|1.||Zhou, Qiang: 8 articles (01/2015 - 02/2004)|
|2.||Shilatifard, Ali: 5 articles (09/2012 - 02/2010)|
|3.||Lin, Chengqi: 5 articles (09/2012 - 02/2010)|
|4.||Luo, Kunxin: 3 articles (01/2015 - 03/2008)|
|5.||Siddiqui, M A Q: 3 articles (11/2012 - 07/2007)|
|6.||Chaqour, Brahim: 3 articles (11/2012 - 07/2007)|
|7.||Smith, Edwin R: 3 articles (12/2011 - 02/2010)|
|8.||He, Nanhai: 3 articles (09/2011 - 03/2008)|
|9.||Lu, Huasong: 2 articles (01/2015 - 01/2014)|
|10.||Xue, Yuhua: 2 articles (01/2015 - 09/2011)|
01/01/2015 - "Because the i-CDK9-induced MYC expression and binding to P-TEFb compensate for P-TEFb's loss of activity, only simultaneously inhibiting CDK9 and MYC/BRD4 can efficiently induce growth arrest and apoptosis of cancer cells, suggesting the potential of a combinatorial treatment strategy. "
01/01/2014 - "Brd4 and HEXIM1: multiple roles in P-TEFb regulation and cancer."
08/01/2010 - "P-TEFb joins the family of cdks in oncology, promotes cell growth of cancer cells."
01/01/2010 - "Abrogation of the interaction between P-TEFb and Brd4 thus provides a mechanism for E2-mediated repression of the viral oncogenes from the integrated viral genomes in cancer cells."
03/14/2008 - "Consistent with the tumor suppressor role of a Drosophila homolog of PIP7S, loss of PIP7S function shifts the P-TEFb equilibrium toward the active state, disrupts epithelial differentiation, and causes P-TEFb-dependent malignant transformation. "
09/24/2010 - "Importantly, P-TEFb directs H1 phosphorylation in response to wild-type HIV-1 infection, but not Tat-mutant HIV-1 infection. "
06/22/1999 - "For this report, we studied the requirement for P-TEFb in HIV-1 infection, and we now show that P-TEFb is both essential and limiting for HIV-1 replication. "
11/01/2010 - "Taken together, this study showed that P-TEFb and DENV core protein work in concert to enhance IL-8 gene expression by DENV infection. "
12/16/2014 - "We propose that SRSF1 activates transcription in the early stages of viral infection by recruiting P-TEFb to TAR from the 7SK snRNP. "
02/01/2012 - "In addition, the HIV-1 Tat protein also releases P-TEFb from the 7SK/HEXIM complex during viral infection to promote viral transcription and replication. "
|3.||Acquired Immunodeficiency Syndrome (AIDS)
01/01/2013 - "These studies define the mechanism of scaffold recognition by P-TEFb and reveal an unanticipated intersubunit pocket on the AFF4 SEC that potentially represents a target for therapeutic intervention against HIV/AIDS. "
06/01/2011 - "Given their roles in HIV-1/AIDS and cancer, further characterization of 7SK snRNP and SEC will help develop strategies to suppress aberrant transcriptional elongation caused by uncontrolled P-TEFb activation. "
05/01/2008 - "CDK9 is the kinase of the TAK complex (Tat-associated kinase complex), and binds to Tat protein of HIV, suggesting a possible role for CDK9 in AIDS progression. "
07/30/2013 - "The positive transcription elongation factor b (P-TEFb) is involved in physiological and pathological events including inflammation, cancer, AIDS, and cardiac hypertrophy. "
08/01/2007 - "Hexamethylene bis-acetamide inducible protein 1 (HEXIM1) is an inhibitor of positive transcription elongation factor b (P-TEFb) that has recently been shown to be involved in cancers, AIDS, cardiac hypertrophy and inflammation. "
|4.||Thymoma (Thymic Carcinoma)
02/01/2008 - "In this study, using looping chromatin immunoprecipitation and chromatin conformation capture assays, we demonstrated that interactions between Runx1 and positive elongation factor b (P-TEFb) appose the silencer and enhancer in CD4-negative thymoma cells and double-negative immature thymocytes. "
|5.||Cardiomegaly (Heart Hypertrophy)
02/01/2012 - "Importantly, cardiac hypertrophy and development of various types of human malignancies have been associated with increased P-TEFb activity, consequence of a disruption of this regulatory equilibrium. "
08/01/2008 - "Thus, P-TEFb activity responds to variations in global cellular transcriptional activity and to physiological conditions linked to cell differentiation, proliferation or cardiac hypertrophy. "
07/01/2007 - "We found that CLP-1 is expressed along with P-TEFb components in developing heart during the period in which knockout mice lacking the CLP-1 gene develop cardiac hypertrophy and die. "
04/01/2009 - "7SK RNA is released from P-TEFb/HEXIM/7SK complexes upon an arrest in transcription and physiological stimulations such as cardiac hypertrophy, leading to P-TEFb activation. "
02/16/2007 - "Through phosphorylation of the C-terminal domain of the RNA polymerase II largest subunit, distinct P-TEFb species regulate the transcriptional elongation of specific genes that play central roles in human physiology and disease development, including cardiac hypertrophy and human immunodeficiency virus-1 pathogenesis. "
|1.||Positive Transcriptional Elongation Factor B
|4.||DNA (Deoxyribonucleic Acid)
|6.||Small Nuclear RNA (snRNA)
|7.||Peptide Elongation Factors (Elongation Factor)
|10.||Interleukin-8 (Interleukin 8)