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Question

Gene Research for Functional Annotation

⚠️ CRITICAL: Gene/Protein Identification Context

BEFORE YOU BEGIN RESEARCH: You MUST verify you are researching the CORRECT gene/protein. Gene symbols can be ambiguous, especially for less well-characterized genes from non-model organisms.

Target Gene/Protein Identity (from UniProt):

• UniProt Accession: Q9QWV9
• Protein Description: RecName: Full=Cyclin-T1; Short=CycT1; Short=Cyclin-T;
• Gene Information: Name=Ccnt1;
• Organism (full): Mus musculus (Mouse).
• Protein Family: Belongs to the cyclin family. Cyclin C subfamily.
• Key Domains: Cyclin-like_dom. (IPR013763); Cyclin-like_sf. (IPR036915); Cyclin/Ssn8. (IPR043198); CYCLIN_CCNT1_rpt2. (IPR047320); Cyclin_N. (IPR006671)

MANDATORY VERIFICATION STEPS:

1. Check if the gene symbol "Ccnt1" matches the protein description above
2. Verify the organism is correct: Mus musculus (Mouse).
3. Check if protein family/domains align with what you find in literature
4. If you find literature for a DIFFERENT gene with the same or similar symbol, STOP

If Gene Symbol is Ambiguous or You Cannot Find Relevant Literature:

DO NOT PROCEED WITH RESEARCH ON A DIFFERENT GENE. Instead:
- State clearly: "The gene symbol 'Ccnt1' is ambiguous or literature is limited for this specific protein"
- Explain what you found (e.g., "Found extensive literature on a different gene with the same symbol in a different organism")
- Describe the protein based ONLY on the UniProt information provided above
- Suggest that the protein function can be inferred from domain/family information

Research Target:

Please provide a comprehensive research report on the gene Ccnt1 (gene ID: Ccnt1, UniProt: Q9QWV9) in mouse.

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Output

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on:
1. Key concepts and definitions with current understanding
2. Recent developments and latest research (prioritize 2023-2024 sources)
3. Current applications and real-world implementations
4. Expert opinions and analysis from authoritative sources
5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available.
Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Gene Research for Functional Annotation

⚠️ CRITICAL: Gene/Protein Identification Context

BEFORE YOU BEGIN RESEARCH: You MUST verify you are researching the CORRECT gene/protein. Gene symbols can be ambiguous, especially for less well-characterized genes from non-model organisms.

Target Gene/Protein Identity (from UniProt):

• UniProt Accession: Q9QWV9
• Protein Description: RecName: Full=Cyclin-T1; Short=CycT1; Short=Cyclin-T;
• Gene Information: Name=Ccnt1;
• Organism (full): Mus musculus (Mouse).
• Protein Family: Belongs to the cyclin family. Cyclin C subfamily.
• Key Domains: Cyclin-like_dom. (IPR013763); Cyclin-like_sf. (IPR036915); Cyclin/Ssn8. (IPR043198); CYCLIN_CCNT1_rpt2. (IPR047320); Cyclin_N. (IPR006671)

MANDATORY VERIFICATION STEPS:

1. Check if the gene symbol "Ccnt1" matches the protein description above
2. Verify the organism is correct: Mus musculus (Mouse).
3. Check if protein family/domains align with what you find in literature
4. If you find literature for a DIFFERENT gene with the same or similar symbol, STOP

If Gene Symbol is Ambiguous or You Cannot Find Relevant Literature:

DO NOT PROCEED WITH RESEARCH ON A DIFFERENT GENE. Instead:
- State clearly: "The gene symbol 'Ccnt1' is ambiguous or literature is limited for this specific protein"
- Explain what you found (e.g., "Found extensive literature on a different gene with the same symbol in a different organism")
- Describe the protein based ONLY on the UniProt information provided above
- Suggest that the protein function can be inferred from domain/family information

Research Target:

Please provide a comprehensive research report on the gene Ccnt1 (gene ID: Ccnt1, UniProt: Q9QWV9) in mouse.

