Affinage

CCNT1

Cyclin-T1 · UniProt O60563

Length
726 aa
Mass
80.7 kDa
Annotated
2026-06-09
91 papers in source corpus 38 papers cited in narrative 38 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CCNT1 (Cyclin T1) is the regulatory cyclin subunit of the P-TEFb kinase complex, which drives RNA polymerase II transcription elongation, and is the host cofactor that is absolutely required for HIV-1 latency reversal (PMID:37766271, PMID:10393900). CycT1 partners with the kinase CDK9, and a histidine-rich stretch in its C-terminal region (residues 481-551) directly binds the RNAPII CTD, an interaction required for P-TEFb to activate productive elongation (PMID:11739744); the same CTD-binding region is the target of repressive CTD analogs and the elongation repressor PIE-1 (PMID:12651893). In HIV-1, the cyclin domain of CycT1 is necessary and sufficient to bind Tat and to cooperatively engage TAR RNA through a conformationally flexible Tat-TAR recognition motif (TRM) at the C-terminal edge of the cyclin domain, a zinc-dependent interaction requiring Cys261 (PMID:9832504, PMID:14972556, PMID:12009901); recruitment of CycT1/P-TEFb is the sole rate-limiting event, since artificial tethering of CycT1 renders Tat and TAR dispensable (PMID:10393900). High-resolution structures define how the TRM, Tat, and the SEC scaffold AFF4 assemble cooperatively on TAR, with AFF4 ordering the TRM and increasing TAR affinity, and CDK9 autophosphorylation gating high-affinity complex formation (PMID:23471103, PMID:24843025, PMID:27731797, PMID:30514815, PMID:10958691). P-TEFb availability is controlled by a layered regulatory network: PKC-mediated phosphorylation of CycT1 promotes CDK9 binding while PP1 reverses it (PMID:34821217), free CycT1 not bound to CDK9 is ubiquitinated and degraded by Siah1/Siah2 (PMID:35524561), CycT1 is sequestered in the inhibitory 7SK snRNP via a combinatorial CycT1-HEXIM1 surface (PMID:24917669, PMID:15992410), and stress- or cell-cycle-triggered dissociation allows Brd4/SEC-driven reassembly of active P-TEFb on chromatin (PMID:34935961). Following DNA damage, PARP1 poly(ADP-ribosyl)ates CycT1 histidine residues, disrupting its liquid-liquid phase separation and stalling elongation, a mechanism co-opted in radioresistant nasopharyngeal carcinoma (PMID:35393539, PMID:37407287). Beyond viral and transcriptional roles, CCNT1 is synthetically lethal with TSC1/TSC2 loss (PMID:26350902) and required for Th1 and short-lived effector CTL differentiation (PMID:25148027).

Mechanistic history

Synthesis pass · year-by-year structured walk · 28 steps
  1. 1998 High

    Established the molecular basis for HIV-1 Tat function by showing CycT1's cyclin domain is the species-specific host factor that bridges Tat to TAR RNA, explaining the human-specific permissiveness of HIV transcription.

    Evidence Alanine-scanning mutagenesis, in vitro binding/co-IP, TAR binding and transactivation reporters, with cross-species (human vs murine CycT1) comparison

    PMID:9832504

    Open questions at the time
    • Structural geometry of the ternary complex not resolved
    • Role within general (non-viral) transcription not yet addressed
  2. 1999 High

    Defined the epistatic position of CycT1 by showing recruitment of CycT1/P-TEFb is the sole rate-limiting step, making Tat and TAR dispensable when CycT1 is tethered directly.

    Evidence Artificial RNA tethering, nuclear run-on, dominant-negative CDK9-binding mutants, reporter assays

    PMID:10393900

    Open questions at the time
    • Endogenous recruitment mechanism at native promoters not addressed
    • Identity of CTD-contacting region not yet mapped
  3. 2000 High

    Showed that CDK9 autophosphorylation licenses high-affinity Tat-P-TEFb-TAR assembly and that the CycT1 C-terminus masks Tat-TAR binding until phosphorylation occurs, coupling kinase activity to complex formation.

    Evidence In vitro kinase assays, phosphomimetic mutations, ATP-dependency TAR binding assays

    PMID:10958691

    Open questions at the time
    • Precise phosphosites unmapped at this stage
    • In vivo relevance of masking not demonstrated
  4. 2002 Medium

    Identified the histidine-rich C-terminal region of CycT1 (481-551) as the direct RNAPII CTD-binding module required for productive elongation, linking CycT1 architecture to its core transcriptional output.

    Evidence DNA tethering with deletion/chimera constructs and transcription reporters

    PMID:11739744

    Open questions at the time
    • Single-lab functional mapping without structural confirmation
    • Phospho-dependence of CTD contact not defined
  5. 2002 Medium

    Mapped the molecular contacts of the Tat-CycT1-TAR ternary complex, showing CycT1 loop residues contact the TAR loop and that assembly is highly cooperative with nanomolar affinity, establishing TAR as a scaffold.

    Evidence Photocross-linking, footprinting, EMSA with comprehensive TAR loop mutants and quantitative binding analysis

    PMID:12009901 PMID:12048247

    Open questions at the time
    • Atomic-resolution structure not yet available
    • Conformational changes inferred indirectly
  6. 2002 Medium

    Revealed an alternative DNA/Sp1-dependent route for P-TEFb to activate the HIV LTR, distinct from the RNA-based Tat/TAR pathway, broadening the recruitment logic of CycT1.

    Evidence DNA tethering of CycT1, Sp1 depletion/rescue, reporters in murine cells

    PMID:12458222

    Open questions at the time
    • Physiological prevalence of the Sp1 route unclear
    • Mechanism of Sp1-CycT1 connection not defined
  7. 2003 Medium

    Demonstrated that the CycT1 CTD-binding region is itself a regulatory target, since CTD analogs and the repressor PIE-1 bind it to block elongation, identifying a mode of P-TEFb inhibition.

    Evidence CTD analog competition, tethering reporters, PIE-1 pulldown/binding

    PMID:12651893

    Open questions at the time
    • Whether endogenous repressors use this surface in mammals unaddressed
    • Single-lab functional study
  8. 2004 Medium

    Provided biophysical evidence that the CycT1 TRM is intrinsically flexible/disordered in isolation, supporting a coupled folding-binding model for ternary complex assembly and confirming Cys261's role in metal-dependent assembly.

    Evidence Partial proteolysis, circular dichroism, TRM mutagenesis

    PMID:14972556

    Open questions at the time
    • Disorder shown only for isolated domain
    • Folding transition not captured structurally
  9. 2004 High

    Placed CycT1/P-TEFb within physiological signaling by showing its recruitment with Notch ICD and Mastermind to the HES1 promoter as the elongation arm of Notch transcriptional output.

