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1 putative GRIP1 kinases, casein kinase 2 and cyclin-dependent kinase 9.
3 anscription factor b, P-TEFb, is composed of cyclin-dependent kinase 9 and a regulatory cyclin (T1/T2
4 on elongation factor b (P-TEFb), composed of cyclin-dependent kinase 9 and cyclin T1 or T2, is requir
5 on elongation factor b (P-TEFb), composed of cyclin-dependent kinase 9 and cyclin T1, stimulates the
6 general transcription factor IIB (TFIIB) and cyclin-dependent kinase 9 are upregulated during hypertr
7 factor b (P-TEFb), a complex containing the cyclin-dependent kinase 9 (CDK-9) and cyclin T1 subunits
10 vels in primary MEPs, specific inhibition of cyclin dependent kinase 9 (CDK9) in MEPs leads to both d
11 metry was applied to measure the dynamics of cyclin dependent kinase 9 (CDK9) interactomes during tra
12 ranscriptional elongation complex containing cyclin dependent kinase-9 (CDK9; a kinase necessary for
14 on elongation factor b (P-TEFb), composed of cyclin-dependent kinase 9 (CDK9) and cyclin T, is a glob
15 ion factor b (P-TEFb) complexes, composed of cyclin-dependent kinase 9 (CDK9) and cyclin T1 or T2, ar
16 n elongation factor b (P-TEFb), comprised of cyclin-dependent kinase 9 (CDK9) and cyclins T1 (CycT1)
17 This important factor is a heterodimer of cyclin-dependent kinase 9 (Cdk9) and one of four cyclin
19 defined Myc-driven HCC model, we identified cyclin-dependent kinase 9 (Cdk9) as required for disease
21 infection enhances the activated fraction of cyclin-dependent kinase 9 (CDK9) by promoting its associ
22 is thought to require the kinase activity of cyclin-dependent kinase 9 (CDK9) for the phosphorylation
23 lated cyclins T1, T2a, and T2b interact with cyclin-dependent kinase 9 (CDK9) forming multiple nuclea
24 rgeting transcription via regulators such as cyclin-dependent kinase 9 (CDK9) has potential as a ther
26 Previously, two regions phosphorylated by cyclin-dependent kinase 9 (CDK9) in elongation factor SP
33 we examine the role of the Tat/TAR-specified cyclin-dependent kinase 9 (CDK9) kinase activity in regu
34 cleolytic subunit of Integrator, INTS11, and cyclin-dependent kinase 9 (CDK9) maintain directionality
35 f cyclin T1 and concomitant stabilization of cyclin-dependent kinase 9 (CDK9) may facilitate producti
36 phosphorylation of elongation factor Spt5 by cyclin-dependent kinase 9 (Cdk9) occur during transcript
37 t of an IL-6-inducible complex of STAT3 with cyclin-dependent kinase 9 (CDK9) on gamma-FBG expression
40 ress responses by regulating the activity of cyclin-dependent kinase 9 (CDK9), a protein required for
41 a heterodimer of a cyclin-dependent kinase, cyclin-dependent kinase 9 (Cdk9), and one of four cyclin
42 ofactors of HIV-1 Tat, cyclin T1 (CycT1) and cyclin-dependent kinase 9 (CDK9), are required for LTR-d
43 ted at the mammal-specific threonine 1032 by cyclin-dependent kinase 9 (CDK9), dynamically moves alon
44 ding Ras GTPase-activating protein (RasGAP), cyclin-dependent kinase 9 (Cdk9), fibronectin, and Ras h
45 factor b (P-TEFb), containing cyclin T1 and cyclin-dependent kinase 9 (CDK9), interacts with the hum
46 several components of transcription such as cyclin-dependent kinase 9 (cdk9), localize at these site
47 RMC5 and Pol II requires the transcriptional cyclin-dependent kinase 9 (CDK9), supporting a phospho-d
48 and the enhancer regions, and inhibition of cyclin-dependent kinase 9 (CDK9), that regulates these e
51 on and led to higher enzymatic activities of cyclin-dependent kinase 9 (CDK9), which serves as a tran
52 s 9 (H3K9ac) and 56 (H3K56ac), activation of cyclin-dependent kinase 9 (CDK9)-that phosphorylates NEL
59 tivated by HIV-1 Tat protein, which recruits cyclin-dependent kinase 9 (CDK9)/cyclin T1 and other hos
60 ster orthologs of the vertebrate PITSLRE and cyclin-dependent kinase-9 (CDK9) kinases, as Hh regulato
61 horylated at an N-terminal serine cluster by cyclin-dependent kinase-9 (CDK9), which is recruited int
62 he role of an isoform of the multifunctional cyclin-dependent kinase 9, CDK9-55, in DNA repair, by ge
63 longation factor b (P-TEFb), consisting of a cyclin-dependent kinase 9-cyclin T heterodimer, stimulat
64 anscriptional elongation by sequestering the cyclin dependent kinase 9/cyclin T1 (CDK9/CCNT1) positiv
65 II transcriptional elongation factor P-TEFb (cyclin-dependent kinase 9/cyclin T) is a cellular protei
67 y, we found that Thr 4 was phosphorylated by cyclin-dependent kinase 9 in cells and dephosphorylated
69 pression of HIV-1 transcription by selective cyclin-dependent kinase-9 inhibitors may be a useful the
70 roscovitine, newly identified inhibitors of cyclin-dependent kinase-9, markedly decrease HIV-1 promo
71 e inhibitors of the transcription regulating cyclin-dependent kinase 9 on the development and progres
72 h the diapause-like adaptation by inhibiting cyclin-dependent kinase 9 represent potential therapeuti
73 (P-TEFb) is composed of cyclins T1 or T2 and cyclin-dependent kinase 9 that regulate the elongation p
74 either by expression of a dominant-negative cyclin-dependent kinase 9 transgene or through the use o
75 hat in a cohort of 46 patients with HB, high cyclin-dependent kinase 9 tumor expression was significa
76 FF4-CHD as a substrate for the P-TEFb kinase cyclin-dependent kinase 9, which triggers release of pol