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Research report: Mouse Ccnt1 (Cyclin T1; UniProt Q9QWV9) — functional annotation

0) Target verification (mandatory)

The queried mouse gene Ccnt1 encodes Cyclin T1 (CycT1), the principal cyclin partner of CDK9 in the positive transcription elongation factor b (P-TEFb) complex, consistently matching the UniProt-provided description (Cyclin T1; cyclin family) and the mechanistic context across the retrieved literature (P-TEFb/7SK snRNP/SEC, RNAPII pause release). The main ambiguity risk is confusion with similarly named Cntn1 (Contactin-1), but those papers are unrelated to P-TEFb biology and were excluded from functional claims. (egloff2021cdk9keepsrna pages 1-2, bywater2020reactivationofmyc pages 1-2)

1) Key concepts and definitions (current understanding)

1.1 P-TEFb and RNAPII promoter-proximal pausing

A large fraction of mammalian protein-coding genes are regulated at promoter-proximal pausing, where RNAPII initiates but pauses ~tens of nucleotides downstream, with pausing enforced largely by DSIF and NELF. The transition to productive elongation requires P-TEFb, which phosphorylates RNAPII and pausing factors to enable elongation. (egloff2021cdk9keepsrna pages 1-2, zhou2022disruptingthecdk9cyclin pages 1-2, puidebat2025the7sksnrnp pages 1-3)

Definition (operational): In this context, Cyclin T1 (CCNT1/Ccnt1) is a regulatory cyclin subunit that binds CDK9 to form core P-TEFb and confers substrate recognition/complex behavior required for RNAPII pause release and productive transcription. (egloff2021cdk9keepsrna pages 1-2, zhou2022disruptingthecdk9cyclin pages 1-2)

1.2 Molecular role of Cyclin T1 within P-TEFb

Mechanistically, the core P-TEFb heterodimer is CDK9–Cyclin T1. CDK9 is the catalytic kinase; Cyclin T1 is the cyclin subunit that enables CDK9 activity within transcriptional complexes. When active on chromatin, P-TEFb phosphorylates RNAPII CTD Ser2, and phosphorylates DSIF/NELF to release RNAPII from pause sites and promote processive elongation. (zhou2022disruptingthecdk9cyclin pages 1-2, egloff2021cdk9keepsrna pages 1-2)

1.3 Domain/architecture concepts relevant to function

Cyclin T proteins are described as carrying an N-terminal cyclin box (cyclin fold) and a C-terminal histidine-rich region implicated in substrate recognition, consistent with Cyclin T proteins being cyclin-family regulators rather than enzymes catalyzing a small-molecule reaction. (egloff2021cdk9keepsrna pages 1-2)

2) Molecular function, complexes, and pathways

2.1 Core biochemical function (primary functional annotation)

Primary function: Mouse Cyclin T1 (Ccnt1 product) functions as the CDK9 cyclin partner in P-TEFb, enabling RNAPII transcriptional elongation by supporting phosphorylation events (RNAPII CTD Ser2; DSIF/NELF) required for RNAPII pause release and productive elongation. (zhou2022disruptingthecdk9cyclin pages 1-2, egloff2021cdk9keepsrna pages 1-2, puidebat2025the7sksnrnp pages 1-3)

This is not an enzyme with an independent catalytic reaction; its “substrate specificity” is mediated through its role in assembling and regulating the CDK9 kinase complex and recruitment to transcriptional targets. (egloff2021cdk9keepsrna pages 1-2, zhou2022disruptingthecdk9cyclin pages 1-2)

2.2 Major complexes that contain Cyclin T1

Inactive reservoir: 7SK snRNP (7SK/P-TEFb snRNP). A substantial fraction of P-TEFb is sequestered in an inactive ribonucleoprotein complex organized around 7SK snRNA, with protein components including HEXIM1/2, LARP7, and MePCE, which limits free/active CDK9–Cyclin T1 availability. (zhou2022disruptingthecdk9cyclin pages 1-2, puidebat2025the7sksnrnp pages 1-3, perezpepe20237skmethylationby pages 1-2)