    Evidence ChIP, Co-IP, in vitro kinase assay (CycC:CDK8 on Notch), mutagenesis, immunofluorescence

    PMID:15546612

    Open questions at the time
    • Direct CycT1 contribution inferred from recruitment, not biochemical necessity
    • Generality across Notch targets not tested
  10. 2008 High

    Solved the CDK9/CycT1 crystal structure, revealing a distinctive ~26° cyclin rotation and a flexible CycT1 C-terminal helix, and demonstrated cis autophosphorylation on T186 plus C-terminal sites.

    Evidence X-ray crystallography and autophosphorylation assays with recombinant complex

    PMID:18566585

    Open questions at the time
    • TRM and full C-terminus not resolved in structure
    • How flexibility enables regulatory interactions shown only indirectly
  11. 2008 High

    Identified the splicing factor SC35 as an upstream factor facilitating P-TEFb recruitment, connecting CycT1/CDK9 elongation activity to splicing machinery via CTD Ser2 phosphorylation.

    Evidence siRNA depletion, ChIP, nuclear run-on, recombinant SC35 rescue

    PMID:18641664

    Open questions at the time
    • Direct SC35-CycT1 contact not established
    • Genome-wide scope of SC35-P-TEFb dependence not mapped
  12. 2009 High

    Showed that PCAF acetylation of Tat tunes ternary complex affinity at the CycT1 TRM, linking post-translational modification of the viral partner to CycT1-dependent elongation efficiency.

    Evidence Acetylation assays, ternary complex assembly, in vitro elongation, reporters, viral replication with compensatory mutations

    PMID:19223581

    Open questions at the time
    • Acetylation effect specific to HIV-1 Tat
    • Structural basis of acetyl-TRM enhancement not resolved here
  13. 2012 Medium

    Identified AFF4 as the SEC scaffold that directly binds CycT1 through short hydrophobic regions, establishing CycT1 as the bridging subunit linking P-TEFb to the larger super elongation complex.

    Evidence In vitro and in vivo binding/co-IP mapping of contact regions

    PMID:23251033

    Open questions at the time
    • Structural detail of interface not yet defined at this stage
    • Functional consequence on TAR binding not quantified
  14. 2013 High

    Resolved the P-TEFb-AFF4 interface crystallographically, showing AFF4 contacts only CycT1 and not CDK9 and is positioned to engage Tat, explaining how the SEC organizes around the cyclin surface.

    Evidence X-ray crystallography, interface mutagenesis, transcription reporters, binding assays

    PMID:23471103

    Open questions at the time
    • TAR RNA not included in this structure
    • TRM ordering by AFF4 not yet demonstrated
  15. 2014 High

    Demonstrated that AFF4 binding allosterically orders the CycT1 TRM and increases Tat-P-TEFb affinity for TAR ~30-fold, providing the structural mechanism for SEC preference in HIV transcription.

    Evidence Crystallography of the quaternary complex, quantitative TAR binding, AFF1/AFF4 interface mutagenesis, reporters

    PMID:24843025

    Open questions at the time
    • TAR RNA modeled but not co-crystallized at high resolution here
    • Dynamics of TRM ordering inferred
  16. 2014 Medium

    Defined Val107 in the N-terminal cyclin box as essential for P-TEFb assembly with CDK9, HEXIM1, and 7SK while sparing AFF4 binding, separating assembly from scaffold engagement and providing a latency-enforcing mutant.

    Evidence Mutagenesis, co-IP/pulldown for multiple partners, HIV replication/latency assays in primary CD4+ T cells

    PMID:24985467

    Open questions at the time
    • Structural basis of V107 selectivity not resolved
    • Single-lab mutant characterization
  17. 2014 Medium

    Mapped the combinatorial CycT1-HEXIM1 surface on 7SK stem-loop I, establishing how the 7SK snRNP inhibits CDK9 kinase activity through CycT1 contacts.

    Evidence RNA tethering cell-based assay with HEXIM1/CycT1 7SK-binding mutants and reporters

    PMID:24917669

    Open questions at the time
    • Atomic structure of the 7SK-HEXIM1-CycT1 surface not determined
    • Cell-based genetic readout indirect
  18. 2016 High

    Delivered an integrative structure of the Tat-P-TEFb-AFF4-TAR complex, showing the TAR loop simultaneously contacts the CycT1 TRM and Tat zinc loop and that AFF4 helix 2 stabilization underlies enhanced TAR binding.

    Evidence Cryo-EM/crystallography at 5.9 Å, HDX, SHAPE, SAXS, binding assays

    PMID:27731797

    Open questions at the time
    • Limited resolution for side-chain detail
    • Dynamics during transcription cycle not captured
  19. 2018 High

    Refined the TAR-TRM interface to 3.5 Å, showing TAR loop-CycT1 TRM contacts dominate over Tat ARM-bulge interactions, redefining the affinity determinants of the complex.

    Evidence X-ray crystallography, TRM/Tat mutational analysis, binding assays

    PMID:30514815

    Open questions at the time
    • Full SEC context not in structure
    • Conformational dynamics not addressed
  20. 2018 High

    Established kinase-cascade and chaperone control of P-TEFb assembly: CDK7 phosphorylates CDK9 Ser175 for Tat binding, T186 phosphorylation stabilizes the CDK9/CycT1 interface via E96 of CycT1, and Hsp90/Cdc37 buffer unassembled CDK9.

    Evidence MD simulations, CDK7 inhibitor THZ1, in vitro kinase assays, co-IP, Hsp90 inhibition, arginine-triad mutagenesis

    PMID:29743242

    Open questions at the time
    • In vivo dynamics of the chaperone-assembly cycle not fully resolved
    • CycT1-specific phospho-regulation not separated here
  21. 2021 High

    Identified a PKC-PP1 phosphorylation switch on CycT1 that toggles P-TEFb assembly, explaining loss of P-TEFb in resting and anergic T cells through CycT1 destabilization.

    Evidence PKC inhibitors, PP1 dephosphorylation, degradation assays, co-IP in primary cells

    PMID:34821217

    Open questions at the time
    • Exact CycT1 PKC phosphosites not enumerated here
    • Coupling to degradation machinery defined separately
  22. 2022 High

    Identified Siah1/Siah2 as the E3 ligases degrading free CycT1 via its N-terminal region, defining the proteostatic mechanism that limits P-TEFb in resting cells.

    Evidence Ubiquitination mapping, domain deletion, Siah1/2 inhibition, co-IP, primary cell rescue

    PMID:35524561

    Open questions at the time
    • Upstream signals controlling Siah activity not defined
    • Specific degron lysines among the six not individually resolved
  23. 2022 Medium

    Showed that P-TEFb fully dissociates into monomers under stress and is reassembled on chromatin by Brd4/SEC with CDK9 T186 autophosphorylation, defining a stepwise activation route shared with G1 entry.

