PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33586776-4	2021	This approach has been put forward for exploration based on the activity of didehydro-cortistatin A, an inhibitor of the HIV transcriptional activator Tat.	didehydro-cortistatin A	76-99	tyrosine aminotransferase	Homo sapiens	151-154
33586776-5	2021	Here we review the mechanisms by which didehydro-cortistatin A inhibition of Tat"s feedback loop transcriptional amplification results in epigenetic silencing of the HIV promoter, and we discuss the benefits and limitations of the block-and-lock approach for an HIV cure.	didehydro-cortistatin A	39-62	tyrosine aminotransferase	Homo sapiens	77-80
32276443-7	2020	Two small molecules, didehydro-cortistatin A (dCA) and triptolide, inhibit Tat by different mechanisms: dCA through direct binding and triptolide through enhanced proteasomal degradation.	didehydro-cortistatin A	104-107	tyrosine aminotransferase	Homo sapiens	75-78
31717492-7	2019	In cell-based assays for CDK8 and CDK19 inhibition, Cmpd3, Cmpd4, dCA and 15w showed similar low-nanomolar potency and efficacy against CDK8 and CDK19, while Senexin B was less potent.	didehydro-cortistatin A	66-69	cyclin-dependent kinase 8	Danio rerio	136-140
32276443-7	2020	Two small molecules, didehydro-cortistatin A (dCA) and triptolide, inhibit Tat by different mechanisms: dCA through direct binding and triptolide through enhanced proteasomal degradation.	didehydro-cortistatin A	21-44	tyrosine aminotransferase	Homo sapiens	75-78
32276443-7	2020	Two small molecules, didehydro-cortistatin A (dCA) and triptolide, inhibit Tat by different mechanisms: dCA through direct binding and triptolide through enhanced proteasomal degradation.	didehydro-cortistatin A	46-49	tyrosine aminotransferase	Homo sapiens	75-78
31717492-7	2019	In cell-based assays for CDK8 and CDK19 inhibition, Cmpd3, Cmpd4, dCA and 15w showed similar low-nanomolar potency and efficacy against CDK8 and CDK19, while Senexin B was less potent.	didehydro-cortistatin A	66-69	cyclin-dependent kinase 19	Danio rerio	145-150
31717492-8	2019	Only dCA produced sustained inhibition of CDK8/19-dependent gene expression.	didehydro-cortistatin A	5-8	cyclin-dependent kinase 8	Danio rerio	42-46
31289189-0	2019	Unexpected Mutations in HIV-1 That Confer Resistance to the Tat Inhibitor Didehydro-Cortistatin A.	didehydro-cortistatin A	74-97	Tat	Human immunodeficiency virus 1	60-63
31266880-2	2019	The Tat inhibitor didehydro-cortistatin A (dCA) promotes a state of persistent latency, refractory to viral reactivation.	didehydro-cortistatin A	18-41	tyrosine aminotransferase	Homo sapiens	4-7
31266880-2	2019	The Tat inhibitor didehydro-cortistatin A (dCA) promotes a state of persistent latency, refractory to viral reactivation.	didehydro-cortistatin A	43-46	tyrosine aminotransferase	Homo sapiens	4-7
31266880-10	2019	Didehydro-cortistatin A (dCA) is a potent Tat inhibitor, reducing HIV-1 transcription and preventing viral rebound.	didehydro-cortistatin A	0-23	tyrosine aminotransferase	Homo sapiens	42-45
31266880-10	2019	Didehydro-cortistatin A (dCA) is a potent Tat inhibitor, reducing HIV-1 transcription and preventing viral rebound.	didehydro-cortistatin A	25-28	tyrosine aminotransferase	Homo sapiens	42-45
31289189-1	2019	Didehydro-cortistatin A (dCA) is a human immunodeficiency virus type 1 (HIV-1) Tat inhibitor that functions by selectively binding to the RNA binding domain of Tat.	didehydro-cortistatin A	0-23	Tat	Human immunodeficiency virus 1	79-82
31289189-1	2019	Didehydro-cortistatin A (dCA) is a human immunodeficiency virus type 1 (HIV-1) Tat inhibitor that functions by selectively binding to the RNA binding domain of Tat.	didehydro-cortistatin A	25-28	Tat	Human immunodeficiency virus 1	79-82
31289189-7	2019	dCA holds promise for strategies to achieve a functional cure of HIV-1 infection and justifies efforts to develop additional Tat inhibitors.	didehydro-cortistatin A	0-3	Tat	Human immunodeficiency virus 1	125-128
