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this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.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.
The requested protein is Res2, historically also called Pct1, encoded by res2/pct1 (systematic locus SPAC22F3.09c) in Schizosaccharomyces pombe strain 972 and represented by UniProt P41412. It is an approximately 73-kDa, nonenzymatic DNA-binding transcriptional regulator and a core component of the MluI-binding factor (MBF, also called DSC1). Its primary function is to help recognize MluI cell-cycle box (MCB) promoter elements and regulate genes required for mitotic G1/S progression and premeiotic DNA replication. It has no catalytic reaction or small-molecule substrate; its relevant “substrate” is MCB-containing chromatin, with the canonical motif ACGCGT. (zhu1994pct1+whichencodes pages 1-2, ayte1997thefissionyeast pages 1-2)
Res2 acts primarily in the nucleus on chromatin, in complexes containing Cdc10 and Res1 during vegetative growth and a Res2–Cdc10-centered complex during meiotic differentiation. Its mitotic role overlaps with Res1, whereas its requirement during premeiotic S phase and meiosis is substantially more specialized. (ayte1997thefissionyeast pages 7-7, eshaghi2011deconvolutionofchromatin pages 2-2)
Independent 1994–1997 primary studies identify S. pombe res2 and pct1 as names for the same cell-cycle regulator, described as p73Res2/Pct1. The cloned product binds p85Cdc10, recognizes MCB DNA, contains a Swi4/Mbp1-related N-terminal DNA-binding region and ankyrin repeats, and is especially important for meiosis. These properties agree with the supplied identity—P41412, SPAC22F3.09c, Res2/Pct1—and with the listed KilA/APSES-like HTH, SWI6-like, and ankyrin-repeat annotations. (zhu1994pct1+whichencodes pages 1-2, ayte1995theschizosaccharomycespombe pages 1-1, miyamoto1994res2+anew pages 2-2)
There is an unrelated fission-yeast protein also called Pct1 in later literature: a 303-residue, 35.4-kDa RNA 5′-triphosphatase involved in mRNA capping. That enzyme hydrolyzes the γ-phosphate from nascent RNA, requires divalent metal, and is essential for viability. It is not Res2, lacks the Res2/MBF domain architecture, and was excluded from this annotation. The strong differences in molecular mass, domain family, biochemical activity, and phenotype resolve the ambiguity. (takagi2002divergentsubunitinteractions pages 2-3)
Accordingly, literature about the 303-aa RNA-triphosphatase Pct1—including interactions with Spt5 or Pce1—must not be transferred to UniProt P41412.
Res2 belongs to the fungal Cdc10/Swi4/Mbp1-related family of cell-cycle transcription factors. It has 28% amino-acid identity to Res1 and 17% to Cdc10, with strongest conservation in an N-terminal “Res/Swi4” region corresponding to the DNA-binding APSES/KilA-like helix-turn-helix superfamily. (miyamoto1994res2+anew pages 2-2)
Biochemical deletion analysis maps homodimerization to the first 152 amino acids. Res2 also contains two approximately 33-residue Cdc10/Swi6-like ankyrin repeats in its central/C-terminal region. The repeats were dispensable in reported assays for DNA binding and Cdc10 association, but the central region was nevertheless required for full biological function, consistent with a regulatory or transcriptional-effector role rather than direct sequence recognition. (ayte1997thefissionyeast pages 1-2, zhu1997functionalcharacterizationof pages 9-11)
No experimentally determined full-length Res2 structure was identified. The InterPro assignments therefore provide credible evolutionary/structural classification, but not an atomic mechanism for the intact complex.
