ArticleOncogene2000
Physical interaction between CDK9 and B-Myb results in suppression of B-Myb gene autoregulation.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Transcriptional pause release at enhancers mediates cell identity.NAR cancer · 2025Review
- Article
- TBX2 is a neuroblastoma core regulatory circuitry component enhancing MYCN/FOXM1 reactivation of DREAM targets.Nature communications · 2018Article
- MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis.Cell death & disease · 2017Review
- Structural Basis for the Non-catalytic Functions of Protein Kinases.Structure (London, England : 1993) · 2016Review
- Kinetically Defined Mechanisms and Positions of Action of Two New Modulators of Glucocorticoid Receptor-regulated Gene Induction.The Journal of biological chemistry · 2016Article
- A kinase-independent activity of Cdk9 modulates glucocorticoid receptor-mediated gene induction.Biochemistry · 2014Article
- The elongation complex components BRD4 and MLLT3/AF9 are transcriptional coactivators of nuclear retinoid receptors.PloS one · 2013Article
- Immunohistochemical localization of beta defensins in the endometrium of rat uterus during the postpartum involution period.Veterinary research communications · 2012Article
- Estrogen receptor-α recruits P-TEFb to overcome transcriptional pausing in intron 1 of the MYB gene.Nucleic acids research · 2012Article
- A chemical screen identifies the chemotherapeutic drug topotecan as a specific inhibitor of the B-MYB/MYCN axis in neuroblastoma.Oncotarget · 2012Article
- Herpes simplex virus 1 ICP22 inhibits the transcription of viral gene promoters by binding to and blocking the recruitment of P-TEFb.PloS one · 2012Article
- HIV-1 Tat and host AFF4 recruit two transcription elongation factors into a bifunctional complex for coordinated activation of HIV-1 transcription.Molecular cell · 2010Article
- CDKN1C negatively regulates RNA polymerase II C-terminal domain phosphorylation in an E2F1-dependent manner.The Journal of biological chemistry · 2010Article
- CDK9/cyclin complexes modulate endoderm induction by direct interaction with Mix.3/mixer.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Article
- Nuclear hBD-1 accumulation in malignant salivary gland tumours.BMC cancer · 2008Article
- HIV-1 Tat mimetic of VEGF correlates with increased microvessels density in AIDS-related diffuse large B-cell and Burkitt lymphomas.Journal of hematopathology · 2008Article
- A cell cycle-dependent co-repressor mediates photoreceptor cell-specific nuclear receptor function.The EMBO journal · 2007Article
- The Yin and Yang of P-TEFb regulation: implications for human immunodeficiency virus gene expression and global control of cell growth and differentiation.Microbiology and molecular biology reviews : MMBR · 2006Review
- Activation of cardiac Cdk9 represses PGC-1 and confers a predisposition to heart failure.The EMBO journal · 2004Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-Myb is a transcription factor belonging to the myb family, whose activity has been associated with augmented DNA synthesis and cell cycle progression. We showed recently that B-Myb autoregulates its own expression through promoter transactivation. We report in this study that CDK9, the cyclin T associated kinase, which phosphorylates and activates RNA-Polymerase II, suppresses B-Myb autoregulation through direct interaction with the carboxyl-terminus of the B-Myb protein. Down-regulation of the transactivating ability of B-Myb is independent of the kinase activity of CDK9, because a kinase deficient mutant (dn-CDK9) also represses B-myb gene autoregulation. Overexpression of CDK9 did not result in suppression of p53-dependent transactivation or inhibition of the basal activity of the promoters tested so far, demonstrating that CDK9 is a B-Myb-specific repressor. Rather, transfection of the dominant negative dn-CDK9 construct inhibited the basal activity of the reporter genes, confirming an essential role for CDK9 in gene transcription. In addition, Cyclin T1 restores B-Myb transactivating activity when co-transfected along with CDK9, suggesting that the down-regulatory effect observed on B-Myb is specifically due to CDK9 alone. Thus, our data suggest that CDK9 is involved in the negative regulation of activated transcription mediated by certain transcription factors, such as B-Myb. This may indicate the existence of a feedback loop, mediated by the different activities of CDK9, which links basal with activated transcription.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.