All 53 imported contexts are reviewed. The three natural products and the specific constructs used in experiments remain distinct. This guide joins the accepted original-reading scopes; it does not expand them or infer access from normal-cache flags.
The three source-described products remain distinct: displayed O95718-3 is 433 residues, O95718-1 is 508, and O95718-2 is 500. A shared DNA-binding fragment does not establish equivalent full-length regulation. No new publication quotation or annotation is proposed.
Bombail et al., PMID:18775884, main Methods (human endometrial samples, isoform-specific RT-PCR, antibodies, immunohistochemistry and confocal microscopy) and Results/Figures 3–5, supplies positive human nuclear staining. The antibody recognizes the long and short forms; peptide blocking and separately expressed short-form controls support assignment. Short/long transcripts were detected in endometrium, whereas delta10 was not detected there under the tested conditions. Endogenous staining cannot identify an individual product. These assays establish nucleus but do not distinguish nucleoplasm from every other nuclear compartment. The integrated review refines the location to nucleoplasm using independent human HPA and target-specific Reactome evidence described below, without attributing that finer resolution to this endometrial experiment. Main text/captions were read, not figure pixels or supplemental Figure S1. Main text and a caption differ in placental timing, so no placental timing inference is used.
Xie et al., PMID:19196830, Methods human H1/H9 and mouse ESC culture/differentiation and quantitative PCR; Results nuclear-receptor expression; Discussion ERR-family comparison. The actual cached main original contains the operative text. Human ESC/early embryoid-body expression was negative for ERRbeta under these conditions, and mouse expression and earlier mouse trophoblast studies are discussed. This is not a human placental functional perturbation. The imported NOT embryonic placenta development remains exactly negated and UNDECIDED; neither human absence of function nor a replacement positive is established by this experiment. Supplemental primer tables and figure pixels were not read.
Cho et al., PMID:23836911, actual PMC main original, Experimental Procedures and Figure 1B/adjacent Results: FLAG-ERRbeta adenoviral expression increases Perm1 mRNA in mouse C2C12 myotubes. The inspected original does not identify the ERRbeta insert accession, species or C-terminal product. Mouse host does not determine insert species. The ChIP result tests ERRalpha and FLAG-PGC-1alpha, not ERRbeta. Failed direct-fetch routes and the abstract-only normal cache do not negate the subsequently recovered main-text access. Figure pixels/supplement were not read.
Nakadai et al., PMID:36646760, PMC original, Results on conserved ERR-family mechanisms; Methods Plasmids, Recombinant proteins and In vitro transcription; original Supplementary Figure S5b (human chromatin activation), j (DNA binding), k (WT/DBD-mutant transcription) and l (p52 competitive inhibition). Independently inspected human ERRbeta-L/S proteins activate an ERRE-containing template with RNA polymerase II and transcript readout. S5b chromatin reactions include trace HeLa nuclear extract; the positive naked-DNA transcription reactions and their mutant/p52 controls are distinct. The full S5 caption and page-one pixels were read. The cDNA spreadsheet printed Table S4, Sheet1 rows 5–6, names NP_004443 and AAS15571; the vector/tag spreadsheet printed Table S5, row 5, describes the FLAG constructs. The main's S5/S6 table numbering differs from those actual headings. Files are preserved under their published names at the official BioStudies record: 41422_2022_774_MOESM5_ESM.pdf, 41422_2022_774_MOESM11_ESM.xlsx and 41422_2022_774_MOESM12_ESM.xlsx.
The unversioned table accessions correspond in the recovered current records to 508- and 433-residue products. This verifies current correspondence, not every historical plasmid base; no 500-residue product activity is inferred. The independent positive human reaction resolves the gene's transcription-regulation claim and supports refinement to GO:0045944. It does not retroactively identify the 2013 construct or establish native human PERM1 occupancy.