Res2 is a sequence-specific, nonenzymatic transcription-factor subunit of MBF/DSC1. Original DNA-binding experiments showed that Res2–Cdc10 complexes recognize MCB elements in vitro and in vivo, while failing to recognize SCB or E2F sites. The canonical MCB sequence is 5′-ACGCGT-3′. (zhu1994pct1+whichencodes pages 1-2, ayte1997thefissionyeast pages 1-2)
Full-length Res2 binds DNA only weakly by itself; Cdc10 strongly enhances binding. Res2 can form DNA-binding homodimers and Res1–Res2 heterodimers, while both Res proteins interact with Cdc10. A tetrameric Res2–Cdc10 arrangement has been proposed, but native stoichiometry remains insufficiently resolved. (zhu1997functionalcharacterizationof pages 9-11)
Loss of either Res1 or Res2 disrupts normal MBF DNA-binding activity, supporting a vegetative complex containing Cdc10, Res1, and Res2, rather than a simple model in which mutually exclusive Cdc10–Res1 and Cdc10–Res2 dimers alternate through the cell cycle. Res1 and Res2 remain Cdc10-associated through the mitotic cycle. (ayte1997thefissionyeast pages 7-7, ivanova2013thednadamage pages 47-52)
An early model classified Res1 as an activator and Res2 as a repressor. Later expression profiling showed that this is too simple: each contributes to activation or repression of different MBF targets. Most MBF-dependent transcripts become constitutively derepressed in res2Δ, supporting a major role in transcriptional shutoff, but yox1, cig2, and mik1 can retain near-wild-type expression. Thus, Res2 is best viewed as a gene- and context-dependent DNA-binding regulatory scaffold rather than a universal repressor. (ivanova2013thednadamage pages 47-52, dutta2008thednareplication pages 7-8)
MBF activity peaks around G1/S and drives expression of genes needed for DNA replication and S-phase progression. Supported targets of the broader Res2-containing MBF program include cdc18, cdc22, cdt1, cig2, mik1, mrc1, ssb1, rhp51, ctp1, and pfh1. Direct promoter evidence is strongest for representative MCB-containing genes such as cdc18 and cdc22; assignment of every listed gene specifically to Res2, rather than to MBF collectively, is less certain. (ayte1997thefissionyeast pages 7-7, dutta2008thednareplication pages 7-8, ivanova2011g1stranscriptionand pages 1-3)
Genome-wide ChIP-chip using chromosomally tagged Res2 placed it at MBF-associated promoter and intragenic sites. The study used arrays with approximately 33-bp resolution and found a comparatively stable Cdc10/Res1/Res2 promoter core, whereas recruitment of the coactivator Rep2 was more temporally dynamic. (eshaghi2011deconvolutionofchromatin pages 1-2, eshaghi2011deconvolutionofchromatin pages 2-2)
The res2 deletion is viable, reflecting overlap with Res1, but it impairs growth and normal periodic transcription. Overexpression of Res2 can compensate for defects caused by loss of Res1, while genetic interactions with the Pas1–Pef1 cyclin/CDK module support a specific route that activates the Res2–Cdc10 pathway. (tanaka2000apcllikecyclin pages 10-11, ivanova2013thednadamage pages 47-52)
Res2 has a stronger specialized role in meiosis than in vegetative growth. Its expression/activity rises during nitrogen starvation, conjugation, and premeiotic DNA synthesis; res2/pct1 deletion is viable during vegetative growth but causes severe defects in premeiotic DNA replication and meiotic completion. (zhu1994pct1+whichencodes pages 1-2, ayte1995theschizosaccharomycespombe pages 1-1, ivanova2013thednadamage pages 47-52)
The foundational model proposes that nitrogen starvation reduces Res1 abundance and disrupts the mitotic tripartite MBF complex while Res2 increases and remains associated with Cdc10. This meiotic complex promotes mat1 expression, leading to induction of mei3; Mei3 inhibits Pat1 kinase, permitting activation of the Mei2/Ste11 meiotic program. Evidence is strong that Res2 is required for meiotic progression, but the exact composition and direct genomic targets of meiotic Res2 are less comprehensively mapped than those of mitotic MBF. (ayte1997thefissionyeast pages 7-7)
A March 2024 review confirms the current framework that MBF contains Res1, Res2, and Cdc10, binds MCB elements, and controls G1/S genes such as cig2. It places this module within the broader nutrient-starvation → G1 arrest → mating-type/Mei3 → Pat1 inhibition pathway initiating sexual differentiation. The review focuses chiefly on events leading to conjugation, so it does not resolve the detailed composition of post-conjugation Res2 complexes. Kawamukai, 2024, DOI. (kawamukai2024regulationofsexual pages 1-2)