    Evidence Fractionation, co-IP, ChIP, nocodazole synchronization, stress treatment, pulldowns

    PMID:34935961

    Open questions at the time
    • Single-lab reassembly model
    • Quantitative kinetics of monomer pools not established
  24. 2022 High

    Revealed that PARP1 poly(ADP-ribosyl)ates CycT1 histidine residues after DNA damage, disrupting CycT1 phase separation and stalling elongation to favor DNA repair and survival.

    Evidence PARP1 binding, PARylation site mapping, phase separation assays, Pol II phosphorylation, survival assays

    PMID:35393539

    Open questions at the time
    • Composition of CycT1 condensates not fully defined
    • Reversal/erasure of the modification not characterized
  25. 2023 High

    Established by CRISPR knockout that CCNT1 is dispensable for T cell biology yet absolutely required for HIV-1 latency reversal, nominating it as a host-directed target whose loss does not perturb the host transcriptome.

    Evidence CRISPR knockout in primary CD4+ T cells and latent cell lines, RNA-seq, multiple latency reversal agents

    PMID:37766271

    Open questions at the time
    • Apparent host transcriptome neutrality contrasts with developmental roles elsewhere
    • Compensation by paralogs not examined
  26. 2023 Medium

    Connected EGF signaling to P-TEFb release via METTL3-dependent m6A methylation of 7SK, defining an RNA-methylation switch controlling availability of CycT1-containing P-TEFb.

    Evidence METTL3 phosphorylation, 7SK methylation, P-TEFb release and elongation assays, EGF pathway analysis

    PMID:37163588

    Open questions at the time
    • Not independently replicated
    • Direct effect on CycT1 versus snRNP architecture not separated
  27. 2024 Medium

    Extended the PARylation-phase separation axis to oncology, showing elevated CycT1 PARylation enforces RNAPII pausing and radioresistance in nasopharyngeal carcinoma, reversible by mutating PARylation sites.

    Evidence ChIP-seq, CycT1 PARylation-site mutation, RNAPII pausing analysis, IR resistance assays in NPC cells

    PMID:37407287

    Open questions at the time
    • Single-lab oncology extension
    • Therapeutic targetability not tested in vivo
  28. 2026 Medium

    Uncovered a hypoxia-specific, HIF-independent chromatin role for CycT1 in complex with nuclear Tim8-Tim13 chaperones and BHLHE40, implicating CycT1 in the acute hypoxic transcriptional response.

    Evidence Biochemical purification, co-IP across multiple cell lines, Tim8-Tim13 disruption, BHLHE40 knockdown, transcription assays

    PMID:42160428

    Open questions at the time
    • Newly reported, single lab
    • Mechanism linking CycT1 to hypoxic gene selection unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CycT1 phase separation, partner selection (7SK/SEC/Brd4), and post-translational switches are integrated to direct gene-specific elongation in physiological (non-viral) contexts remains unresolved.
  • Endogenous gene targets of CycT1-driven elongation largely uncatalogued
  • How competing regulatory inputs (PKC/PP1, Siah, PARP1, 7SK) are coordinated in vivo is unknown
  • Physiological role of the hypoxia and developmental interactions mechanistically incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 5 GO:0098772 molecular function regulator activity 4 GO:0140110 transcription regulator activity 3
Localization
GO:0005634 nucleus 4 GO:0005694 chromosome 3
Pathway
R-HSA-1643685 Disease 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-168256 Immune System 2 R-HSA-73894 DNA Repair 2
Partners
AFF4BHLHE40BRD4CDK9HEXIM1PARP1SIAH1TAT (HIV-1)
Complex memberships
7SK snRNPP-TEFb (CDK9/CycT1)super elongation complex (SEC)