Katano et al., PMID:25522312, main Methods, Results/Figure 3 and the original supplemental Materials and Methods (stem0033-1089-sd7.docx, Plasmid construction), reports positive pCAG-Flag-Esrrb rescue of mouse NS-tetoff ESC colonies, growth and pluripotency markers. It is not merely a correlation. The actual supplementary construct methods were read in full, but do not identify an Esrrb species/accession/current product. The human SC102A1 iPSC experiment depletes nucleostemin; it does not demonstrate ESRRB rescue. EpiSC behavior differs from ESC rescue. The gene-level role is retained as KEEP_AS_NON_CORE using independent mouse transcriptional-occupancy and population-maintenance evidence together with conserved human transcriptional capability. The historical insert identity and a human ESRRB-rescue assay remain unverified; this is not a wrong-gene or negative-function claim. Other downloaded supplementary figures were not read or viewed.
Gearhart et al., PMID:12654265, actual primary PDB 1LO1 and deposition mmCIF, identifies the human ESRRB DNA-binding fragment with complementary DNA strands in solution NMR. Protein/source/sequence/sample metadata were inspected; article Methods remain inaccessible. The 98-residue fragment maps to current 97–194. C163A is designated engineered, while S193N is separately flagged SEE REMARK 999; that second designation is not silently recast as engineered. No coordinate-contact analysis or figure inspection is claimed.
Yin et al., PMID:28473536, actual Methods protein production and HT-SELEX/methyl-HT-SELEX, plus original supplemental workbook. Sheet S1 sequence information, row 562, identifies ESRRB and its 109-residue eDBD; it exactly matches current residues 85–193 without substitutions. Sheet S2 PWM models, rows 6418–6427, contains ESRRB methyl-HT-SELEX and ordinary HT-SELEX motif matrices. The selection uses double-stranded ligands. These exact target records support sequence-specific dsDNA binding; no target methylation-preference claim is needed. The fragment is common to all three products, but full-length equivalence was not tested. project_target_evidence.py replays the literal target-table and sequence projection offline.
Current GO:1990837 is an is_a descendant of the broader imported GO:0043565; GO:0045944 is an is_a descendant of GO:0006355. Official definitions and typed closures were captured. The two refinements are source reviews, not NEW annotations.
ERRβ has a sequence-specific DNA-binding domain and activates RNA-polymerase-II transcription. Human long and short constructs have been tested directly; the natural 500-residue product remains distinct. Steroid-specific receptor/binding/signaling assertions are unresolved. Pharmacological modulation is positive evidence and is not excluded by the description of ERRβ as an orphan receptor.
| Source and accessible original | Operative location and scope |
|---|---|
| PMID:36646760, Cell Research original | Main Results on human ERRβ-L/S; Methods on constructs, protein preparation, DNA/chromatin transcription and GST pull-down. Actual Supplementary Figure S5 was inspected, including b (chromatin transcription with trace HeLa extract), j (DNA binding), k (DNA-templated activation and DBD-mutant comparison), l (p52 competitive inhibition), and h/i (TFIIB/TFIIH interactions). The supplementary construct tables list NP_004443/AAS15571; their current sequences match 508/433 residues, without verifying historical plasmid sequences or the 500-residue product. The original supplementary files are also available through BioStudies S-EPMC9892517. |
| PMID:28473536, Science author manuscript | Methods, protein expression and HT-SELEX; original supplementary Table S1 sequence information row 562 and Table S2 PWM models rows 6418–6427. The human extended DNA-binding domain is exactly current residues 85–193. Ordinary and methyl-HT-SELEX identify DNA sequence preference, not a full-length transcriptional or ligand assay. Actual workbook retrieved from BioStudies S-EPMC8009048. |
| PMID:18662995 original | Mouse embryonic-stem-cell Methods and Results, Figures 1–4 captions: Esrrb–Oct4 association with DNA-disruption controls, Nanog regulatory-site EMSA/mutation and Oct4/Sox2 dependence. Transfection into human cells does not establish a human receptor construct. No figure pixels or supplementary experiments inspected. |