At the end of S phase, Nrm1 acts mainly as an adaptor that loads the Yox1 repressor onto MBF. Nrm1/Yox1 therefore terminates the G1/S transcriptional wave. During replication stress, the Cds1 checkpoint kinase phosphorylates Yox1 at Ser114 and Thr115, releases it from MBF, and sustains transcription of genes such as cdc22 and cdc18 to replenish replication capacity and promote recovery. These established modifications affect associated repressors, not Res2 directly. (ivanova2011g1stranscriptionand pages 3-4, ivanova2013thednadamage pages 86-127, ivanova2013thednadamage pages 145-154)
Cds1 can phosphorylate the C-terminal region of Cdc10 in vitro, while phosphomimetic cdc10-2E constitutively activates MBF transcription. Restoring MBF output with cdc10-2E improves hydroxyurea resistance in cds1Δ and rad3Δ backgrounds; Rep2 overexpression also partially suppresses checkpoint-mutant hydroxyurea sensitivity. This shows that sustained S-phase transcription makes a causal contribution to replication-stress survival. (dutta2008thednareplication pages 5-7)
DNA damage produces a distinct response. Chk1 phosphorylates the Cdc10 core subunit and promotes eviction of MBF from chromatin, repressing MBF-dependent transcription. Again, available evidence supports regulation of the Res2-containing complex through Cdc10, Nrm1, Yox1, and Rep2, not direct checkpoint phosphorylation of Res2. (ivanova2013thednadamage pages 86-127)
The INO80 chromatin-remodeling complex physically associates with MBF and is recruited to cdc18 and cdc22 promoters. INO80 occupancy peaks at the M/G1 transition approximately 20 minutes before maximal mRNA accumulation. Depending on the mutated INO80 subunit, Cdc10 promoter occupancy fell to about 60% or below 30% of control, while a cdc22-YFP reporter declined by 10–30%. (knezevic2018theino80complex pages 4-7)
This regulation involves the H2A.Z variant Pht1 and promoter nucleosome organization. A nonacetylatable Pht1-4KR allele reduced MBF reporter output to 62% ± 0.6 of wild type, close to the 56% ± 0.5 observed in rep2Δ. These results indicate that acetylated H2A.Z and INO80 help establish an accessible promoter architecture needed for full, timely MBF transcription. They do not demonstrate an isolated direct INO80–Res2 interaction; the strongest physical evidence is through Cdc10-containing MBF. Knezevic et al., September 2018, DOI. (knezevic2018theino80complex pages 4-7, knezevic2018theino80complex pages 7-10)
The functional site of Res2 is the nucleus, at chromatin associated with MCB-containing genes. This conclusion is supported directly by formaldehyde cross-linking and ChIP-chip detection of tagged Res2 at MBF-bound genomic loci, together with its sequence-specific DNA-binding activity. (eshaghi2011deconvolutionofchromatin pages 1-2, eshaghi2011deconvolutionofchromatin pages 2-2)
However, the retrieved literature did not provide a definitive Res2-specific fluorescence-microscopy study measuring nuclear/cytoplasmic partitioning or cell-cycle-dependent movement. “Nuclear/chromatin-associated” is therefore a strong functional conclusion, while fine-scale localization dynamics remain insufficiently characterized.
| Annotation question | Best-supported conclusion | Evidence type | Confidence / limitation |
|---|---|---|---|
| Identity and synonym ambiguity | Res2/Pct1 is the approximately 73-kDa Schizosaccharomyces pombe Cdc10-binding cell-cycle transcription factor corresponding to P41412. It is distinct from the unrelated S. pombe Pct1 RNA triphosphatase, a 303-aa, 35.4-kDa mRNA-capping enzyme. (zhu1994pct1+whichencodes pages 1-2, ayte1995theschizosaccharomycespombe pages 1-1, takagi2002divergentsubunitinteractions pages 2-3) | Cloning, interaction, DNA-binding, deletion, and enzyme studies | High. Molecular size, domains, function, and essentiality resolve the genuine historical name ambiguity. |
| Primary molecular function | Res2 is a nonenzymatic, sequence-specific transcription-factor subunit of MluI-binding factor, also called MBF or DSC1. It helps recognize MCB promoters and regulate mitotic G1/S and premeiotic-S transcription. (zhu1994pct1+whichencodes pages 1-2, ayte1997thefissionyeast pages 7-7, zhu1997functionalcharacterizationof pages 9-11) | EMSA, genetics, protein-interaction assays, and transcriptional phenotypes | High. No catalytic reaction or enzymatic substrate applies; activity depends on the complete MBF complex. |