Evidence

Reading pass · 38 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 The cyclin domain of human CycT1 is necessary and sufficient to interact with HIV-1 Tat and promote cooperative binding to TAR RNA in vitro and mediate Tat transactivation in vivo. A Tat-TAR recognition motif (TRM) was identified at the carboxy-terminal edge of the cyclin domain. The interaction between Tat and hCycT1 requires zinc and essential cysteine residues in both proteins (C261 in hCycT1); murine CycT1 lacks C261 and forms only a weak, zinc-independent complex with HIV-1 Tat. A point mutation in mCycT1 (Y261C) restores high-affinity, zinc-dependent binding to Tat and TAR in vitro and rescues Tat transactivation in vivo. hCycT1 can interact simultaneously with Tat and CDK9 on TAR RNA in vitro. Alanine-scanning mutagenesis, in vitro binding/co-IP, TAR RNA binding assays, transactivation reporter assays, cloning and characterization of murine CycT1 Genes & development High 9832504
1999 Recruitment of CycT1/P-TEFb to the HIV-1 LTR promoter-proximal RNA target is fully sufficient to activate transcription elongation from that promoter; Tat and TAR become dispensable when CycT1 is artificially tethered. Activation by CycT1 required the ability to bind the CDK9 component of P-TEFb. The sole role of the Tat/TAR axis is to permit recruitment of CycT1/P-TEFb. Artificial RNA tethering assay, reporter gene assays, dominant-negative CDK9 binding mutants, nuclear run-on transcription assays Proceedings of the National Academy of Sciences of the United States of America High 10393900
2000 CDK9 autophosphorylation at multiple C-terminal Ser/Thr residues is required for high-affinity binding of the Tat-P-TEFb complex to TAR RNA. The C-terminal half of CycT1 (beyond residue 303) masks Tat-TAR binding in the absence of ATP/phosphorylation; full-length CycT1 (1-728) is also phosphorylated by CDK9. Replacing CDK9 phosphorylation sites with negatively charged residues restores TAR binding to a catalytically inactive CDK9 mutant. P-TEFb also phosphorylates RNA polymerase II CTD substrates in vitro. In vitro kinase assays, TAR RNA binding assays, ATP-dependency studies, phosphomimetic mutations, affinity-purified complexes Molecular and cellular biology High 10958691
2002 The histidine-rich stretch in the C-terminal region of CycT1 (positions 481-551) directly binds the CTD of RNA polymerase II, and this binding is required for P-TEFb to activate transcription of full-length transcripts from target genes when tethered to DNA upstream or downstream of promoters. Tethering assay to DNA, deletion/chimera constructs of CycT1 C-terminus, transcriptional activation reporter assays Molecular and cellular biology Medium 11739744
2002 TAR RNA loop residues 252-260 of CycT1 directly contact the TAR RNA loop, enhancing the interaction of Tat residue K50 with the opposite side of the loop, as shown by systematic RNA-protein photocross-linking and protein footprinting. TAR RNA provides a scaffold for assembly of the Tat-CycT1 regulatory complex. RNA-protein photocross-linking, Western blot analysis, protein footprinting Proceedings of the National Academy of Sciences of the United States of America Medium 12048247
2002 CycT1-Tat binding to TAR RNA is highly cooperative (Hill coefficient 2.7, KD ~2.45 nM for the ternary complex). CycT1 does not bind TAR RNA in the absence of Tat. The C30-G34 base pair and functional groups O6 and N7 at positions 32 and 34 in the TAR loop are essential for CycT1-Tat interactions with TAR RNA. Gel electrophoresis mobility shift assay with comprehensive TAR loop mutants, quantitative binding analysis Biochemistry Medium 12009901
2002 Both human and murine CycT1, when DNA-tethered, can activate the HIV-1 LTR in a Tat- and TAR-independent manner, and this activity requires Sp1. This demonstrates that P-TEFb can stimulate HIV-1 LTR transcription via a DNA/Sp1-dependent mechanism distinct from the RNA-based Tat/TAR pathway. DNA tethering of CycT1, Sp1 depletion/rescue, reporter assays in murine cells The Journal of biological chemistry Medium 12458222
2003 CTD analog heptapeptide repeats containing alanine substitutions (non-phosphorylatable) bind CycT1 via its histidine-rich region and block P-TEFb-mediated transcription elongation when placed near transcription units. The C. elegans transcriptional repressor PIE-1 similarly binds CycT1 via an alanine-containing heptapeptide repeat to inhibit transcriptional elongation. CTD analog competition, tethering reporter assays, pulldown/binding assays with PIE-1 Genes & development Medium 12651893
2004 CycC:CDK8 (not CycT1:CDK9/P-TEFb) phosphorylates the Notch ICD within its TAD and PEST domains; Mastermind (MAM) interacts directly with CDK8 and recruits both CycC:CDK8 and CycT1:CDK9/P-TEFb to the HES1 promoter. CycT1:CDK9/P-TEFb is recruited with Notch and coactivators to HES1 in signaling cells as part of the transcription elongation machinery. Chromatin immunoprecipitation (ChIP), Co-IP, recombinant CycC:CDK8 in vitro kinase assay on Notch ICD, point mutations of PEST Ser residues, subnuclear localization by immunofluorescence Molecular cell High 15546612
2004 The TRM (Tat-TAR recognition motif) region of CycT1 (C-terminal ~20 residues of the cyclin domain) is conformationally flexible or disordered in isolation, as assessed by partial proteolysis and circular dichroism, suggesting that conformational rearrangements accompany CycT1-Tat-TAR ternary complex formation. A cysteine at position 261 (absent in bovine CycT1) is required for metal binding in HIV ternary complex formation. Partial proteolysis, circular dichroism spectroscopy, mutagenesis of TRM residues Virology Medium 14972556
2008 Crystal structure of CDK9/CycT1 determined at high resolution. CycT1 is rotated ~26° relative to CDK9 compared to CDK2/CycA, showing plasticity in CDK-cyclin interactions. CDK9 autophosphorylates on Thr186 in the activation segment and three C-terminal sites; all autophosphorylation occurs in cis. The CycT1 C-terminal helix is flexible, which may be important for interactions with HIV TAT and HEXIM. X-ray crystallography, autophosphorylation assays with recombinant CDK9/CycT1 The EMBO journal High 18566585
2008 SC35 (splicing factor) affects transcriptional elongation by facilitating P-TEFb (CycT1-CDK9) recruitment to target genes. SC35 depletion induced Pol II accumulation within gene bodies, reduced CTD Ser2 phosphorylation, and was correlated with defective P-TEFb recruitment. Recombinant SC35 rescued the elongation defect in nuclear run-on experiments. siRNA depletion, ChIP, nuclear run-on, recombinant SC35 rescue, CTD phosphorylation analysis Nature structural & molecular biology High 18641664
2009 Tat acetylation of Lys-28 by PCAF modulates the affinity and stability of HIV-1 Tat-CycT1-TAR complexes by enhancing interaction with the CycT1 Tat-TAR recognition motif (TRM). High-affinity assembly of the ternary complex correlates strongly with stimulation of transcription elongation in vitro and Tat activation in vivo. Bovine lentiviral Tat proteins evolved high-affinity TAR interaction independent of PCAF acetylation or CycT1. Tat acetylation assays, ternary complex assembly assays, transcription elongation in vitro, reporter assays in vivo, viral replication assays with compensatory mutations Proceedings of the National Academy of Sciences of the United States of America High 19223581
