Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
DNA topoisomerase II distribution in mouse preimplantation embryos.
DNA topoisomerase II is essential for preimplantation mouse development.
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Topoisomerase II is essential for preimplantation mouse development: inhibition blocked cleavage in the majority of embryos, demonstrating an essential in vivo requirement for chromosome condensation and segregation.
"Topoisomerase II (topo II) is an essential enzyme that alters DNA topology."
Characterization of cDNA encoding the mouse DNA topoisomerase II that can complement the budding yeast top2 mutation.
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Mouse DNA topoisomerase II cDNA (1528 aa) was characterized and shown to complement the budding-yeast top2 mutation, providing direct genetic evidence for conserved type II topoisomerase activity.
"Characterization of cDNA encoding the mouse DNA topoisomerase II that can complement the budding yeast top2 mutation."
Possible role of DNA topoisomerase II on transcription of the homeobox gene Hox-2.1 in F9 embryonal carcinoma cells.
Condensins I and II are essential for construction of bivalent chromosomes in mouse oocytes.
BAF complexes facilitate decatenation of DNA by topoisomerase IIα.
Haploinsufficiency of SAMD9L, an endosome fusion facilitator, causes myeloid malignancies in mice mimicking human diseases with monosomy 7.
Shikonin shortens the circadian period: possible involvement of Top2 inhibition.
Condensin confers the longitudinal rigidity of chromosomes.
Conditional mutation of Smc5 in mouse embryonic stem cells perturbs condensin localization and mitotic progression.
GCNA Interacts with Spartan and Topoisomerase II to Regulate Genome Stability.
Modulation of topoisomerase activities by tumor necrosis factor.
Mutant isolation of mouse DNA topoisomerase II alpha in yeast.
Analysis of expression and function of topoisomerase I and II during meiosis in male mice.
Cellular distribution of mammalian DNA topoisomerase II is determined by its catalytically dispensable C-terminal domain.
Falcon deep research report on mouse Top2a (DNA topoisomerase 2-alpha, Q01320)
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Top2a is an ATP-dependent type IIA DNA topoisomerase that creates a transient enzyme-linked double-strand break in one DNA duplex and passes a second duplex through before religation, thereby relaxing supercoils and decatenating interlinked duplexes.
"**Top2a/TOP2A** is an **ATP-dependent type IIA DNA topoisomerase** that resolves topological stress by creating a **transient, enzyme-linked double-strand break** in one DNA duplex (the “gate” segment) and transporting a second duplex (the “transport” segment) through the break before **re-ligating** the DNA. This activity changes DNA topology and enables both **relaxation of supercoils** and **decatenation** (unlinking) of interlinked DNA duplexes"
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The substrate is double-stranded DNA in topologically constrained forms in vivo: supercoiled DNA from replication/transcription and catenated sister chromatids from DNA replication; the central outputs are supercoil relaxation and decatenation for chromosome segregation.
"Functionally, TOP2A’s substrate is **double-stranded DNA** in topologically constrained forms encountered in vivo: **supercoiled DNA** produced by replication/transcription and **catenated sister chromatids** produced by DNA replication. Its central physiological outputs are (i) **relaxation of supercoiling** and (ii) **decatenation** required for chromosome segregation"
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The catalytic cycle uses an ATPase/N-gate (ATP binding/hydrolysis controls dimer closure), a DNA-gate where cleavage/religation occurs, and a C-gate; assembly of the cleavage-religation center involves TOPRIM-mediated metal (Mg2+) coordination.
"The catalytic cycle is commonly described in terms of gates: an **ATPase/N-gate** (ATP binding/hydrolysis controls dimer closure), a **DNA-gate** where cleavage/religation occurs, and a **C-gate** that allows release after transport."
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In mouse NIH3T3 cells Top2a is chromatin-associated and enriched at heterochromatin; catalytic inhibition by ICRF-193 increases its chromatin association/retention, consistent with inhibitor-induced trapping on chromatin.
"In mouse NIH3T3 fibroblasts, Top2α is **chromatin-associated** and described as **enriched at heterochromatin**. Importantly, **catalytic inhibition** with **ICRF-193** (a catalytic Top2 inhibitor) increases Top2α chromatin association and retention (including under high-salt extraction conditions) and reduces its mobility by FRAP, consistent with inhibitor-induced trapping on chromatin rather than free diffusion"
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Top2a expression is proliferation-coupled: low in quiescent cells, rising through S phase and peaking at G2/M, consistent with its role managing DNA topology during replication completion and mitosis.
"TOP2A expression is tightly linked to proliferation: it is low in quiescent cells, increases through **S phase**, and peaks during **G2/M**, consistent with its specialized role in managing DNA topology during replication completion and mitosis"
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Sister chromatid decatenation by Top2a is required for individualization and faithful segregation; catalytic inhibition can activate a decatenation/G2 checkpoint, and depletion/inhibition causes chromosome decompaction, bridges, and segregation failure.
"TOP2A decatenation is required to enable sister chromatid individualization and faithful segregation, and catalytic inhibition can activate a **decatenation checkpoint**/G2 arrest phenotype in cell-based contexts"
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Mouse Top2a knockout is embryonic lethal very early (arrest reported as early as the 4-8 cell stage), indicating an essential requirement during cleavage-stage development.
"A frequently cited mammalian genetic result is that **mouse Top2a null embryos are lethal very early**, with arrest reported **as early as the 4–8 cell stage**, supporting an essential requirement during cleavage-stage development"
RanBP2 Sumoylates Top2a with Sumo1