| Protein family and domains | Res2 belongs to the Cdc10/Swi4/Mbp1-related class. Its N-terminal APSES/KilA-like helix-turn-helix region supports DNA binding and dimerization, while two approximately 33-aa ankyrin/Cdc10-Swi6 repeats occur centrally or toward the C terminus. Res2 has 28% identity to Res1 and 17% identity to Cdc10. (miyamoto1994res2+anew pages 2-2, ayte1997thefissionyeast pages 1-2, zhu1997functionalcharacterizationof pages 9-11) | Sequence comparison and truncation/domain-function experiments | High for architecture and homology; moderate for exact mechanism. Ankyrin repeats were dispensable for DNA binding and Cdc10 association in reported assays but required for full biological function. |
| Complex partners | Res2 associates with Cdc10 and can form DNA-binding homodimers and Res1–Res2 heterodimers. Mitotic MBF contains Cdc10, Res1, and Res2; Rep2 acts as a dynamically recruited coactivator in this setting. (zhu1994pct1+whichencodes pages 1-2, zhu1997functionalcharacterizationof pages 9-11, eshaghi2011deconvolutionofchromatin pages 2-2, ivanova2013thednadamage pages 47-52) | Co-immunoprecipitation, EMSA/supershift, deletion analysis, and ChIP-chip | High for Cdc10 and Res1 associations; moderate for native stoichiometry. A proposed Res2–Cdc10 tetramer remains unconfirmed. |
| DNA recognition | Res2-containing MBF recognizes the six-base MluI cell-cycle box, MCB: ACGCGT, and did not recognize SCB or E2F sites in original specificity experiments. Cdc10 strongly enhances the otherwise weak DNA binding of full-length Res2. (zhu1994pct1+whichencodes pages 1-2, ayte1997thefissionyeast pages 1-2, zhu1997functionalcharacterizationof pages 9-11) | In-vitro and in-vivo DNA-binding assays and EMSA | High for MCB specificity. No modern dissociation constant or comprehensive Res2-only motif-selection dataset was identified. |
| Mitotic G1/S targets | Res2-containing MBF controls genes needed for DNA synthesis and S-phase progression. Supported MBF targets include cdc18, cdc22, cdt1, cig2, mik1, mrc1, ssb1, rhp51, ctp1, and pfh1. (ayte1997thefissionyeast pages 7-7, dutta2008thednareplication pages 7-8, ivanova2011g1stranscriptionand pages 1-3) | Mutant expression analysis, promoter binding, arrays, and ChIP | High for MBF-level regulation; moderate for assigning every target specifically to Res2. Res2 can activate some targets and repress others. |
| Mitotic phenotype | res2 deletion is viable but perturbs growth and periodic MBF transcription. Most MBF-dependent genes become derepressed, whereas yox1, cig2, and mik1 can retain near-wild-type expression. Res2 and Res1 have overlapping mitotic functions. (ayte1997thefissionyeast pages 1-2, ivanova2013thednadamage pages 47-52) | Deletion genetics, rescue, and expression profiling | High for viability and altered transcription. Gene-specific effects rule out a simple universal-repressor model. |
| Meiotic role | Res2 is particularly important for premeiotic DNA synthesis and meiotic progression. Its abundance or activity rises during nitrogen starvation and premeiotic S phase, while deletion causes severe meiotic-DNA-synthesis and sporulation defects. Res2–Cdc10 activity has also been connected to mat1 expression and the downstream mei3–Pat1–Mei2 pathway. (ayte1997thefissionyeast pages 7-7, ayte1995theschizosaccharomycespombe pages 1-1, kawamukai2024regulationofsexual pages 1-2) | Starvation/meiosis time courses, deletions, overexpression, DNA-binding, and expression assays | High for meiotic requirement; moderate for the detailed mat1-to-mei3 causal model, which rests mainly on foundational studies. |
| Checkpoint regulation | Replication stress maintains MBF transcription through Cds1, which phosphorylates Yox1 at S114/T115 and regulates Nrm1/Cdc10-linked repression. DNA damage activates Chk1, which phosphorylates Cdc10 and removes MBF from chromatin. These pathways regulate the Res2-containing complex but have not been shown to modify Res2 directly. (ivanova2011g1stranscriptionand pages 3-4, ivanova2013thednadamage pages 86-127, ivanova2013thednadamage pages 145-154, dutta2008thednareplication pages 5-7) | Phosphorylation assays, phosphomutants, ChIP, and stress-survival assays | High for regulation through Yox1, Nrm1, and Cdc10; direct checkpoint phosphorylation of Res2 is unsupported. |
