CSNK2A1 evidence notes

2026-10-13 — source-specific review

CSNK2A1 encodes CK2 alpha, a protein serine/threonine kinase. The compact core is the performed phosphorylation reaction, protein phosphorylation, nuclear and cytosolic contexts, and membership in the CK2 complex. This accommodates diverse substrate outcomes without treating each downstream response as a separate core activity. In the human PTEN study, commercial recombinant CK2 was a holoenzyme; cell experiments used human MCF7 and monkey COS7 hosts. The alpha/alpha-prime distinction and the tested reagent matter. PMID:11035045(https://pubmed.ncbi.nlm.nih.gov/11035045/) reports “a cluster of Ser/Thr residues”.

Direct catalytic evidence is distinct from downstream regulation. The RAD51 experiments join PLK1-dependent Ser14 priming to CK2-dependent Thr13 phosphorylation; they do not make CSNK2A1 a DNA-repair scaffold. PMID:22325354(https://pubmed.ncbi.nlm.nih.gov/22325354/) describes “S14 phosphorylation licenses subsequent Rad51 phosphorylation at threonine 13”. In the TEL2 study, the main Methods identify recombinant CK2 alpha 1, while additional cellular assays establish the TEL2 phosphorylation context; the author-hosted original was read, without a supplementary-page or figure-pixel claim. PMID:20864032(https://pubmed.ncbi.nlm.nih.gov/20864032/). The MRE11, HSJ1, FNIP1 and FMRP studies likewise support positive substrate-specific effects, with their cell, fragment and reconstitution limits preserved in the review and evidence index.

The current GO:0106310 comment recommends its use for serine-specific enzymes. CK2 performs both serine and threonine phosphorylation. The thirteen experimental serine-activity assertions and the RHEA-derived assertion are therefore refined to GO:0004674 at the target level. This retains the genuine serine reaction and does not claim a false RHEA mapping, a typed child relationship, or absence of serine activity. The comment's inconsistent cross-reference is retained as an ontology question. Current term, RHEA:17989.

Products and constructs

The two official products reconstruct exactly: P68400-1 has 391 residues; P68400-2 has 255 after VSP_041925 removes residues 1–136. The deletion removes the annotated ATP-binding region and part of the kinase domain. Sequence evidence does not establish either equivalent activity or complete inactivity of the shorter product. Source product slots remain unchanged. UniProt P68400.

The deposited 4DGL alpha construct has 335 residues and an R at the position corresponding to canonical Y125, while the deposition describes an R125Y mutation. This sequence/label discrepancy is retained rather than silently repaired. Structural evidence supports canonical CK2 assembly; it does not assay the endogenous 255-residue product. PDB 4DGL, PMID:22506723(https://pubmed.ncbi.nlm.nih.gov/22506723/).

Interaction evidence

All 175 generic protein-binding source assertions remain positive. Forty-six receive a more informative partner-class term, and 129 remain non-core under the project's standing positive-binding instruction. A binding term classifies the bound partner; it does not transfer that partner's activity to CK2 or establish a native regulatory mechanism. Refinements use literal assay pairs, sequence/construct checks and reviewed partner classes. The public YAML evidence index retains the actual interaction records, their provenance and the precise limits.

The current IntAct/MINT captures contain 810 complete 42-field records. There are 179 reviewed source joins (including non-generic binding), 265 unique positive used records and 530 participant sequence checks. Every computed ROGID matches its recorded backbone. Fragment coordinates, tags, host organisms, negative flags and assay types remain distinct from full-length physiological claims. Current-feed absence is not a negative interaction result. The OpenCell table has 242 target-bearing rows and 22 source joins; grouped CSNK2A1/CSNK2A3 prey assignments remain grouped and non-core. IntAct, OpenCell.

Several source boundaries change the interpretation of a positive pair. PMID:22113938 records phosphorylation assays using bead-immobilized cell-lysate preparations, not measurements of stable binary binding affinity. In PMID:21968188, direct SIRT1 contact is assigned to CK2 beta, whereas alpha occurs in the associated complex. The CBX/PRC1 studies distinguish CK2-alpha association with CBX-containing complexes from direct CBX4–CK2-beta binding. None is converted into an unsupported alpha adaptor or direct-contact mechanism. PMID:22113938(https://pubmed.ncbi.nlm.nih.gov/22113938/), PMID:21968188(https://pubmed.ncbi.nlm.nih.gov/21968188/), PMID:21282530(https://pubmed.ncbi.nlm.nih.gov/21282530/).

Product-specific evidence overrides a gene-level partner label. The POU6F2 interaction tests residues 9–691 of displayed P78424 isoform 1; all three literal HuRI records retain the insertion absent from isoform 2. The official record assigns lack of DNA binding to isoform 1. That positive interaction remains generic/non-core rather than acquiring a DNA-binding transcription-factor class from another product. TRIM41 likewise retains positive binding without an E3-class refinement from a fragment lacking its RING region. POU6F2 record, HuRI PMID:32296183.

Propagation, locations and pathway contexts

The actual PANTHER v19 PTHR24054 tree contains 540 nodes. The human target PTN002513964 is on a 23-node path and its ungapped sequence matches the official 391 residues exactly. All six seeded IBA terms have matching on-path IBD assertions. Proximate PTNs are recorded in the review; extant evidence and complete literal donor records are retained separately. The target's own experimental annotation is legitimate descendant grounding, not circularity. Forty-eight donor joins resolve to 871 captured records with 183 exact supporting occurrences. PANTHER family, PAINT.

All 27 ARBA00027460 condition branches were evaluated against the official InterPro, FunFam and taxonomic fields. Only zero-based branch 4 matches: the two recorded FunFams and Haplorrhini. Its actual GO:0042176 output is preserved as a broad non-core regulatory context, not an unexplained failed inference. ARBA00027460.