Active recruitment complexes: Active P-TEFb is recruited to chromatin via BRD4–P-TEFb or via incorporation into the Super Elongation Complex (SEC), which is particularly important for stimulus-responsive transcription programs. (zhou2022disruptingthecdk9cyclin pages 1-2, puidebat2025the7sksnrnp pages 1-3, galbraith2019therapeutictargetingof pages 6-7)

Switching mechanism: Stress- or signal-induced 7SK disruption releases P-TEFb; one mechanistic study reports that released CDK9/Cyclin T1 can dissociate into monomers, and BRD4 or SEC can recruit these monomers to reassemble active P-TEFb on chromatin, including reactivation steps involving CDK9 T-loop autophosphorylation (T186). (zhou2022disruptingthecdk9cyclin pages 1-2)

2.3 Signaling-pathway coupling (example: EGF→METTL3→7SK m6A)

A 2023 study provides a concrete signaling-to-transcription mechanism: EGF signaling induces phosphorylation of METTL3, which methylates 7SK RNA (m6A). This methylation increases binding of HNRNP proteins and promotes release of HEXIM1/P-TEFb (CDK9/CCNT1), thereby enhancing transcriptional elongation. (perezpepe20237skmethylationby pages 1-2)

The associated figures include direct biochemical/omics evidence of 7SK m6A and a model connecting EGF/ERK, METTL3, 7SK methylation, and P-TEFb release. (perezpepe20237skmethylationby media 160b1369, perezpepe20237skmethylationby media b39d83df)

3) Cellular localization and where Cyclin T1 acts

Nuclear/transcriptional compartmentalization: CDK9 is described as a nuclear protein, and P-TEFb function is inherently nuclear and chromatin-associated when active. (egloff2021cdk9keepsrna pages 1-2, zhou2022disruptingthecdk9cyclin pages 1-2)

Chromatin-free vs chromatin-associated pools: Inactive 7SK-bound P-TEFb is described as largely chromatin-free, whereas BRD4- or SEC-associated P-TEFb is chromatin-associated. (zhou2022disruptingthecdk9cyclin pages 1-2)

Nuclear speckle association and isoform-dependent localization: Work discussing Cyclin T1 isoforms reports Cyclin T1 localization in nuclear speckle-rich regions and suggests truncated isoforms can display altered localization (including cytoplasmic presence) with functional consequences in viral transcription contexts. (alberio2024atruncatedisoform pages 13-14)

Mouse embryo nuclear foci: In mouse early embryos, maternal TDP-43 co-occupies with RNAPII as nuclear foci and biochemical evidence indicates TDP-43 binds Cyclin T1, supporting a role for Cyclin T1 in proper RNAPII configuration and zygotic genome activation (ZGA). (nie2023maternaltdp43interacts pages 1-2)

4) Mouse biology, phenotypes, and in vivo functional contexts

4.1 Heart: Cyclin T1 as a limiting determinant of P-TEFb output

Mouse cardiomyocyte studies emphasize that Cyclin T1 levels limit P-TEFb abundance and CDK9 stability, and that increased P-TEFb activity correlates with increased RNAPII phosphorylation and transcriptional output. Overexpression of Cyclin T1 in the mouse heart increases CDK9 and phosphorylated RNAPII; sustained elevation across development is associated with cardiac hypertrophy in transgenic contexts. (boikova2022hrasandmyc pages 1-2)

In a mouse model context, constitutive HRas activity increased Cyclin T1 expression; HRas plus Myc promoted cardiomyocyte cell-cycle progression but also cell death, whereas Myc plus Cyclin T1 supported extensive cardiomyocyte proliferation (supporting the idea that Cyclin T1/P-TEFb availability gates Myc-driven transcriptional programs in heart). (boikova2022hrasandmyc pages 1-2, bywater2020reactivationofmyc pages 1-2)