| Chromatin regulation and quantitative effects | INO80 associates with MBF and reaches cdc18/cdc22 promoters about 20 minutes before maximal mRNA accumulation. INO80-subunit mutants reduce Cdc10 occupancy to approximately 60% or below 30% and lower a cdc22-YFP reporter by 10–30%. Nonacetylatable H2A.Z/Pht1-4KR lowers reporter output to 62% ± 0.6 of wild type, compared with 56% ± 0.5 for rep2Δ. (knezevic2018theino80complex pages 4-7, knezevic2018theino80complex pages 7-10) | Affinity purification, co-IP, synchronized ChIP, reporter assays, and nucleosome mapping | High for MBF-level chromatin regulation. INO80 association was demonstrated chiefly through Cdc10, not as an isolated direct INO80–Res2 interaction. |
| Cellular localization | Res2 acts in the nucleus on chromatin. Formaldehyde ChIP-chip with HA-tagged Res2 mapped it to MBF-associated promoter and intragenic sites at approximately 33-bp resolution. (eshaghi2011deconvolutionofchromatin pages 1-2, eshaghi2011deconvolutionofchromatin pages 2-2) | Genome-wide ChIP-chip and promoter-occupancy analysis | Moderate to high for chromatin association and nuclear action. Direct microscopy or live-cell compartmental dynamics were not identified, so nuclear localization is partly a functional inference. |
| Applications and model relevance | Res2/MBF provides a tractable model for conserved G1/S transcription, checkpoint–transcription coupling, negative feedback, and chromatin-remodeler/H2A.Z control. Constitutive MBF activation can improve hydroxyurea resistance in checkpoint mutants, enabling mechanistic tests of replication-stress survival. (ivanova2011g1stranscriptionand pages 5-5, dutta2008thednareplication pages 5-7, knezevic2018theino80complex pages 4-7) | Synchronization, reporter strains, checkpoint genetics, ChIP, and chromatin perturbation | High as a basic-research model. No direct clinical or industrial implementation specific to Res2 was identified. |
| Overall annotation | Chromatin-associated DNA-binding regulatory subunit of the fission-yeast MBF transcription complex that controls mitotic G1/S transcription and has a stronger specialized requirement in premeiotic S phase and meiosis. (ivanova2013thednadamage pages 47-52, zhu1997functionalcharacterizationof pages 9-11, eshaghi2011deconvolutionofchromatin pages 2-2) | Integrated biochemical, genetic, genomic, and evolutionary evidence | High. Remaining gaps include native complex structure, quantitative Res2-only DNA affinity, direct live-cell localization, and possible Res2-specific post-translational regulation. |
Table: Evidence-weighted annotation of fission-yeast Res2/Pct1 (UniProt P41412), covering identity, molecular function, pathways, localization, quantitative findings, and remaining limitations.
The direct mechanistic literature on Res2 itself is concentrated in 1994–2000. More recent work has shifted from identifying the subunit to resolving how the Res2-containing MBF system is controlled by checkpoint signaling, dynamic cofactor recruitment, and chromatin architecture. Major developments include genome-wide Res2/MBF occupancy mapping, identification of Cds1–Yox1 and Chk1–Cdc10 checkpoint inputs, and demonstration that INO80 and acetylated H2A.Z are required for full temporal activation of MBF promoters. (eshaghi2011deconvolutionofchromatin pages 2-2, ivanova2013thednadamage pages 86-127, knezevic2018theino80complex pages 4-7)
No Res2-focused primary paper from 2023–2024 was identified. The most relevant 2024 authoritative source is the sexual-differentiation review cited above, which retains Res2 within the established MBF/meiotic-entry framework rather than proposing a substantially revised molecular function. (kawamukai2024regulationofsexual pages 1-2)
Current applications are principally experimental rather than clinical:
No direct therapeutic, diagnostic, or industrial implementation specific to Res2 was found.
The strongest annotation is:
Res2 is a chromatin-associated DNA-binding regulatory subunit of the fission-yeast MBF transcription complex. It recognizes MCB-containing promoters in cooperation with Cdc10 and Res1, contributes context-dependent activation and repression of mitotic G1/S genes, and is specifically required for premeiotic DNA replication and meiotic progression.