| PMID:27723719 deposited author manuscript | Results/Figure 1 and Methods: mouse ES-cell mitotic chromosome association by GFP, endogenous TdTomato and immunostaining, Dox-withdrawal controls, and DNA-binding mutants. Mouse embryo injections are a separate experiment. Selected manuscript text was read; page pixels and complete supplements were not inspected. |
| PMID:23019124 original | Mouse ES-cell Methods/Results, especially Figure 6F–H: Esrrb/Ncoa3/polymerase-II association and its Ncoa3 dependence. Positive complex-mediated association is distinguished from a purified binary contact. No figure pixels or supplements inspected. |
| PMID:26206133 original | Mouse trophoblast-stem-cell Methods/Results; depletion/rescue and markers, Eomes/Elf5 enhancer binding/reporters, Figure 5 nuclear proteomics and INTS1/INTS9 co-IP. Integrator association does not establish universal stoichiometric membership or snRNA-cleavage activity. No figure pixels or raw supplementary proteomics inspected. |
| PMID:23040477 original | Mouse Methods/Results and figure captions: conditional self-renewal, EpiSC reversion and somatic reprogramming, with marker/transgene/chimera endpoints. No universal necessity across culture conditions or human product equivalence inferred. |
| PMID:23040478 original | Mouse Methods/Results: clonal self-renewal, Esrrb depletion/knockout and rescue, with viability and LIF/GSK3-context controls. No figure pixels or supplements inspected. |
| PMID:34397088 original | Mouse ES-cell Methods/Results: Esrrb/Nr5a2 single/double perturbation, occupancy, colony maintenance and differentiation. Functional redundancy is explicit. No figure pixels or supplements inspected. |
| PMID:20534447 original | Main Methods/Results and Figures 1–5 captions: rhodopsin-promoter reporter modulation, conditional mouse retinal genetics, rod maintenance and rescue. Figure 1K is a 293T reporter assay; the receptor insert was not assigned a human accession in the inspected main text. Complete SI Methods/pixels were not read. |
| PMID:39361745 deposited author manuscript | Mouse maternal/zygotic single and double knockout Methods; Results/Figures 3–4 distinguish an earlier Esrrb transcriptional contribution from the dominant Nr5a2 morula phenotype. Normal Esrrb-null development is not proof of no participation; the specific transferred morula-formation role remains unresolved. Selected manuscript text, no pixels or supplements. |
| PMID:17765677 publisher record | Verified positive mouse inner-ear-development abstract. Operative full Methods/Results unavailable; the precise developmental transfer remains unresolved. |
| PMID:24315836 publisher preview | Verified marine 4-methylenesterol-antagonist abstract and partial human ERRβ-LBD/GAL4 construction/reporter Methods. Complete Results, doses, direct binding and product sequence unavailable. Pocket models are theoretical. The positive sterol lead is retained rather than dismissed. |
| PMID:16332939 publisher record | Verified abstract describing three human products with differing ERE-reporter activity and localization signals. Full Methods/Results unavailable; not treated as a newly inspected direct binding assay. ERE DNA binding is distinct from estrogen ligand binding. |
All publication and machine source caches are preserved exactly. Normal-cache access flags describe the original fetch; separately recovered manuscripts and supplements are described above without rewriting those caches. No publication quotations were added.
The human endometrial experiment in PMID:18775884(https://doi.org/10.1093/humrep/den298) supports nuclear staining. The more precise nucleoplasm replacement is grounded separately in the human ESRRB HPA record and the explicit ESRRB participant in R-HSA-376419 and R-HSA-382096. HPA uses a shared antigen and Reactome represents residues 1–433; neither establishes every natural product in every tissue. The endometrial source keeps its own broader experimental scope. GO:0005654 is the current specific compartment used for the replacement.