2012 AFF4 serves as the central scaffold of the HIV-1 Tat super elongation complex (SEC), directly binding CycT1 (along with ELL2 and ENL/AF9) through short hydrophobic regions along its disordered axis. Mapping of binding sites was performed in vitro and in vivo, establishing that CycT1 is a direct binding partner of AFF4 and a bridging component linking P-TEFb to the larger elongation complex. In vitro binding assays mapping contact regions, in vivo co-IP, identification of binding partners Proceedings of the National Academy of Sciences of the United States of America Medium 23251033
2013 Crystal structure of a tripartite P-TEFb–AFF4 complex shows AFF4 meanders over the surface of the CycT1 subunit but makes no stable contacts with CDK9. Interface mutations reduced CycT1-AFF4 binding and AFF4-dependent transcription. AFF4 is positioned to make direct contacts with HIV Tat, and Tat enhances P-TEFb affinity for AFF4. X-ray crystallography, interface mutagenesis, transcription reporter assays, in vitro binding assays eLife High 23471103
2014 AFF4 binding to Tat-P-TEFb partially orders the CycT1 Tat-TAR recognition motif (TRM) and increases the affinity of Tat-P-TEFb for TAR RNA 30-fold. Crystal structure of a quaternary Tat-P-TEFb-AFF4 complex determined; AFF4 and Tat interact directly on the CycT1 surface, and AFF4 helix 2 stabilization (even without RNA contact) explains SEC preference. X-ray crystallography, in vitro TAR binding assays, interface mutagenesis of AFF1/AFF4, Tat-dependent transcription reporter assays eLife High 24843025
2016 5.9 Å cryo-EM/crystal structure of HIV-1 TAR in complex with Tat, AFF4, CDK9, and CycT1. The TAR central loop contacts the CycT1 TRM and the second Tat Zn2+-binding loop. AFF4 helix 2 is stabilized in the TAR complex (shown by HDX), explaining its 50-fold enhancement of TAR binding to the SEC. The Tat ARM enters the TAR major groove between the bulge and central loop. X-ray crystallography (5.9 Å), hydrogen-deuterium exchange (HDX), RNA SHAPE, SAXS, functional binding assays eLife High 27731797
2018 Crystal structure of TAR loop in complex with Tat and the SEC core (CycT1 TRM) at 3.5 Å resolution. The TAR central loop is stabilized by cross-loop hydrogen bonds and makes structure-specific contacts with CycT1 TRM side chains and Tat zinc-coordinating loop. Mutational analysis confirmed that TAR loop-CycT1 TRM interactions contribute importantly to binding affinity, and these interactions dominate over TAR bulge-Tat ARM interactions. X-ray crystallography, mutational analysis of CycT1 TRM and Tat, binding assays Proceedings of the National Academy of Sciences of the United States of America High 30514815
2018 CDK7-mediated phosphorylation of CDK9 at Ser-175 (confirmed by selective CDK7 inhibitor THZ1 and in vitro kinase assays) is required for Tat binding and proviral HIV reactivation but does not affect CDK9 kinase activity or P-TEFb assembly. Thr-186 phosphorylation stabilizes CDK9/CycT1 interface via arginine triad and E96 of CycT1; disruption of this interface causes accumulation of dephosphorylated CDK9 associated with cytoplasmic Hsp90/Cdc37 chaperone. Hsp90 inhibition blocks P-TEFb assembly and Thr-186 phosphorylation. Molecular dynamics simulations, CDK7 inhibitor (THZ1), in vitro kinase assays, co-IP, Hsp90 inhibition, site-directed mutagenesis of arginine triad The Journal of biological chemistry High 29743242
2021 PKC-mediated phosphorylation of CycT1 promotes productive CycT1:CDK9 interactions (P-TEFb assembly) in human cells, while dephosphorylation of CycT1 by PP1 reverses this process. CycT1 not bound to CDK9 is rapidly degraded in resting/quiescent cells. PKC inhibitors or chronic PKC depletion cause P-TEFb disassembly and CycT1 degradation, recapitulating P-TEFb depletion in resting CD4+ T cells and anergic T cells. PKC inhibitor treatment, PP1 dephosphorylation assays, CycT1 degradation assays, primary cell experiments, co-IP eLife High 34821217
2022 Siah1 and Siah2 are the E3 ubiquitin ligases responsible for ubiquitination and degradation of free CycT1 (not bound to CDK9) in resting and quiescent cells. The ubiquitination and degradation of free CycT1 was mapped to its N-terminal region (positions 1-280) and involves six lysine residues. Inhibition of Siah1/2 rescued CycT1 expression in both proliferating and resting primary cells. Ubiquitination mapping, domain deletion analysis, Siah1/2 inhibition, co-IP, primary cell experiments Nucleic acids research High 35524561
2022 PARP1, activated by DNA damage, binds to transcriptionally engaged P-TEFb and poly(ADP-ribosyl)ates CycT1 at multiple positions including histidine residues. This modification prevents CycT1 from undergoing liquid-liquid phase separation required for CDK9 to hyperphosphorylate Pol II and stimulate elongation. Poly(ADP-ribosyl)ation of CycT1 promotes DNA repair and cell survival after DNA damage. PARP1 binding assays, PARylation site mapping (including histidine residues), phase separation assays, Pol II phosphorylation assays, cell survival assays Nature cell biology High 35393539
2022 Under stress, the CDK9/CycT1 heterodimer released from 7SK snRNP completely dissociates into monomers. Brd4 or SEC then recruits monomeric CDK9 and CycT1 to reassemble active P-TEFb on chromatin, inducing CDK9 autophosphorylation of T186. The same mechanism operates during entry into G1 phase after nocodazole release. Biochemical fractionation, co-IP, ChIP, cell cycle synchronization (nocodazole), stress treatment, pulldown assays Nucleic acids research Medium 34935961
2023 CCNT1 knockout (via CRISPR) prevents HIV-1 latency reactivation by a wide variety of latency reversal agents in primary CD4+ T cells and latently infected cell lines, without affecting T cell activation itself. RNA-seq showed CCNT1 regulates HIV-1 proviral genes to a larger extent than any other host gene but has no significant effects on host RNA transcripts in primary T cells after activation. CCNT1 function is non-essential for T cell biology but absolutely required for HIV latency reversal. CRISPR gene knockout screen, primary CD4+ T cell latency model, RNA-seq, multiple latency reversal agents Viruses High 37766271
2023 7SK RNA methylation by METTL3 (induced by EGF signaling via phosphorylation of METTL3) enhances 7SK binding to heterogeneous nuclear ribonucleoproteins, causing release of the HEXIM1/P-TEFb complex (CDK9/CycT1) from the inhibitory 7SK snRNP and inducing transcriptional elongation. This establishes an m6A-based RNA methylation switch controlling CycT1-containing P-TEFb availability. METTL3 phosphorylation assays, 7SK methylation assays, P-TEFb release assays, transcription elongation assays, EGF signaling pathway analysis Science advances Medium 37163588
