 inhibits immunoprecipitated P-TEFb kinase activity from UV-irradiated cells and preferentially decreases UV-induced serine 2 phosphorylation of soluble, rather than chromatin bound, RNAPII
Shimizu et al., AIDS 2007 : Tat dependent transcriptional elongation is crucial for the replication of HIV-1 and depends on positive transcription elongation factor b complex ( P-TEFb ), composed of cyclin dependent kinase 9 (CDK9) and cyclin T. Hexamethylene bisacetamide induced protein 1 ( HEXIM1 ) inhibits P-TEFb in cooperation with 7SK RNA, but direct evidence that this inhibition limits the replication of HIV-1 has been lacking
He et al., Cold Spring Harb Symp Quant Biol 2006 : Together with the HEXIM1 protein, 7SK sequesters P-TEFb into a kinase-inactive complex, where it mediates HEXIM1 's inhibition of P-TEFb
Espinoza-Derout et al., Cardiovasc Res 2007 (Cardiomegaly) : Pivotal role of cardiac lineage protein-1 (CLP-1) in transcriptional elongation factor P-TEFb complex formation in cardiac hypertrophy
Cho et al., J Virol 2007 : Our lab has recently demonstrated that P-TEFb is required for Tax transactivation of the viral long terminal repeat ( LTR )
Radhakrishnan et al., Oncogene 2008 : In this study, we found that P-TEFb inhibitors block the phosphorylation of p53 induced by doxorubicin
Chen et al., Genes Dev 2008 (Calcium Signaling) : PP2B and PP1alpha cooperatively disrupt 7SK snRNP to release P-TEFb for transcription in response to Ca2+ signaling
Ogba et al., Cancer Res 2008 : Whereas there have been previous reports on HEXIM1 inhibition of P-TEFb activity, our studies add a new dimension by showing that E ( 2 ) /ER is an important regulator of the HEXIM1/P-TEFb functional unit in breast cells
Zhou et al., J Virol 2009 : Here we provide evidence that Brd4 regulates P-TEFb kinase activity by inducing a negative pathway
Wang et al., Mini Rev Med Chem 2009 (HIV Infections) : The positive elongation factor P-TEFb , a heterodimer containing a catalytic subunit ( CDK9 ) and unique regulatory cyclins ( CycT1 ), is required for HIV-1 Tat transcriptional activation
Kohoutek et al., Mol Cell Biol 2009 : Thus, CycT1 and CycT2 are not redundant, and these different P-TEFb complexes regulate subsets of distinct genes that are important for embryonic development
Cho et al., Cell cycle (Georgetown, Tex.) 2010 : CYCLINg through transcription : posttranslational modifications of P-TEFb regulate transcription elongation
Tahirov et al., Nature 2010 : Importantly, Tat induces significant conformational changes in P-TEFb
O'Brien et al., J Biol Chem 2010 (HIV Infections) : We identify histone H1 as a novel P-TEFb substrate, and our results suggest new roles for P-TEFb in both cellular and HIV-1 transcription
Flynn et al., Proc Natl Acad Sci U S A 2011 : Antisense RNA polymerase II divergent transcripts are P-TEFb dependent and substrates for the RNA exosome
Žumer et al., Nucleic Acids Res 2011 (Polyendocrinopathies, Autoimmune) : Thus, AIRE requires P-TEFb to activate transcription elongation and co-transcriptional processing of target genes
Peterlin et al., Wiley Interdiscip Rev RNA 2012 : The release of active P-TEFb is closely followed by release of HEXIM proteins and both are replaced by heterogeneous nuclear ribonucleoproteins ( hnRNPs )
Yamamura et al., Carcinogenesis 2012 (Carcinoma, Renal Cell...) : miR-34a was also found to repress the c-Myc-P-TEFb transcription elongation complex, indicating one of the mechanisms by which miR-34a has profound effects on cellular functions
Okamura et al., Genes Dev 2012 : The expression of p15(INK4b) , a cyclin dependent kinase inhibitor (CDKI) gene, in PGCs is selectively activated by P-TEFb and its recruiting molecule, Brd4, when the amount of active P-TEFb is increased due to reduction of the 7SK snRNP, and PGCs consequently undergo growth arrest
Wang et al., Transcription 2013 : Instead, Med23 depletion results in a significant decrease in P-TEFb and RNAP II ( Ser2P ) binding at the coding region, but no changes for several other elongation regulators, such as DSIF and NELF
Bowman et al., Development 2013 : Phosphorylation of RNA polymerase II is independent of P-TEFb in the C. elegans germline
Ding et al., PloS one 2013 : Since no changes in CDK9 and cyclin T1 were observed in the LY294002 treated cells, increased levels of HEXIM1 might lead to inhibition of P-TEFb activity