C/EBPalpha is a bZIP DNA-binding transcription factor whose differentiation programs are coupled to proliferative restraint. The review retains all 143 normal source assertions and all four UniProt products. No new annotation row is proposed. There was no prior CEBPA notes file at the checked main snapshot, so this is the first journal entry.
The central activity is sequence-specific transcriptional regulation. Human CEBPA binds and activates granulocyte targets, and AML-associated mutations alter that output (PMID:11242107(https://doi.org/10.1038/85820), Methods and Figures 3–5; genuine full publisher PDF inspected). Human CYP3A4 promoter-site mutations, reporters and endogenous expression provide independent evidence (PMID:12695546(https://doi.org/10.1124/mol.63.5.1180), abstract). EVI2B promoter occupancy and mutant reporters directly connect human CEBPA to a myeloid target (PMID:28186500(https://pubmed.ncbi.nlm.nih.gov/28186500/), full publisher Methods, Figure 2 and supplemental Methods). Human U937 endogenous ChIP and human CEBPA/K562 reporters are distinct from the rat p42/p30 reporter comparison in Figure 3a; the separate ER-induction constructs are human. The published correction changes only an acknowledged grant number. Short verbatim anchors appear at the relevant YAML decisions, with distinct excerpts and at most 25 newly quoted words per paper across the whole packet.
The normal UniProt record displays P49715-1. P49715-2 is named p42 and lacks the displayed sequence's first 14 residues; P49715-3 is p30 and lacks its first 119 residues. P49715-4 has an extended N terminus. These source names, identifiers and sequence notes are preserved exactly. An untagged GOA assertion is not silently converted to a product-specific assertion.
The original p30/WT work directly tests human CEBPA, but its reduced p30 DNA binding is specific to the tested probe and conditions. It does not mean p30 cannot bind any DNA. SWI/SNF-dependent proliferation arrest in PMID:14660596(https://doi.org/10.1074/jbc.M312709200) was read in the selected original author-uploaded Methods/Results and uses rat p42/p30 constructs. Cell-count outcomes are not cell-size measurements.
The extended-product work (PMID:20075868(https://pmc.ncbi.nlm.nih.gov/articles/PMC2810377/), full normal Methods/Results) links nucleolar retention to rDNA regulation and cell-size changes. Many engineered localization and functional assays use rat constructs in human cells. Human endogenous localization and translation-initiation experiments are separate evidence. Both p42 and extended products associate with UBF1; this is not an extended-only interaction or intrinsic RNA-polymerase activity. The nucleolar location remains non-core at the gene level.
The source-evidence artifact contains exact machine-field IntAct records, source queries/hashes, bZIP target measurements and ortholog-source links. The accompanying extractor regenerates these machine fields from the immutable seed and genuine downloaded IntAct, ComplexPortal, GOA and bZIP source inputs. Its input hashes and public source locations are recorded in the artifact; reproduction was checked before publication. Empty query matches are not negative interaction results. Curated records link a target to an assay/publication; they are not independent experimental replications. HaloMS and BioPlex co-capture can report complex-associated interactions without proving isolated direct contact. IL32beta is retained as the exact P24001-2 source partner, including recorded fragment limits.
For PMID:20102225(https://doi.org/10.1021/bi902065k), the genuine publisher supplement Figure S2/Table S2 was inspected, including target cells and the heatmap. Its SHA256 is 34b9a53a9762e0bcaf10b2a7637dc751d87d9fe0e400512c355e180aa570dc21. The experiment measures purified human leucine-zipper domains. Array intensities are not dissociation constants, and weak asymmetric pairs are not called high-affinity physiological complexes.
For PMID:23661758(https://doi.org/10.1126/science.1233465), the original full primary Methods and source-linked ComplexPortal entries were read. The released 2013 supplement was not recovered. Exact human partner affinities were instead inspected in the first author's 2012 MIT thesis, Chapter 5 Methods and Table 5.2, printed page 195; SHA256 23aac751d497316468d1e2f134b583628651c22a66b378d64b078f2b93ecdc9c. These values are explicitly thesis measurements and are not relabeled as the 2013 published table or as independent replication. Together with the curated source links and conserved biochemical activity, they support bounded dimerization refinements. No untested cellular transcriptional program is inferred from a pair's affinity.