The evidence is strongest for protein identity, Cdc10 association, MCB specificity, MBF membership, and meiotic requirement. Important unresolved questions are the native stoichiometry and full-length structure of MBF; quantitative Res2-only DNA-binding affinity; the complete direct target set in meiosis; direct live-cell localization dynamics; and whether Res2 itself undergoes regulatory post-translational modification. Current checkpoint evidence should not be overinterpreted as direct Res2 regulation because the experimentally demonstrated targets are chiefly Cdc10, Yox1, Nrm1, and Rep2-associated mechanisms. (zhu1997functionalcharacterizationof pages 9-11, ivanova2011g1stranscriptionand pages 3-4, ivanova2013thednadamage pages 86-127)
References
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(ayte1997thefissionyeast pages 7-7): José Ayté, José F. Leis, and James A. DeCaprio. The fission yeast protein p73res2 is an essential component of the mitotic mbf complex and a master regulator of meiosis. Molecular and Cellular Biology, 17:6246-6254, Nov 1997. URL: https://doi.org/10.1128/mcb.17.11.6246, doi:10.1128/mcb.17.11.6246. This article has 38 citations and is from a domain leading peer-reviewed journal.
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(kawamukai2024regulationofsexual pages 1-2): Makoto Kawamukai. Regulation of sexual differentiation initiation in schizosaccharomyces pombe. Bioscience, biotechnology, and biochemistry, 88:475-492, Mar 2024. URL: https://doi.org/10.1093/bbb/zbae019, doi:10.1093/bbb/zbae019. This article has 17 citations.
(ivanova2011g1stranscriptionand pages 3-4): Tsvetomira Ivanova, Blanca Gómez-Escoda, Elena Hidalgo, and José Ayté. G1/s transcription and the dna synthesis checkpoint: common regulatory mechanisms. Cell Cycle, 10:912-915, Mar 2011. URL: https://doi.org/10.4161/cc.10.6.14963, doi:10.4161/cc.10.6.14963. This article has 29 citations and is from a peer-reviewed journal.
(ivanova2013thednadamage pages 86-127): Tsvetomira Ivanova, Isabel Alves-Rodrigues, Blanca Gómez-Escoda, Chaitali Dutta, James A. DeCaprio, Nick Rhind, Elena Hidalgo, and José Ayté. The dna damage and the dna replication checkpoints converge at the mbf transcription factor. Molecular Biology of the Cell, 24(21):3350-3357, Nov 2013. URL: https://doi.org/10.1091/mbc.e13-05-0257, doi:10.1091/mbc.e13-05-0257. This article has 37 citations and is from a domain leading peer-reviewed journal.
(ivanova2013thednadamage pages 145-154): Tsvetomira Ivanova, Isabel Alves-Rodrigues, Blanca Gómez-Escoda, Chaitali Dutta, James A. DeCaprio, Nick Rhind, Elena Hidalgo, and José Ayté. The dna damage and the dna replication checkpoints converge at the mbf transcription factor. Molecular Biology of the Cell, 24(21):3350-3357, Nov 2013. URL: https://doi.org/10.1091/mbc.e13-05-0257, doi:10.1091/mbc.e13-05-0257. This article has 37 citations and is from a domain leading peer-reviewed journal.
(dutta2008thednareplication pages 5-7): Chaitali Dutta, Prasanta K. Patel, Adam Rosebrock, Anna Oliva, Janet Leatherwood, and Nicholas Rhind. The dna replication checkpoint directly regulates mbf-dependent g1/s transcription. Oct 2008. URL: https://doi.org/10.1128/mcb.00596-08, doi:10.1128/mcb.00596-08. This article has 69 citations and is from a domain leading peer-reviewed journal.
(knezevic2018theino80complex pages 4-7): Iva Knezevic, Alberto González‐Medina, Laura Gaspa, Elena Hidalgo, and José Ayté. The ino80 complex activates the transcription of s‐phase genes in a cell cycle‐regulated manner. The FEBS Journal, 285:3870-3881, Sep 2018. URL: https://doi.org/10.1111/febs.14640, doi:10.1111/febs.14640. This article has 17 citations.
(knezevic2018theino80complex pages 7-10): Iva Knezevic, Alberto González‐Medina, Laura Gaspa, Elena Hidalgo, and José Ayté. The ino80 complex activates the transcription of s‐phase genes in a cell cycle‐regulated manner. The FEBS Journal, 285:3870-3881, Sep 2018. URL: https://doi.org/10.1111/febs.14640, doi:10.1111/febs.14640. This article has 17 citations.
(ivanova2011g1stranscriptionand pages 5-5): Tsvetomira Ivanova, Blanca Gómez-Escoda, Elena Hidalgo, and José Ayté. G1/s transcription and the dna synthesis checkpoint: common regulatory mechanisms. Cell Cycle, 10:912-915, Mar 2011. URL: https://doi.org/10.4161/cc.10.6.14963, doi:10.4161/cc.10.6.14963. This article has 29 citations and is from a peer-reviewed journal.