2014 A CycT1 mutant (V107E) eliminates binding to Hexim1, CDK9, and assembly on HIV TAR RNA or 7SK snRNA, yet retains strong AFF4 binding and slightly impaired Tat association. CycT1-V107E potently inhibits HIV replication and enforces viral latency in primary CD4+ T cells, defining Val107 in the N-terminal cyclin box as essential for P-TEFb assembly with its major partners. Mutagenesis, co-IP/pulldown binding assays for Hexim1/CDK9/AFF4/Tat, HIV replication and latency reporter assays in primary CD4+ T cells Retrovirology Medium 24985467
2012 Nine novel CDK9/CCNT1-associated protein complexes (CCAPs) were identified in HeLa cell nuclei. siRNA depletion of five CCAPs (PPP1R10/TOX3/WDR82; TTF2; TPR; WRNIP1; FBXO11/CUL1/SKP1) enhanced Tat activation of integrated HIV-1 LTR, suggesting they negatively regulate P-TEFb availability similar to the 7SK snRNP. Co-IP/complexome mining, siRNA depletion, integrated HIV-1 LTR-luciferase reporter assays Retrovirology Low 23110726
2014 A cell-based genetic analysis of 7SK snRNP mapped 7SK HEXIM1-binding to the 5'U-U bulge and central loop of stem-loop I; CycT1 and HEXIM1 form a combinatorial binding surface for 7SK. HEXIM1 inhibits CDK9 kinase activity via interactions between 7SK, HEXIM1, and CycT1. A tyrosine-to-alanine mutation in HEXIM1 (critical for CDK9 inhibition) converts HEXIM1 into a transcriptional activator. RNA tethering cell-based assay, HEXIM1/CycT1 7SK-binding mutants, reporter gene assays The Journal of biological chemistry Medium 24917669
2011 Residues Q46, Q50, and F176 in the N-terminal region of human CycT1 play critical and distinctive roles in Tat-mediated transactivation. Q46 and Q50 are required for binding to Tat (in vitro pull-down); Q50 and F176 (along with C261) are required for Tat transactivation activity. A triple mutant (Q46A/Q50A/F176A) completely abolishes transcriptional activity. Alanine substitution mutagenesis based on 3D crystal structure, in vitro pull-down, luciferase reporter assays on HIV-1 LTR Journal of molecular biology Medium 21763494
2012 A CCNT1 splice variant (CYCT1b/dE7) that lacks exon 7 (generating a frameshift and premature stop codon) encodes a ~23 kDa protein covering ~70% of the cyclin box. This protein physically interacts with CDK9 and competes with full-length CCNT1 for CDK9 binding, acting dominant-negatively to inhibit HIV-1 transcription and Tat/LTR-driven transcription. The dE7/FL transcript ratio is high in quiescent PBMCs and low in proliferating cells. RT-PCR, ectopic expression, co-IP of dE7 with CDK9, luciferase reporter assays for Tat/LTR transcription, HIV-1 replication assays, NMD analysis The Journal of biological chemistry Medium 23569210
2005 HEXIM1 inhibits Tat transactivation by repressing transcription mediated through direct activation of P-TEFb (via GAL4-CycT1 tethering). Effective Tat-inhibition requires the 7SK snRNA basic recognition motif of HEXIM1 as well as its C-terminus region required for interaction with CycT1. HEXIM1-mediated repression of Tat is not due to global inhibition of cellular transcription. HEXIM1/HEXIM2 co-expression, GAL4-CycT1 artificial tethering assay, HEXIM1 deletion/mutation analysis, reporter assays Retrovirology Medium 15992410
2026 CycT1 (CCNT1) forms a hypoxia-specific, chromatin-associated interaction with nuclear-localized mitochondrial chaperone Tim8-Tim13 complexes and the hypoxia-inducible transcription factor BHLHE40. Tim8-Tim13 complex disruption and BHLHE40 silencing both impair the transcriptional response to acute hypoxia. This interaction is HIF-independent. Biochemical purification, co-IP validation across multiple human cell lines, Tim8-Tim13 disruption, BHLHE40 siRNA knockdown, transcriptional response assays Science advances Medium 42160428
2002 CycT1 is required as an essential cofactor for HIV-2 Tat and SIVmnd Tat function, in addition to HIV-1 Tat. Tat2 and Tat-M can also bind CycT2, but Tat-CycT2 complexes fail to bind TAR and are abortive. A single mutation in CycT2 (N260C) rescues TAR binding and Tat function for all three Tat proteins, demonstrating that C260/C261 is the key CycT1 residue for TAR binding in the context of multiple lentiviral Tats. Co-IP, in vitro binding assays (Tat-CycT1 and Tat-CycT2), TAR RNA binding assay, Tat transactivation reporter assay, site-directed mutagenesis of CycT2 Journal of virology Medium 10364329
2021 FACT complex protein SUPT16H interferes with the association of Cyclin T1 (CCNT1) with the Tat-LTR axis. Depletion of SUPT16H enhances Tat-mediated HIV-1 LTR activity and spontaneously reverses HIV-1 latency, suggesting FACT suppresses HIV transcription in part by blocking CycT1/P-TEFb recruitment to the LTR. Co-IP (HIV Tat with SUPT16H), siRNA depletion, HIV-1 LTR reporter assays, HIV latency reversal assays in U1/HIV and J-LAT cells and primary CD4+ T cells The Journal of biological chemistry Medium 26378236
2024 Poly(ADP-ribosyl)ation of CycT1 is elevated in ionizing radiation (IR)-resistant nasopharyngeal carcinoma (NPC) cells, disrupting CycT1 phase separation, increasing RNA Pol II pausing, and contributing to IR resistance. Mutation of the major PARylation sites of CycT1 decreases RNAPII pausing and restores IR sensitivity in NPC cells. ChIP-seq, CycT1 PARylation site mutation, RNAPII pausing analysis, IR resistance assays in NPC cells Journal of molecular cell biology Medium 37407287
2014 Cyclin T1 (CCNT1, CycT) is synthetically lethal with TSC1 and TSC2 mutations in Drosophila and mammalian cells. Individual knockdown of CycT (ortholog of CCNT1) reduced population growth rate of Drosophila cells lacking TSC1 or TSC2 but not wild-type cells; the same was true for mammalian TSC2-deficient cells including human tumor-derived cells. CRISPR-based Drosophila cell knockouts combined with RNAi screen, cross-species validation in mammalian TSC2-deficient and human tumor cells Science signaling Medium 26350902
2014 Both Cyclin T1 (Ccnt1) and its catalytic partner Cdk9 are required for development of Th1 cells and short-lived effector CTLs during viral infection; inhibiting Ccnt1 expression impaired these effector fates and enhanced Tfh and memory precursor CTL formation in vivo. Demonstrated by in vivo shRNAmir screens in TCR-transgenic CD4+ and CD8+ T cells responding to LCMV. In vivo pooled shRNAmir screen in TCR-transgenic T cells during LCMV infection, flow cytometric analysis of T cell differentiation phenotypes Immunity Medium 25148027
2021 Fosl1 interacts with JunB (shown by co-IP) and promotes expression of Cyclin T1 (Ccnt1) during Xenopus tropicalis and mouse heart regeneration, as demonstrated by ChIP and luciferase reporter assays. Overexpression of Fosl1 promoted cardiomyocyte proliferation, and its knockdown suppressed it; Ccnt1 is a downstream transcriptional target of the Fosl1/JunB complex in this regenerative context. Co-immunoprecipitation (Fosl1-JunB interaction), luciferase reporter assay (Fosl1/JunB driving Ccnt1 promoter), ChIP analysis, in vivo overexpression/knockdown in Xenopus and neonatal mouse NPJ Regenerative medicine Medium 34188056