HPA metadata identify two antibodies and human cell lines supporting nucleoplasm. The metadata and antibody/cell-line distinctions were read; fluorescence pixels were not independently inspected. Twelve Reactome event roots were followed through 43 objects and 27 target-bearing paths. Ten cached GO-CAM models contain eleven target activities, including MDC1/TOPBP1, FMRP, RAD9, HTATSF1, MRE11 and other contexts. These are positive curated pathway roles, with their original source and participant distinctions retained; they do not require a new core for every substrate or a new annotation. HPA CSNK2A1, Reactome.

Remaining source uncertainty and access

Three assertions remain undecided. The heterochromatin-formation assertion requires unresolved target-specific supplementary evidence from PMID:22325352. The alpha self-binding assertion from the Drosophila circadian paper PMID:24013921 is not resolved by the main text's commercial human CK2 assay. The TAFII250–CK2–Mdm2 paper demonstrates association and phosphorylation but explicitly presents the p53-turnover consequence as a model requiring further molecular and cell studies. These are source-specific limitations, not claims that the positive molecular data are false. PMID:22325352(https://pubmed.ncbi.nlm.nih.gov/22325352/), PMID:24013921(https://pubmed.ncbi.nlm.nih.gov/24013921/), PMID:18548200(https://pubmed.ncbi.nlm.nih.gov/18548200/).

All 98 reference identities were reconciled to genuine selected metadata. Five reference-support assessments remain UNVERIFIED where the target assay/table was not established in the actual read: 20439735, 21630459, 22325352, 24013921 and 40205054. Identity verification and source-support verification are separate. Abstract-only evidence that explicitly identifies the target can support a positive judgment; inaccessible details are not evidence of a wrong target. Main-text availability is separate from the repository cache's full_text_available field and from the exact pages/paragraphs personally read.

Original source access was expanded without replacing repository caches. The owner read selected original Methods/Results/Discussion for the sources enumerated in the evidence index. The independent core consultation read the full scientific main sections of 11035045, 12700239 and 18548200; its 217/157/225 source main texts remained unavailable, with the 4DGL deposition available separately. No universal full-paper or figure-pixel read is claimed. For 24657168, the actual plasmid list specifies alpha-prime while Results use alpha; that ambiguity remains explicit. Its later correction PMID:32822581 repairs duplicated Figure 1 panels and reports unchanged conclusions. Separate corrections to author names or funding were not treated as scientific retractions.

Source preservation and review provenance

This is manual synthesis following a genuine normal fetch. One default Falcon attempt timed out; the configured perplexity-lite fallback failed with HTTP 401 quota information. No provider output was fabricated and no retry was used. There was no historical CSNK2A1 review to overwrite. All 281 seeded assertion objects, ordinary qualifiers, two official products and 98 reference identities are retained; one seeded TODO reference title was repaired from its genuine cached title. No NEW assertion is added.

Existing repository source bytes were selected intact. Of 43 normal-fetch versus repository publication variants, 31 have equal normalized bodies and 12 differ in extraction coverage. Fuller normal variants remain separately authenticated research inputs, with both hashes and exact read scopes in the public index; they are not silently substituted for shared caches. The final sidecar is manually compiled evidence, not a primary paper or provider-generated report: CSNK2A1 source evidence. It retains portable public source locators, literal records and the distinction between measured evidence, curated provenance and this review's judgments.

2026-10-13 finite review follow-up

The fourteen residue-specific serine assertions remain MODIFY to the established CK2 Ser/Thr enzyme class, with every positive serine reaction and original source object preserved. This follows the actual GO issue 20114 final disposition and its enzyme-class rationale, rather than an assumption that CK2 lacks serine activity. UniProt/RHEA records individual substrate reactions; the GO convention describes the specificity of the known enzyme. The thirteen same-PMID EXP and IDA rows have different evidence types and are not identical source objects. The RHEA GO_REF:0000116 source is likewise distinct from the broader GO_REF:0000120 assertion. Duplicates are not being removed.

Fresh QuickGO is_a closures and OLS records confirm that GO:0106310 and GO:0004674 have no typed parent/child relationship. The GO:0106310 comment retains a real inconsistent label/GO:0004712 cross-reference. The documented final convention nevertheless distinguishes the unusual serine-specific class from known Ser/Thr enzymes. GO:0106311 is obsolete/replaced by GO:0004674; QuickGO resolves a request for the former directly to the latter. No NEW annotation is warranted. The exact current selected fields and public request URLs are recorded in the evidence index follow-up section.

Two limited-access sources now have short catalytic anchors without implying recovered Methods: PMID:20545769, "phosphorylates serines 341 and 387" and PMID:22017874, "phosphorylates S403 of p62 directly". Both complete cached abstracts were read; original assay details remain unavailable. The MDC1 row's association-only anchor was replaced by the measured kinase result from original Results, supported by its recombinant CK2 assay Methods (PMID:18411307, Results/Figure 4 and CK2 kinase assay). This does not assign every reagent specifically to isolated CK2 alpha or claim supplemental figure access.

The ZNF440, ZNF558 and ZNF670 partner-class reasons now name the actual reviewed UniProt IBA:GO_Central provenance. Positive binary-screen evidence and the inferred partner class remain separate premises; no CK2 transcription-factor function or new partner DNA-binding experiment is asserted.

The evidence sidecar retains the lossless gene-relevant interaction/donor/tree records. Its public database URLs, identifiers and literal records support independent source lookup; authenticated-capture hashes are integrity metadata for private receipts, not portable biological evidence or citations to repository files. The follow-up appends compact ontology context and updates affected mirrors/quote counts. It does not cite the authored index as an independent experimental source or discard the raw evidence merely to reduce file size.