Supported remaining generic interactions are retained as non-core under the explicit campaign curation instruction: supported, correct protein binding is kept as non-core when no better supported molecular function is established. This is the applicable user-authorized instruction; no shared validator or policy is changed.
Direct CDK inhibition is reported in the authentic abstract of PMID:11684017(https://doi.org/10.1016/S1097-2765(01)00366-5). Its full construct-level Methods were not recovered. The reported inhibitory core is explicitly context dependent, and the reference assessment states the construct-access limit. The original source-specific kinase-binding rows are refined only to protein kinase binding, preserving their IPI event. Selected full indexed PMID:15107404(https://pmc.ncbi.nlm.nih.gov/articles/PMC395850/) Methods/Results and Figure 8 contain genuine human normal/tumor liver associations with CDK2, CDK4 and BRM; separate phosphorylation mutagenesis uses mouse constructs. The existing short normal cache is partial despite its full-text flag. Official PubMed XML checked on 2026-10-10 has no linked correction/retraction record or retraction publication type for either paper; the direct publisher status requests were blocked. This is a dated database-status observation, not a guarantee against every possible concern. E2F repression in mouse alleles (PMID:11672531(https://doi.org/10.1016/S0092-8674(01)00516-5)) supplies a distinct mechanistic route to arrest and differentiation, not the direct kinase-inhibition assay.
A separate primary test limits the physiological generalization. In PMID:16428455(https://pmc.ncbi.nlm.nih.gov/articles/PMC1347024/), the genuine full Methods, Results/Figures 1–2 and 5–7 and Discussion were read externally. Rat expression constructs and a mouse/rat hybrid knock-in retain growth repression after deleting the proposed PHR kinase-interaction region. Fetal-liver BrdU incorporation and CDK2 histone-H1 kinase activity, myeloid replating, and the measured response to partial hepatectomy show no corresponding growth defect in the tested systems. The authors could not recover CDK2 co-IP under their extraction conditions and explicitly discuss possible high-salt disruption; that does not disprove the separate binding evidence. Thus direct CDK inhibition remains a reported context-dependent mechanism, not an obligatory explanation of all CEBPA growth repression. The normal cache is abstract-only, whereas the externally inspected full source is available at the linked PMCID.
The CHOP-focused review PMID:14685163(https://doi.org/10.1038/sj.cdd.4401373) actually discusses CEBPA-mediated CDK turnover and arrest in its original full author-uploaded text. Independent PMID:11867521(https://pubmed.ncbi.nlm.nih.gov/11867521/) abstract and primary Figure 2/6 legends support CDK4 ubiquitination/turnover and MG132 sensitivity. This is a regulatory process, not evidence that CEBPA is an E3 enzyme; it is not generalized to CDK2 degradation.
The white-fat proliferation assertion is refined to fat-cell differentiation. In PMID:36228616(https://doi.org/10.1016/j.cmet.2022.09.018), selected full Figure 6 Results and Methods show CEBPA DNA binding, reporter activation and adipogenic promoter occupancy. Ovol2 perturbations alter Oil Red O and mature markers during differentiation; tissue hyperplasia is not a demonstrated CEBPA-dependent division assay. Human OVOL2 experiments do not establish an independently manipulated human CEBPA result. The leptin-promoter source PMID:8643605(https://doi.org/10.1073/pnas.93.11.5507) positively establishes transcriptional activation; its broad energy-generation term is refined to that performed step, not interpreted as CEBPA catalyzing energy-producing chemistry. Full scanned body access remains incomplete, and no claim excludes all possible metabolic regulatory roles.
The STAT3-focused PMID:16946298(https://doi.org/10.1182/blood-2006-07-033969) explicitly contains CEBPA-siRNA and promoter-deletion experiments in human Huh7 cells, Figure 3. The original indexed full Results were inspected; the title/abstract alone would miss them. Human IL6-dependent CEBPA/PU.1/STAT3 complexes, promoter occupancy and reporter cooperation were read in PMID:24429361(https://doi.org/10.1128/JVI.03060-13), selected publisher Methods/Results and Figures 3–4. These co-IP, ChIP and reporter experiments use primary human hepatocytes; the separate nuclear-colocalization experiment uses HepG2. Other organ/metabolic effects retain their rodent transfer scope and remain non-core.