Source papers

Stage 0 corpus · 91 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Mastermind recruits CycC:CDK8 to phosphorylate the Notch ICD and coordinate activation with turnover. Molecular cell 495 15546612
1998 The interaction between HIV-1 Tat and human cyclin T1 requires zinc and a critical cysteine residue that is not conserved in the murine CycT1 protein. Genes & development 387 9832504
2008 The structure of P-TEFb (CDK9/cyclin T1), its complex with flavopiridol and regulation by phosphorylation. The EMBO journal 304 18566585
2008 The splicing factor SC35 has an active role in transcriptional elongation. Nature structural & molecular biology 304 18641664
2009 TFIIH-associated Cdk7 kinase functions in phosphorylation of C-terminal domain Ser7 residues, promoter-proximal pausing, and termination by RNA polymerase II. Molecular and cellular biology 286 19667075
2008 The multi-tasking P-TEFb complex. Current opinion in cell biology 188 18513937
1999 Recruitment of cyclin T1/P-TEFb to an HIV type 1 long terminal repeat promoter proximal RNA target is both necessary and sufficient for full activation of transcription. Proceedings of the National Academy of Sciences of the United States of America 160 10393900
2000 CDK9 autophosphorylation regulates high-affinity binding of the human immunodeficiency virus type 1 tat-P-TEFb complex to TAR RNA. Molecular and cellular biology 142 10958691
2018 A Cdk9-PP1 switch regulates the elongation-termination transition of RNA polymerase II. Nature 129 29899453
2015 Identification of potential drug targets for tuberous sclerosis complex by synthetic screens combining CRISPR-based knockouts with RNAi. Science signaling 111 26350902
2014 In vivo RNA interference screens identify regulators of antiviral CD4(+) and CD8(+) T cell differentiation. Immunity 106 25148027
2002 Interaction between P-TEFb and the C-terminal domain of RNA polymerase II activates transcriptional elongation from sites upstream or downstream of target genes. Molecular and cellular biology 94 11739744
2003 A model of repression: CTD analogs and PIE-1 inhibit transcriptional elongation by P-TEFb. Genes & development 92 12651893
2002 TAR RNA loop: a scaffold for the assembly of a regulatory switch in HIV replication. Proceedings of the National Academy of Sciences of the United States of America 82 12048247
2012 HIV-1 Tat recruits transcription elongation factors dispersed along a flexible AFF4 scaffold. Proceedings of the National Academy of Sciences of the United States of America 79 23251033
2013 The AFF4 scaffold binds human P-TEFb adjacent to HIV Tat. eLife 75 23471103
2002 Transient induction of cyclin T1 during human macrophage differentiation regulates human immunodeficiency virus type 1 Tat transactivation function. Journal of virology 72 12368300
2000 HIV-1 TAR RNA enhances the interaction between Tat and cyclin T1. The Journal of biological chemistry 71 10944537
2002 Tat and trans-activation-responsive (TAR) RNA-independent induction of HIV-1 long terminal repeat by human and murine cyclin T1 requires Sp1. The Journal of biological chemistry 70 12458222
2002 Specific HIV-1 TAR RNA loop sequence and functional groups are required for human cyclin T1-Tat-TAR ternary complex formation. Biochemistry 65 12009901
2022 Poly(ADP-ribosylation) of P-TEFb by PARP1 disrupts phase separation to inhibit global transcription after DNA damage. Nature cell biology 63 35393539
2018 Structural mechanism for HIV-1 TAR loop recognition by Tat and the super elongation complex. Proceedings of the National Academy of Sciences of the United States of America 63 30514815
2018 Cyclin-dependent kinase 7 (CDK7)-mediated phosphorylation of the CDK9 activation loop promotes P-TEFb assembly with Tat and proviral HIV reactivation. The Journal of biological chemistry 56 29743242
2009 Tat acetylation modulates assembly of a viral-host RNA-protein transcription complex. Proceedings of the National Academy of Sciences of the United States of America 56 19223581
2002 P-TEFb containing cyclin K and Cdk9 can activate transcription via RNA. The Journal of biological chemistry 54 11884399
2014 Synthesis and evaluation of phosphorus containing, specific CDK9/CycT1 inhibitors. Journal of medicinal chemistry 51 24742150
2014 AFF4 binding to Tat-P-TEFb indirectly stimulates TAR recognition of super elongation complexes at the HIV promoter. eLife 51 24843025
2016 Insights into HIV-1 proviral transcription from integrative structure and dynamics of the Tat:AFF4:P-TEFb:TAR complex. eLife 45 27731797
2015 FACT Proteins, SUPT16H and SSRP1, Are Transcriptional Suppressors of HIV-1 and HTLV-1 That Facilitate Viral Latency. The Journal of biological chemistry 45 26378236
2009 Cyclin T2 is essential for mouse embryogenesis. Molecular and cellular biology 44 19364821
2020 Genome-wide association study of word reading: Overlap with risk genes for neurodevelopmental disorders. Genes, brain, and behavior 41 32108986
2021 Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention. Proceedings of the National Academy of Sciences of the United States of America 37 33619107
2005 Inhibition of Tat activity by the HEXIM1 protein. Retrovirology 34 15992410
1999 Analysis of the effect of natural sequence variation in Tat and in cyclin T on the formation and RNA binding properties of Tat-cyclin T complexes. Journal of virology 34 10364329
2020 Preferential Expression of B7-H6 in Glioma Stem-Like Cells Enhances Tumor Cell Proliferation via the c-Myc/RNMT Axis. Journal of immunology research 30 32322592
2010 Atomistic theory of amyloid fibril nucleation. The Journal of chemical physics 27 21171698
2008 Increased in vivo activation of microglia and astrocytes in the brains of mice transgenic for an infectious R5 human immunodeficiency virus type 1 provirus and for CD4-specific expression of human cyclin T1 in response to stimulation by lipopolysaccharides. Journal of virology 25 18353948
2006 TAR-RNA recognition by a novel cyclic aminoglycoside analogue. Nucleic acids research 23 16855296
2021 Fosl1 is vital to heart regeneration upon apex resection in adult Xenopus tropicalis. NPJ Regenerative medicine 22 34188056
2023 7SK methylation by METTL3 promotes transcriptional activity. Science advances 21 37163588
2018 HIV-1 Vif's Capacity To Manipulate the Cell Cycle Is Species Specific. Journal of virology 21 29321323
2012 Modulation of intracellular restriction factors contributes to methamphetamine-mediated enhancement of acquired immune deficiency syndrome virus infection of macrophages. Current HIV research 21 22591364
2012 Identification of novel inhibitors of human immunodeficiency virus type 1 replication by in silico screening targeting cyclin T1/Tat interaction. Antimicrobial agents and chemotherapy 20 23274668
2012 Identification of novel CDK9 and Cyclin T1-associated protein complexes (CCAPs) whose siRNA depletion enhances HIV-1 Tat function. Retrovirology 19 23110726