31021670-0	2019	The Tat inhibitor didehydro-cortistatin A suppresses SIV replication and reactivation.	didehydro-cortistatin A	18-41	tyrosine aminotransferase	Homo sapiens	4-7
31021670-3	2019	We reported that didehydro-cortistatin A (dCA) inhibits HIV-1 Tat activity.	didehydro-cortistatin A	17-40	tyrosine aminotransferase	Homo sapiens	62-65
31021670-3	2019	We reported that didehydro-cortistatin A (dCA) inhibits HIV-1 Tat activity.	didehydro-cortistatin A	42-45	tyrosine aminotransferase	Homo sapiens	62-65
31021670-7	2019	Here, we demonstrate, using in vitro and cell-based assays, that dCA directly binds to SIV Tat"s basic domain.	didehydro-cortistatin A	65-68	tyrosine aminotransferase	Homo sapiens	91-94
31021670-8	2019	dCA specifically inhibits SIV Tat binding to TAR, but not a Tat-Rev fusion protein, which activates transcription when Rev binds to its cognate RNA binding site replacing the apical region of TAR.	didehydro-cortistatin A	0-3	tyrosine aminotransferase	Homo sapiens	30-33
29045830-2	2017	We postulated a "block-and-lock" functional cure approach based on properties of the Tat inhibitor didehydro-Cortistatin A (dCA).	didehydro-cortistatin A	99-122	tyrosine aminotransferase	Homo sapiens	85-88
30992052-0	2019	Tat inhibition by didehydro-Cortistatin A promotes heterochromatin formation at the HIV-1 long terminal repeat.	didehydro-cortistatin A	18-41	Tat	Human immunodeficiency virus 1	0-3
30992052-3	2019	The Tat inhibitor didehydro-Cortistatin A (dCA) inhibits transcription and overtime, the lack of low-grade transcriptional events, triggers epigenetic changes at the latent loci that "lock" HIV transcription in a latent state.	didehydro-cortistatin A	18-41	tyrosine aminotransferase	Homo sapiens	4-7
30992052-3	2019	The Tat inhibitor didehydro-Cortistatin A (dCA) inhibits transcription and overtime, the lack of low-grade transcriptional events, triggers epigenetic changes at the latent loci that "lock" HIV transcription in a latent state.	didehydro-cortistatin A	43-46	tyrosine aminotransferase	Homo sapiens	4-7
30992052-9	2019	CONCLUSIONS: We characterized the dCA-mediated epigenetic signature on the HIV genome, which translates into potent blocking effects on HIV expression, further strengthening the potential of Tat inhibitors in "block-and-lock" functional cure approaches.	didehydro-cortistatin A	34-37	tyrosine aminotransferase	Homo sapiens	191-194
30723126-7	2019	These features are distinct from the ones required for inhibition of cyclin-dependent kinase 8 (CDK8), the only other known ligand of dCA.	didehydro-cortistatin A	134-137	cyclin dependent kinase 8	Homo sapiens	69-94
30723126-7	2019	These features are distinct from the ones required for inhibition of cyclin-dependent kinase 8 (CDK8), the only other known ligand of dCA.	didehydro-cortistatin A	134-137	cyclin dependent kinase 8	Homo sapiens	96-100
30723126-17	2019	dCA features required for Tat inhibition are distinct from features needed for inhibition of cyclin-dependent kinase 8 (CDK8), the only other known target of dCA.	didehydro-cortistatin A	158-161	cyclin dependent kinase 8	Homo sapiens	93-118
30723126-17	2019	dCA features required for Tat inhibition are distinct from features needed for inhibition of cyclin-dependent kinase 8 (CDK8), the only other known target of dCA.	didehydro-cortistatin A	158-161	cyclin dependent kinase 8	Homo sapiens	120-124
29045830-2	2017	We postulated a "block-and-lock" functional cure approach based on properties of the Tat inhibitor didehydro-Cortistatin A (dCA).	didehydro-cortistatin A	124-127	tyrosine aminotransferase	Homo sapiens	85-88
26152583-0	2015	The Tat Inhibitor Didehydro-Cortistatin A Prevents HIV-1 Reactivation from Latency.	didehydro-cortistatin A	18-41	Tat	Human immunodeficiency virus 1	4-7