The initial normal R-HSA-9622363 retrieval and first bounded retry failed, and those receipts remain preserved. A later genuine normal retry recovered the human CEBPA–KLF5 promoter-binding event; its curated nucleoplasm assertion is therefore retained as non-core, consistent with independent human nuclear evidence. Integrated stress signaling remains undecided: the genuine CEBPA–ATF4 ComplexPortal entry links to PMID:28566324(https://pmc.ncbi.nlm.nih.gov/articles/PMC5496626/), but the read full primary experiments do not resolve the specific heterodimer's functional contribution. This is not called a wrong-gene error or rejected merely because the paper emphasizes ATF4.
The initial normal seed and all normal source bytes remain unchanged. The genuine Falcon attempt timed out at 90 seconds; its explicit Perplexity-lite fallback returned HTTP 401 for insufficient quota. No provider report was fabricated. Manual primary-source research continued. Several saved PMC/BioC/publisher requests contain recaptcha, 403 or no-result bodies; file extensions and HTTP 200 were not treated as proof of full text. Source-by-source access notes in the YAML distinguish normal cache content, externally inspected primary text, curated assay records, and unresolved source details. The reviewed CEBPA main/alias trees and complete open-PR inventory were clear at main e94991ceada8507158f48e9902087033919dd36b.
This entry supersedes the preceding entry's characterization of CDK inhibition as a separate headline core. The biological report is retained, with its access and context limits. The TF core now includes the already-supported negative-cell-cycle process and E2F-dependent proliferative restraint. PHR dispensability in selected models does not disprove direct biochemical inhibition. No source assertion or per-row action changes in this follow-up; the 143 source objects, all four products and original journal prefix remain unchanged.
The earlier PR explanation that a NEW GO:0004861 assertion would be redundant with binding was incorrect. The current official is_a/part_of ancestry does not include GO:0005515, GO:0019900 or GO:0019901, and intersects none of this review's source terms or proposed replacements. The decision not to add that assertion rests on the unresolved human assay scope and core prominence, not ontology redundancy. A bounded query found no GO:0004861 annotations for human CEBPA, CEBPB or CEBPD, but family membership does not establish identical mechanistic roles and annotation absence does not refute inhibition.
Short excerpts are used within the session's source quotation limit; the limit is an external quotation constraint, not a repository curation rule. A decision is supported by the full source-specific read and assay locator, not by quote count. The two generic bZIP background excerpts were removed: the exact CEBPA partner measurements in the source artifact, indexed by immutable source identity, supply the target-specific evidence. Nucleolar row70 now quotes the retention result rather than alternative translation initiation.
The extractor instructions and input manifest now give actual retrieval commands, public locations and expected SHA256 hashes. The extractor joins source tuples rather than annotation positions, declares its Python dependency, records a computed supplement MD5 and fails informatively for missing/changed snapshots or unknown partners. This is a primary-record extraction, not a computational function-prediction analysis. Public database responses can change; a mismatch is reported rather than accepted as the reviewed historical input. Reordering the review's rows preserves the extracted result.
The TF parent GO:0000981 is retained because the biology includes promoter-dependent activation and repression. The source-specific energy/transcription, cell-cycle/negative-regulation and adipocyte-proliferation/differentiation refinements are retained: MODIFY records the positively supported performed process even when another source independently supplies the same destination. No REMOVE or OVER quota is imposed. Generic-binding rows were explicitly assessed for functional specificity, but supported residual associations remain non-core under the campaign instruction. The unresolved stress-response row stays UNDECIDED.
The prior history's statement about retaining both assigning-source versions refers to preservation in the raw 144-row GOA archive. The normal seed deterministically projects those two nucleus IDA records to one assertion, producing 143 reviewed rows; it does not contain two separately reviewed copies. Existing history is append-only and is not rewritten.