4.2 Early development: ZGA and transcriptional elongation control

Maternal TDP-43 deletion caused mouse embryos to arrest at the two-cell stage; TDP-43 binds Polr2a and Cyclin T1, and depletion reduced Pol II chromatin binding at major ZGA genes, implicating Cyclin T1/P-TEFb-related elongation control as part of the mechanism enabling major ZGA. (nie2023maternaltdp43interacts pages 1-2)

5) Mouse-specific sequence feature (important for species differences)

A widely used functional marker of rodent Cyclin T1 is the residue corresponding to human Cys261, which is critical for Tat-dependent HIV transcriptional activation. Mouse Cyclin T1 carries a Tyr at this position (mouse-like “C261Y” relative to human), reducing Tat/TAR-dependent transactivation and contributing to rodent non-permissivity for HIV-1 transcription. (behrens2023exploitingarodent pages 12-14, alberio2024atruncatedisoform pages 13-14)

A 2023 gene-editing study recoded this region in human CD4+ T cells to encode CCNT1.C261Y, yielding viable isogenic clones with little effect on host proliferation/basal CCNT1 but near-total inactivation of viral gene expression across multiple HIV-1 strains and related primate lentiviruses—demonstrating that this single mouse-informed change can be sufficient to block Tat-dependent transcriptional amplification. (behrens2023exploitingarodent pages 12-14)

6) Recent developments (prioritizing 2023–2024)

6.1 2023 — Signal-responsive 7SK modification couples growth-factor signaling to P-TEFb

Perez-Pepe et al. (Science Advances; 10 May 2023; https://doi.org/10.1126/sciadv.ade7500) established a mechanism in which METTL3-mediated m6A methylation of 7SK promotes release of HEXIM1/P-TEFb, enabling enhanced elongation in response to EGF signaling. This provides a modern model of how extracellular cues can “unlock” CDK9/CCNT1 activity. (perezpepe20237skmethylationby pages 1-2, perezpepe20237skmethylationby media b39d83df)

6.2 2023 — Mouse early embryo: Cyclin T1 in ZGA regulatory machinery

Nie et al. (Nature Communications; accepted 30 June 2023; https://doi.org/10.1038/s41467-023-39924-1) provides in vivo mouse evidence linking Cyclin T1 binding partners (maternal TDP-43) to RNAPII nuclear organization and major ZGA gene activation. (nie2023maternaltdp43interacts pages 1-2)

6.3 2023 — Functional separation in T cells: CCNT1 non-essential for many host transcripts but essential for HIV latency reactivation

Hafer et al. (Viruses; Aug 2023; https://doi.org/10.3390/v15091863) reported CCNT1 as the top hit in a CRISPR screen for HIV latency reactivation. In primary CD4+ T cell latency models, CCNT1 knockout prevented latency reactivation without impairing T cell activation, and RNA-seq suggested CCNT1 had minimal detectable impact on host transcripts after activation while strongly affecting proviral transcription. (hafer2023acrisprscreen pages 1-2)

6.4 2024 — Releasing P-TEFb from SEC as a latency reversal approach

Cisneros et al. (PLOS Pathogens; published 11 Sep 2024; https://doi.org/10.1371/journal.ppat.1012083) tested a small molecule inhibitor (KL-2) of P-TEFb/SEC interaction; KL-2 increased viral transcription and synergized with other latency reversing agents in cell models and enhanced reactivation in PBMCs from people living with HIV on suppressive ART, supporting SEC-bound P-TEFb as a therapeutically relevant reservoir of CDK9/CCNT1. (cisneros2024releaseofptefb pages 1-2)

7) Current applications and real-world implementations

7.1 Regenerative biology (mouse heart)

Mouse work suggests that elevating P-TEFb (CDK9–Cyclin T1) can re-engage Myc-driven transcription and proliferative potential in cardiomyocytes, positioning P-TEFb/Ccnt1 modulation as a candidate strategy for cardiac regeneration research. (bywater2020reactivationofmyc pages 1-2, boikova2022hrasandmyc pages 1-2)