The single unit uses GO:0001228, DNA-binding transcription activator activity specific to RNA polymerase II, in chromatin, directly involved in positive regulation of RNA-polymerase-II transcription. The MF is a typed part_of child of that BP; this is a cross-aspect activity-to-process connection, not two redundant BP assertions. Only one MF, one BP and one location are used. The chromosome, nucleus and general transcription-regulation ancestors are not added as duplicate coverage.
The 2023 primary original, Results on conservation across ERR-family members and Methods Plasmids, Recombinant proteins and In vitro transcription, identifies human ERRβ-L/S and measures regulatory-template binding and RNA production. Supplementary Figure S5j measures DNA binding, S5k compares WT and DBD-mutant transcription, and S5l tests p52 competitive inhibition. The core phase reread the operative text and full S5 caption; the earlier direct/database and independent ROOT readings of S5 pixels remain recorded separately. Human S5b chromatin-template activation uses coactivators and trace HeLa nuclear extract. This is positive chromatin-associated activation, not a completely defined human chromatin reaction or evidence that every observed protein contact is an isolated binary interaction.
The transcription factor performs regulatory work by recognizing the template and promoting transcript production with the polymerase machinery. RNA polymerase II performs RNA synthesis. The positive activation endpoint is therefore more than necessity inferred from a developmental perturbation. Mouse chromatin bookmarking and stem-cell phenotypes support conserved context but are not substituted for the human activation assays or promoted into additional core processes.
The exact human eDBD in the 2017 original, Methods protein expression and HT-SELEX/methyl-SELEX, and original Table S1 row 562/Table S2 rows 6418–6427, independently supports sequence-specific double-stranded-DNA recognition. It is a 109-residue fragment matching current positions 85–193. It does not establish full-length product equivalence, a preferred methylation state or steroid binding. The 2023 supplementary table and current-accession correspondence are detailed above: the printed tables identify historical L/S reagents but are not resequenced plasmids; no activity is assigned to the natural 500-residue product by this core.
The current official ontology definitions and explicit is-a closures were checked. Chromatin is a cellular anatomical entity, not a protein-containing-complex assertion in this representation. The core makes no fixed Integrator or RNA-polymerase-complex membership claim. The core-synthesis phase retained its reference assessments; the later source-scope clarifications are recorded below. Publication caches remain unchanged, and no new publication quotation was added.
Collin et al., PMID:18179891, DOI 10.1016/j.ajhg.2007.09.008: Methods Clinical evaluations, Genetic linkage and Mutation analysis; Results Figures 1–3/Table 2 establish five families with cosegregating biallelic ESRRB variants. Figure 4 describes structural predictions, not measured variant activity. Figure 5 uses isoform-directed RT-PCR on human fetal cochlea; Figure 6 is mouse embryonic in situ; Figure 7 is P4 rat immunohistochemistry. The original body, table and captions were read, but figure pixels and supplements were not independently inspected. The normal cache remains its genuine abstract-only acquisition. Public original access does not change those bytes.
GO:0048839 describes progression from inner-ear formation to the mature structure. Human auditory genetics and expression are relevant positive evidence, but do not on their own assign the timing and executed developmental step. The separate mouse PMID:17765677 retains its positive abstract and unread operative Methods/Results boundary. The precise developmental transfer therefore remains UNDECIDED. No additional process annotation is introduced.
The contextual parent GO:0019827 is now retained consistently with the supported maintenance descendants: PMID:25522312 Figures 3–4 rescue, PMID:34397088 Figures 1–3 occupancy/population assays and PMID:23040478 Figures 3–4 culture-dependent self-renewal are the relevant original locators. The human rescue-insert identity and equal activity of natural products remain unresolved. No wrong-product source defect is inferred from a missing accession.
The original PMID:20534447 Results/Figure 1K was independently read for receptor-dependent reporter pharmacology. Its 293T host is not proof of the receptor insert’s species. This public locator explains why the review can discuss experiments not present in the immutable abstract-only normal cache.