2008 Dominant negative mutant cyclin T1 proteins inhibit HIV transcription by specifically degrading Tat. Retrovirology 19 18620576
2015 Targeting polyamine biosynthetic pathway through RNAi causes the abrogation of MCF 7 breast cancer cell line. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 18 26277788
2014 Genetic analysis of the structure and function of 7SK small nuclear ribonucleoprotein (snRNP) in cells. The Journal of biological chemistry 18 24917669
2004 Evidence for conformational flexibility in the Tat-TAR recognition motif of cyclin T1. Virology 17 14972556
2022 Disrupting the Cdk9/Cyclin T1 heterodimer of 7SK snRNP for the Brd4 and AFF1/4 guided reconstitution of active P-TEFb. Nucleic acids research 16 34935961
2021 Reversible phosphorylation of cyclin T1 promotes assembly and stability of P-TEFb. eLife 16 34821217
2003 Additive activity between the trans-activation response RNA-binding protein, TRBP2, and cyclin T1 on HIV type 1 expression and viral production in murine cells. AIDS research and human retroviruses 16 14585207
2002 Cyclin T1 expression is mediated by a complex and constitutively active promoter and does not limit human immunodeficiency virus type 1 Tat function in unstimulated primary lymphocytes. Journal of virology 16 11739686
2021 Deubiquitinating Enzyme USP21 Inhibits HIV-1 Replication by Downregulating Tat Expression. Journal of virology 15 33827943
2009 Synergistic effect of human CycT1 and CRM1 on HIV-1 propagation in rat T cells and macrophages. Retrovirology 15 19435492
2020 The landscape of alternative splicing in HIV-1 infected CD4 T-cells. BMC medical genomics 13 32241262
2018 Graphene Oxide-Facilitated Comprehensive Analysis of Cellular Nucleic Acid Binding Proteins for Lung Cancer. ACS applied materials & interfaces 13 29722257
2012 Preventing the formation of positive transcription elongation factor b by human cyclin T1-binding RNA aptamer for anti-HIV transcription. AIDS (London, England) 13 22569018
2000 Isolation and characterization of the human cyclin T1 promoter. Gene 13 10903436
2022 The chaperone protein p32 stabilizes HIV-1 Tat and strengthens the p-TEFb/RNAPII/TAR complex promoting HIV transcription elongation. Proceedings of the National Academy of Sciences of the United States of America 12 36584296
2021 A novel methylation signature predicts inferior outcome of patients with PDAC. Aging 12 33550277
2021 Pharmacological Modulation of BET Family in Sepsis. Frontiers in pharmacology 12 33776776
2012 Regulation of cyclin T1 expression and function by an alternative splice variant that skips exon 7 and contains a premature termination codon. Gene 12 22692005
2011 Functional characterization of human cyclin T1 N-terminal region for human immunodeficiency virus-1 Tat transcriptional activation. Journal of molecular biology 11 21763494
2004 Transcriptional activity and substrate recognition of cyclin T2 from P-TEFb. Gene 11 15563843
2019 Regulation of cyclin T1 during HIV replication and latency establishment in human memory CD4 T cells. Virology journal 10 30786885
2004 A uniform procedure for the purification of CDK7/CycH/MAT1, CDK8/CycC and CDK9/CycT1. Biological procedures online 10 15328539
2022 P-TEFb is degraded by Siah1/2 in quiescent cells. Nucleic acids research 9 35524561
2022 Castration-resistant prostate cancer cells are dependent on the high activity of CDK7. Journal of cancer research and clinical oncology 9 36401094
2014 A single point mutation in cyclin T1 eliminates binding to Hexim1, Cdk9 and RNA but not to AFF4 and enforces repression of HIV transcription. Retrovirology 9 24985467
2013 Inhibition of HIV-1 transcription and replication by a newly identified cyclin T1 splice variant. The Journal of biological chemistry 9 23569210
2023 The relationship between pepsinogen C and gastric carcinogenesis: a transgene and population study. BMC cancer 8 37291517
2015 Molecular dynamics simulation and experimental verification of the interaction between cyclin T1 and HIV-1 Tat proteins. PloS one 8 25781978
2017 MD simulation of the Tat/Cyclin T1/CDK9 complex revealing the hidden catalytic cavity within the CDK9 molecule upon Tat binding. PloS one 7 28178316
2023 A CRISPR Screen of HIV Dependency Factors Reveals That CCNT1 Is Non-Essential in T Cells but Required for HIV-1 Reactivation from Latency. Viruses 6 37766271
2020 Enhanced conductivity and structure stability of BiPO4@void@C/CNT particles for high-performance bismuth-based batteries. Dalton transactions (Cambridge, England : 2003) 6 32285058
2020 Proteasomal Inhibition Potentiates Latent HIV Reactivation. AIDS research and human retroviruses 6 32683901
2024 Differentially localized protein identification for breast cancer based on deep learning in immunohistochemical images. Communications biology 4 39095659
2024 Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma. Journal of molecular cell biology 3 37407287
2022 Genome-wide identification, expression and functional analysis of the core cell cycle gene family during the early somatic embryogenesis of Dimocarpus longan Lour. Gene 3 35176425
2025 Vitamin D Decreases Susceptibility of CD4+ T Cells to HIV Infection by Reducing AKT Phosphorylation and Glucose Uptake: A Bioinformatic and In Vitro Approach. Biomolecules 2 40149968
2024 The Biological Significance of AFF4: Promoting Transcription Elongation, Osteogenic Differentiation and Tumor Progression. Combinatorial chemistry & high throughput screening 2 37815186
2024 Expanding RNA editing toolkit using an IDR-based strategy. Molecular therapy. Nucleic acids 1 38721279
2024 Development of BODIPY FL SNS 032 as a Versatile Probe for Constitutive Androstane Receptor and Multiple Kinases. ACS medicinal chemistry letters 1 39563813
2024 Expression of Concern: Bimetal-Organic-Framework Derivation of Ball-Cactus-Like Ni-Sn-P@C-CNT as Long-Cycle Anode for Lithium Ion Battery. Small (Weinheim an der Bergstrasse, Germany) 1 39580691
2016 Expression and Purification of Recombinant CDKs: CDK7, CDK8, and CDK9. Methods in molecular biology (Clifton, N.J.) 1 26231705
2003 Development of a mouse model for HIV/AIDS. Research initiative, treatment action : RITA 1 12845774
2026 Selective reactivation of latent HIV using CyclinT1-Tat-containing virus-like particles. Virology 0 41534351
2026 Hypoxia-responsive interaction between P-TEFb, BHLHE40, and Tim8-Tim13 regulates hypoxic gene transcription. Science advances 0 42160428
2025 Discovery of a Potent Tat-Binding Antiretroviral Compound Using a Two-Step Screening Approach. Biochemistry 0 41312763
2024 Effect of Nanostructure and Crosslinks on Impact Resistance of Carbon Nanotube Films Under Micro-Ballistic Impact. Small (Weinheim an der Bergstrasse, Germany) 0 39460491
2023 A CRISPR screen of HIV dependency factors reveals CCNT1 is non-essential in T cells but required for HIV-1 reactivation from latency. bioRxiv : the preprint server for biology 0 37546973

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