7.2 HIV cure and antiviral strategies (leveraging rodent CCNT1 biology)

Several 2023–2024 studies use CCNT1 biology in applied directions:
- Gene editing (C261Y “mousification”) as a host-directed strategy to create Tat-resistant human T cells. (behrens2023exploitingarodent pages 12-14)
- Latency reversal approaches that manipulate P-TEFb pools (SEC release; PAF1C disruption discussed as a pausing regulator that interfaces with P-TEFb recruitment). (cisneros2024releaseofptefb pages 1-2, soliman2023enhancinghiv1latency pages 1-2)

These are not mouse therapies per se, but directly exploit the conserved CCNT1/P-TEFb mechanism and a mouse-specific residue difference to inform intervention design. (behrens2023exploitingarodent pages 12-14)

8) Expert opinions and authoritative synthesis

A detailed review of CDK9/P-TEFb emphasizes that CDK9 (with Cyclin T partners) is essential for productive transcription of most RNAPII genes via promoter-proximal pause release and that P-TEFb impacts initiation/termination and broader gene-expression coordination; this framing supports Cyclin T1 as a core transcriptional control node rather than a cell-cycle cyclin. (egloff2021cdk9keepsrna pages 1-2)

A mechanistic synthesis of 7SK snRNP regulation frames 7SK-bound P-TEFb as a dynamic “buffer” controlling CDK9 availability and highlights recruitment of active P-TEFb via BRD4 and SEC, and links dysregulation of this axis to disease states. (puidebat2025the7sksnrnp pages 1-3)

9) Quantitative statistics and data points from recent studies

Note: Many mechanistic P-TEFb studies report qualitative switching mechanisms; a limited number of retrieved texts provide directly stated quantitative effects.

• In mouse females with oocyte-specific TDP-43 knockout, control females produced 8.8 ± 2.1 pups/litter, whereas TDP-43 oocyte knockout females produced no pups after extended mating, supporting essentiality of the pathway in early development (with Cyclin T1 as a binding partner in the mechanism). (nie2023maternaltdp43interacts pages 1-2)
• In a comprehensive HIV latency reactivation CRISPR screen, CCNT1 was the top hit and had the largest effect on latency reversal across multiple LRAs; in primary CD4+ T cells, CCNT1 knockout blocked latency reactivation without affecting T cell activation. (hafer2023acrisprscreen pages 1-2)

10) Evidence map table (for rapid functional annotation)

Table: This table summarizes the functional annotation of mouse Ccnt1/Cyclin T1 across identity, mechanism, complexes, regulation, localization, pathways, species-specific features, recent studies, and applications. It is designed as a compact evidence map with direct citation IDs, URLs, and dates for rapid use in the final report.

11) Summary functional annotation (mouse Ccnt1 / Cyclin T1)

Mouse Ccnt1 encodes Cyclin T1, a nuclear cyclin-family regulatory subunit that forms P-TEFb with CDK9. Its primary role is to enable RNAPII pause release and productive transcription elongation through P-TEFb’s kinase activity on RNAPII CTD Ser2 and associated pausing factors, with its availability controlled by dynamic sequestration in 7SK snRNP and recruitment by BRD4 and SEC to chromatin. In mouse biology, Cyclin T1 levels can gate transcriptional programs in differentiated cardiomyocytes and contribute to early embryonic transcriptional activation (ZGA). A key mouse-specific residue (Tyr at the position corresponding to human Cys261) is functionally important in species differences for HIV Tat transactivation and has been leveraged to engineer Tat-resistant human T cells. (boikova2022hrasandmyc pages 1-2, zhou2022disruptingthecdk9cyclin pages 1-2, perezpepe20237skmethylationby pages 1-2, nie2023maternaltdp43interacts pages 1-2, behrens2023exploitingarodent pages 12-14)

References

1. (egloff2021cdk9keepsrna pages 1-2): Sylvain Egloff. Cdk9 keeps rna polymerase ii on track. Cellular and Molecular Life Sciences: CMLS, 78:5543-5567, Jun 2021. URL: https://doi.org/10.1007/s00018-021-03878-8, doi:10.1007/s00018-021-03878-8. This article has 106 citations.