26152583-3	2015	Here we show that the Tat inhibitor didehydro-cortistatin A (dCA), unlike other antiretrovirals, reduces residual levels of viral transcription in several models of HIV latency, breaks the Tat-mediated transcriptional feedback loop, and establishes a nearly permanent state of latency, which greatly diminishes the capacity for virus reactivation.	didehydro-cortistatin A	36-59	tyrosine aminotransferase	Homo sapiens	22-25
26152583-3	2015	Here we show that the Tat inhibitor didehydro-cortistatin A (dCA), unlike other antiretrovirals, reduces residual levels of viral transcription in several models of HIV latency, breaks the Tat-mediated transcriptional feedback loop, and establishes a nearly permanent state of latency, which greatly diminishes the capacity for virus reactivation.	didehydro-cortistatin A	36-59	tyrosine aminotransferase	Homo sapiens	189-192
26152583-3	2015	Here we show that the Tat inhibitor didehydro-cortistatin A (dCA), unlike other antiretrovirals, reduces residual levels of viral transcription in several models of HIV latency, breaks the Tat-mediated transcriptional feedback loop, and establishes a nearly permanent state of latency, which greatly diminishes the capacity for virus reactivation.	didehydro-cortistatin A	61-64	tyrosine aminotransferase	Homo sapiens	22-25
26152583-3	2015	Here we show that the Tat inhibitor didehydro-cortistatin A (dCA), unlike other antiretrovirals, reduces residual levels of viral transcription in several models of HIV latency, breaks the Tat-mediated transcriptional feedback loop, and establishes a nearly permanent state of latency, which greatly diminishes the capacity for virus reactivation.	didehydro-cortistatin A	61-64	tyrosine aminotransferase	Homo sapiens	189-192
26152583-5	2015	Critically, dCA inhibits viral reactivation upon CD3/CD28 or prostratin stimulation of latently infected CD4(+) T cells from HIV-infected subjects receiving suppressive ART.	didehydro-cortistatin A	12-15	CD28 molecule	Homo sapiens	53-57
26152583-5	2015	Critically, dCA inhibits viral reactivation upon CD3/CD28 or prostratin stimulation of latently infected CD4(+) T cells from HIV-infected subjects receiving suppressive ART.	didehydro-cortistatin A	12-15	CD4 molecule	Homo sapiens	105-108
26152583-8	2015	Based on the mode of action of didehydro-cortistatin A (dCA), a Tat-dependent transcription inhibitor, our work highlights an alternative approach to current HIV-1 eradication strategies to decrease the latent reservoir.	didehydro-cortistatin A	31-54	Tat	Human immunodeficiency virus 1	64-67
26152583-8	2015	Based on the mode of action of didehydro-cortistatin A (dCA), a Tat-dependent transcription inhibitor, our work highlights an alternative approach to current HIV-1 eradication strategies to decrease the latent reservoir.	didehydro-cortistatin A	56-59	Tat	Human immunodeficiency virus 1	64-67
26152583-9	2015	In our model, dCA blocks the Tat feedback loop initiated after low-level basal reactivation, blocking transcriptional elongation and hence viral production from latently infected cells.	didehydro-cortistatin A	14-17	tyrosine aminotransferase	Homo sapiens	29-32
25613133-5	2015	In addition, dCA potently inhibits Tat mediated dysregulation of IL-1beta, TNF-alpha and MCP-1, key neuroinflammatory signaling proteins.	didehydro-cortistatin A	13-16	interleukin 1 beta	Homo sapiens	65-73
25613133-5	2015	In addition, dCA potently inhibits Tat mediated dysregulation of IL-1beta, TNF-alpha and MCP-1, key neuroinflammatory signaling proteins.	didehydro-cortistatin A	13-16	tumor necrosis factor	Homo sapiens	75-84
25613133-5	2015	In addition, dCA potently inhibits Tat mediated dysregulation of IL-1beta, TNF-alpha and MCP-1, key neuroinflammatory signaling proteins.	didehydro-cortistatin A	13-16	C-C motif chemokine ligand 2	Homo sapiens	89-94
22817991-5	2012	Importantly, dCA abrogates spontaneous viral particle release from CD4(+)T cells from virally suppressed subjects on highly active antiretroviral therapy (HAART).	didehydro-cortistatin A	13-16	CD4 molecule	Homo sapiens	67-70