DYRK1A source and assay guide

This guide gives source access, organism/construct and measurement limits for the reviewed assertions. It is an authored navigation aid; the primary papers and deposited records remain the evidence. Zero-based row indices refer to the 125-row review. No new verbatim paper quotation is reproduced.

Decisive original locators

The source-specific reference assessments below record body access independently of the normal cache flag. For PMID:23602568, authentic indexed main text and a supplemental validation caption were read, but complete Methods and all selected validation figures were not recovered. For PMID:25556849 the accessible original was an indexed author-uploaded manuscript; later papers displayed on that page were excluded. Original publication title/identifier verification does not certify an unresolved specific assay.

Deposited interaction evidence

The reproducible extracts retain original workbook rows, network attributes and CSV fields. The chromosome-21 Table S3 has multiple DYRK1A bait labels, including a polyhistidine deletion and a separately labeled isoforme3; none is silently mapped onto a current human natural product. Relevant imported pairs include worksheet rows 710 (WT/USP54), 724 (WT/FAM53C), 782 (delta-polyHis/DYNLL1), 819 (delta-polyHis/USP54) and 824 (delta-polyHis/TRAF2). Nucleotide prey boundaries, PBS values and original labels are preserved.

The induced-neuron mmc4 workbook contains twelve selected partner identities in Interaction_Annotations and matching Interactor_Lists rows. The Broad-specific rows and aggregate rows are not counted twice as independent evidence. The OpenCell DYNLL1-bait record is physical CSV line 7906 (zero-based data index 7904), with a mixed DYRK1A/DYRK1B prey group. The two selected 2025 graph edges point from LZTS2 or DCAF7 bait to DYRK1A prey.

IntAct and MINT source joins were checked by literal publication, target and partner identifiers, retaining method, host, feature and reference-sequence fields. Their absence for some historic rows is not a negative experiment. A sufficient-binding-region feature and a parent-sequence ROGID answer different questions; neither alone proves an archived bait is unmodified full length.

Complete binding annotation index

The activity of the partner and the assay supporting the pair are checked separately. A class refinement is not a claim that DYRK1A performs the partner's activity. Ordinary project-supported generic binding remains non-core where no evidence-backed subclass was established.

Propagation and compartment provenance

Five IBA records were joined to their exact PAINT IBD nodes in the actual PTHR24058 tree. The 1,390-node tree and 1,390-sequence MSA contain the target PTN002514217 and exact 763-residue human sequence. Target-path descent, not donor count or the mere presence of a family name, grounds the transfer. The transcription/coactivator ancestor includes experimental human DYRK1B evidence, supplemented by target-specific human CTD/chromatin studies. The target appearing among donors is valid experimental grounding.

Mouse and rat donor annotation records were inspected directly. Mouse nuclear-speckle support includes human/rat transfers and location-vocabulary mapping; it is not reported as an independently read mouse microscopy experiment. Mouse axon/dendrite IDA records cite PMID:21878370, whose complete target-specific body was unavailable. Rat splice-factor sources were recovered and read. This distinction preserves curator evidence without fabricating a source assay.

HPA target HTML, rather than its overall XML score, supplied individual-location reliability: supported nucleoplasm and nuclear speckles, uncertain centrosome and cytosol. These uncertain calls are not used to negate separate positive cytoplasmic evidence or add a new centrosomal assertion.

Reactome R-HSA-1362270 was traced through catalytic activity 1362272 to human DYRK1A entity 1362267, residues 1–763 in nucleoplasm, and the LIN52 phosphorylation step. The existing DNA-repair GO-CAM 617b481400003575 was considered alongside the actual RNF169 experiments; a curator-modeled positive branch does not erase opposite knockout results.

Reference access inventory

The full source-specific assessments are recorded once in the review YAML. Body access below records the actual operative original or database record, not just the machine-cache flag. It does not imply that all supplementary files or image pixels were read.

Official partner identities

The binding index above identifies the exact partner accession for every row. These directly read official records establish the partner class, separately from the source experiment establishing association. The record and the source-specific review reason disclose inferred versus direct activity support.