2. (bywater2020reactivationofmyc pages 1-2): Megan J. Bywater, Deborah L. Burkhart, Jasmin Straube, Arianna Sabò, Vera Pendino, James E. Hudson, Gregory A. Quaife-Ryan, Enzo R. Porrello, James Rae, Robert G. Parton, Theresia R. Kress, Bruno Amati, Trevor D. Littlewood, Gerard I. Evan, and Catherine H. Wilson. Reactivation of myc transcription in the mouse heart unlocks its proliferative capacity. Nature Communications, Apr 2020. URL: https://doi.org/10.1038/s41467-020-15552-x, doi:10.1038/s41467-020-15552-x. This article has 64 citations and is from a highest quality peer-reviewed journal.

3. (zhou2022disruptingthecdk9cyclin pages 1-2): Kai Zhou, Songkuan Zhuang, Fulong Liu, Yanheng Chen, You Li, Shihui Wang, Yuxuan Li, Huixin Wen, Xiaohua Lin, Jie Wang, Yue Huang, Cailing He, Nan Xu, Zongshu Li, Lang Xu, Zixuan Zhang, Lin-Feng Chen, Ruichuan Chen, and Min Liu. Disrupting the cdk9/cyclin t1 heterodimer of 7sk snrnp for the brd4 and aff1/4 guided reconstitution of active p-tefb. Nucleic Acids Research, 50:750-762, Dec 2022. URL: https://doi.org/10.1093/nar/gkab1228, doi:10.1093/nar/gkab1228. This article has 19 citations and is from a highest quality peer-reviewed journal.

4. (puidebat2025the7sksnrnp pages 1-3): Oriana Puidebat and Sylvain Egloff. The 7sk snrnp complex: a critical regulator in carcinogenesis. Biochimie, May 2025. URL: https://doi.org/10.1016/j.biochi.2025.05.003, doi:10.1016/j.biochi.2025.05.003. This article has 2 citations and is from a peer-reviewed journal.

5. (perezpepe20237skmethylationby pages 1-2): Marcelo Perez-Pepe, Anthony W. Desotell, Hengyi Li, Wenxue Li, Bing Han, Qishan Lin, Daryl E. Klein, Yansheng Liu, Hani Goodarzi, and Claudio R. Alarcón. 7sk methylation by mettl3 promotes transcriptional activity. Science Advances, May 2023. URL: https://doi.org/10.1126/sciadv.ade7500, doi:10.1126/sciadv.ade7500. This article has 24 citations and is from a highest quality peer-reviewed journal.

6. (galbraith2019therapeutictargetingof pages 6-7): Matthew D. Galbraith, Heather Bender, and Joaquín M. Espinosa. Therapeutic targeting of transcriptional cyclin-dependent kinases. Transcription, 10:118-136, Nov 2019. URL: https://doi.org/10.1080/21541264.2018.1539615, doi:10.1080/21541264.2018.1539615. This article has 107 citations and is from a peer-reviewed journal.

7. (perezpepe20237skmethylationby media 160b1369): Marcelo Perez-Pepe, Anthony W. Desotell, Hengyi Li, Wenxue Li, Bing Han, Qishan Lin, Daryl E. Klein, Yansheng Liu, Hani Goodarzi, and Claudio R. Alarcón. 7sk methylation by mettl3 promotes transcriptional activity. Science Advances, May 2023. URL: https://doi.org/10.1126/sciadv.ade7500, doi:10.1126/sciadv.ade7500. This article has 24 citations and is from a highest quality peer-reviewed journal.