• Q96S59: Ran-binding protein 9.
• P61962: DDB1- and CUL4-associated factor 7.
• Q92561: Phytanoyl-CoA hydroxylase-interacting protein.
• Q7Z698: Sprouty-related, EVH1 domain-containing protein 2.
• Q7Z699: Sprouty-related, EVH1 domain-containing protein 1.
• P06400: Retinoblastoma-associated protein.
• P28749: Retinoblastoma-like protein 1.
• P63167: Dynein light chain 1, cytoplasmic.
• Q12815: Tastin.
• Q9BRK4: Leucine zipper putative tumor suppressor 2.
• Q9NYF3: Protein FAM53C.
• Q12933: TNF receptor-associated factor 2.
• Q5T749: Keratinocyte proline-rich protein.
• Q70EL1: Ubiquitin carboxyl-terminal hydrolase 54.
• O00425: Insulin-like growth factor 2 mRNA-binding protein 3.
• Q01826: DNA-binding protein SATB1.
• Q06787: Fragile X messenger ribonucleoprotein 1.
• Q12926: ELAV-like protein 2.
• Q14576: ELAV-like protein 3.
• Q14669: E3 ubiquitin-protein ligase TRIP12.
• Q9NZI8: Insulin-like growth factor 2 mRNA-binding protein 1.
• Q9ULU4: MYND-type zinc finger-containing chromatin reader ZMYND8.
• Q9Y6M1: Insulin-like growth factor 2 mRNA-binding protein 2.
• Q13627: Dual specificity tyrosine-phosphorylation-regulated kinase 1A.

Review-response source locators

The author-uploaded original of PMID:25556849 is identified by DOI 10.1111/jnc.13018 and the matching article title. The Methods for recombinant kinase activity and Figure 2 support the human kinase/Tau assay; cortical-neuron culture, insoluble-Tau extraction and Figure 5 define the rat aggregation endpoint; Figure 6 defines the human HEK293-APP Aβ40 experiment. The indexed original text was inspected, including the captions, but no original PDF download or figure-pixel inspection is claimed. The preserved normal cache is abstract-only. Access to the original, rather than the cache flag alone, grounds the source-specific decisions.

For PMID:30773093(https://pmc.ncbi.nlm.nih.gov/articles/PMC6464593/), the Results distinguish kinase-dependent RNF169/53BP1 experiments from DYRK1A knockout and DR-GFP repair measurements. The production GO-CAM source explicitly links DYRK1A activity 617b481400003576 to RNF169 activity 617b481400003584 by positive regulation. That curator model is consistent with the measured branch, not an independent experiment or a replacement for the opposing knockout result. PMID:31024071(https://pmc.ncbi.nlm.nih.gov/articles/PMC6483993/) supplies the separate early recruitment, abundance and inhibitor-control context.

PMID:24327345(https://pubmed.ncbi.nlm.nih.gov/24327345/) Methods specify human frontal cortex, controlled subcellular fractionation and immunoprecipitation from the human brain cytoskeletal fraction. Figures 2 and 3 distinguish the cytoskeleton-associated pool from a claim of purified filament binding. The original colocalizes_with qualifier remains unchanged. Later murine phosphorylation experiments are not relabeled human.

The current official USP54 record provides the partner-class evidence through its experimentally supported FUNCTION and CATALYTIC ACTIVITY sections, rather than through the protein name or GO annotations. The cited enzymology is curated evidence; those underlying original bodies were not independently reread for this review. The positive DYRK1A–USP54 associations and their original bait/fragment limitations are separately documented above.

PMID:29849146(https://pmc.ncbi.nlm.nih.gov/articles/PMC6475116/) Figure 3 compares DYRK1A CTD targeting with a histidine-region deletion. Extended Data Figure 6 tests a GFP-tagged DYRK1A IDR fragment in vitro, while the live-cell phase-separation experiments predominantly concern cyclin T1. The new questions distinguish these assays from unresolved endogenous intact-DYRK1A and natural-product behavior.

Cached evidence anchors

The review now includes brief literal excerpts for the decisive kinase, scaffold-partner, exon-choice, cytoskeletal and Tau-aggregation statements. Selected reference findings provide the biological interpretation once; related source rows retain their individual evidence contexts. The final paragraph of the preserved PMID:25556849 abstract explicitly reports Tau aggregation, so a phosphorylation-only account of that paper would be incomplete. Its separately accessed original remains the source for the detailed insoluble-Tau assay described above. Aggregation does not, by itself, demonstrate neurofibrillary-tangle assembly.