8. (perezpepe20237skmethylationby media b39d83df): Marcelo Perez-Pepe, Anthony W. Desotell, Hengyi Li, Wenxue Li, Bing Han, Qishan Lin, Daryl E. Klein, Yansheng Liu, Hani Goodarzi, and Claudio R. Alarcón. 7sk methylation by mettl3 promotes transcriptional activity. Science Advances, May 2023. URL: https://doi.org/10.1126/sciadv.ade7500, doi:10.1126/sciadv.ade7500. This article has 24 citations and is from a highest quality peer-reviewed journal.

9. (alberio2024atruncatedisoform pages 13-14): Tiziana Alberio, Mariam Shallak, Amruth Kaleem Basha Shaik, Roberto Sergio Accolla, and Greta Forlani. A truncated isoform of cyclin t1 could contribute to the non-permissive hiv-1 phenotype of u937 promonocytic cells. Viruses, 16:1176, Jul 2024. URL: https://doi.org/10.3390/v16081176, doi:10.3390/v16081176. This article has 0 citations.

10. (nie2023maternaltdp43interacts pages 1-2): Xiaoqing Nie, Qianhua Xu, Chengpeng Xu, Fengling Chen, Qizhi Wang, Dandan Qin, Rui Wang, Zheng Gao, Xukun Lu, Xinai Yang, Yu Wu, Chen Gu, Wei Xie, and Lei Li. Maternal tdp-43 interacts with rna pol ii and regulates zygotic genome activation. Nature Communications, Jul 2023. URL: https://doi.org/10.1038/s41467-023-39924-1, doi:10.1038/s41467-023-39924-1. This article has 19 citations and is from a highest quality peer-reviewed journal.

11. (boikova2022hrasandmyc pages 1-2): Aleksandra Boikova, Megan J. Bywater, Gregory A. Quaife-Ryan, Jasmin Straube, Lucy Thompson, Camilla Ascanelli, Trevor D. Littlewood, Gerard I. Evan, James E. Hudson, and Catherine H. Wilson. Hras and myc synergistically induce cell cycle progression and apoptosis of murine cardiomyocytes. Frontiers in Cardiovascular Medicine, Oct 2022. URL: https://doi.org/10.3389/fcvm.2022.948281, doi:10.3389/fcvm.2022.948281. This article has 4 citations and is from a peer-reviewed journal.

12. (behrens2023exploitingarodent pages 12-14): Ryan T. Behrens, Jyothi Krishnaswamy Rajashekar, James W. Bruce, Edward L. Evans, Amelia M. Hansen, Natalia Salazar-Quiroz, Lacy M. Simons, Paul Ahlquist, Judd F. Hultquist, Priti Kumar, and Nathan M. Sherer. Exploiting a rodent cell block for intrinsic resistance to hiv-1 gene expression in human t cells. mBio, Oct 2023. URL: https://doi.org/10.1128/mbio.00420-23, doi:10.1128/mbio.00420-23. This article has 4 citations and is from a domain leading peer-reviewed journal.

13. (hafer2023acrisprscreen pages 1-2): Terry L. Hafer, Abby Felton, Yennifer Delgado, Harini Srinivasan, and Michael Emerman. 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, 15:1863, Aug 2023. URL: https://doi.org/10.3390/v15091863, doi:10.3390/v15091863. This article has 9 citations.

14. (cisneros2024releaseofptefb pages 1-2): William J. Cisneros, S. Soliman, Miriam Walter, L. Simons, Daphne Cornish, Simone De Fabritiis, Ariel W. Halle, Eun-Young Kim, Steven M. Wolinsky, Ramon Lorenzo-Redondo, A. Shilatifard, and J. Hultquist. Release of p-tefb from the super elongation complex promotes hiv-1 latency reversal. PLOS Pathogens, Sep 2024. URL: https://doi.org/10.1371/journal.ppat.1012083, doi:10.1371/journal.ppat.1012083. This article has 5 citations and is from a highest quality peer-reviewed journal.

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