The review retains the 48 genuinely fetched source assertions and both official product slots. Its compact core is the performed structural muscle activity at the Z disc, contributing to sarcomere organization. No new annotation is proposed. This manually compiled review uses primary evidence and an independently checked bounded core consultation. The genuine Falcon attempt timed out and the configured fallback returned HTTP 401; no provider report was fabricated.
Direct assays establish human MLP binding and cross-linking of actin. The 2014 study removed the GST tag before the biochemical experiments and used rabbit muscle actin; cellular human-MLP expression experiments used mouse C2C12/HL-1 cells and other heterologous contexts. PMID:24934443(https://doi.org/10.1128/MCB.00651-14), Results: “MLP functions as an actin-bundling protein in vitro”. This supports a performed structural role without claiming native human-cell stoichiometry.
The original stretch-sensor study was available as indexed author-uploaded article text, including its actual Methods, Results, Discussion and captions. The protected repository cache remains abstract-only. Mouse papillary-muscle and neonatal-cell experiments, rat colocalization and human disease/binding observations remain separate. MLP-null cells lose stretch-induced BNP/ANF responses while some hormonal responses remain; these endpoints are not measured cell enlargement. Telethonin binding and redistribution support structural retention, but directed movement to the Z disc remains unresolved. PMID:12507422(https://doi.org/10.1016/S0092-8674(02)01226-6), abstract: “MLP interacts with and colocalizes with telethonin”. The paper proposes titin as the intrinsic elastic sensor rather than showing autonomous MLP force sensing.
The recovered Springer PDF supplies the complete scientific Methods and results of human MLP, ACTN2 and N-RAP fragment experiments. Purified recombinant binding and competition support the specific muscle-alpha-actinin and cytoskeletal-partner refinements. PMID:15205937(https://doi.org/10.1007/s00441-004-0873-y), abstract: “MLP can form a ternary complex”. This is not a native-complex stoichiometry measurement. Actual indexed JACC Methods identify human MLP 1–194 and TCAP constructs in yeast two-hybrid and purified recombinant competition assays; target-bearing Results and Table 3 corroborate the telethonin interaction. PMID:15582318(https://www.jacc.org/doi/10.1016/j.jacc.2004.08.058). Direct publisher access returned 403, but the separately retained indexed original text provides genuine assay access.
Current UniProt products independently reconstruct to 194 and 58 residues. The short product retains 37 canonical residues followed by 21 alternative residues. The historical author deposition JN898958.1/AFH66949.1 instead encodes 59 residues: the current 58-residue sequence plus a terminal histidine. The original historical construct is therefore retained as 59 residues, and its activity is not claimed to have been remeasured for the current 58-residue sequence. The older cofilin paper calls full-length MLP 1–195, whereas the later paper calls the reused construct 1–194; the exact older insert was not recovered.
PMID:24860983(https://doi.org/10.1111/febs.12859) distinguishes MLP-a/MLP-b binding from full-length self-association. Its historical MLP-b binds MLP-a, associates with alpha-actinin/telethonin in tissue pull-downs, and attenuates differentiation after expression in mouse C2C12 cells. It does not show the direct CFL2, MyoD or myogenin interactions measured for MLP-a. Results state cardiac extract whereas Methods state skeletal homogenate; the discrepancy is not silently resolved. MINT's displayed 194-residue backbone can coexist with an experimental comment naming MLP-b, so a matching ROGID does not identify the tested short construct. The independently demonstrated full-length self-association in PMID:24934443 supports the retained identical-protein-binding function; the original hetero-isoform experiment alone does not.
The authentic full PMID:19752190(https://doi.org/10.1128/MCB.00654-09) was read in the bounded consultation and selected Methods/captions were independently read by the owner. Tagged MBP-MLP/GST-CFL2 experiments report maximal depolymerization enhancement at a 2:1 ratio and suppression at 4:1. PMID:24860983 reuses tagged assays and shows MLP-b attenuation without displacement of MLP-a/CFL2 binding. In contrast, tag-cleaved MLP in PMID:24934443 binds, bundles and protects actin and explicitly disagrees with the enhancement interpretation. Preparation and assay differences are real, but a causal reconciliation was not experimentally established. Both findings remain; no universal depolymerase activity is asserted.
The complete PMID:9234731(https://doi.org/10.1128/MCB.17.8.4750) abstract directly describes nuclear/cytoplasmic MLP, myogenic-factor interaction and enhanced MyoD–E47 DNA binding, while stating that “MLP lacks a functional transcription activation domain”. The new notes normalize whitespace in that short excerpt; the review's supporting text preserves the literal cache newline. Full original recovery was unsuccessful, so MyoD-specific results are not relabeled as independent MRF4 assays. The complete PMID:7954791(https://doi.org/10.1016/0092-8674(94)90192-9) abstract supports myogenic differentiation, but unrecovered construct details remain unasserted. These nuclear/developmental contexts are retained separately from the compact structural core.
Mouse P50462 carries exact IGI annotations from PMID:10555147(https://doi.org/10.1016/S0092-8674(00)81662-1) for cardiac force, intracellular calcium homeostasis and cardiac muscle development. Its abstract describes calcium-cycling rescue; the independently read 12507422 original explicitly identifies the MLP/PLN model and discusses stress-related structural rescue. The 10555147 full original remains unavailable: the successful Elsevier HTTP response contains metadata only. These source assertions are retained as contextual physiology, without a direct calcium-pump or embryonic-specification claim.
PMID:27353086(https://doi.org/10.1038/ncomms12120) directly measures reduced PKC-alpha autophosphorylation and phosphorylation of a competing phospholamban fragment in the presence of GST-MLP. MLP is also phosphorylated. Whether MLP has an inhibitory regulatory interaction beyond alternative-phosphoacceptor competition remains a question; no dedicated inhibitor annotation is manufactured from this experiment. Human disease samples and mouse knockout/rescue results remain distinct from the biochemical assay.
All eight IBA rows have matching IBD assertions at the literal ancestors on the verified PTHR24215 human target path. The 252-node tree and MSA reconstruct the official 194-residue target exactly. Human descendant evidence is not circular, and donor counts do not grade ancestral inference. Complete current donor joins preserve 488 records and 41 source links, including both current zebrafish products associated with the original ZFIN identifier. Electronic subcellular and Ensembl routes retain their actual source identities; the unresolved directed-localization issue is shared by source and target.
The actual HPA XML reports cytosol in U2OS and THP-1, plus THP-1 nucleoplasm. Its overall reliability is uncertain while the antibody subassay validation is supported. Image pixels were not inspected. The HTT interaction is supported by three complete IntAct records using an N-terminal HTT construct; this does not establish a physiological neural role. The LDHD pair is explicit in its source abstract and is retained as supported generic binding under the project instruction.
The structured evidence index retains original source objects, full literal interaction/donor records, sequence checks, term captures, source-selection hashes, access limits and current decisions. The public index is authored provenance, not a replacement machine cache or provider report. Existing publication caches and the GO-CAM index remain byte-exact. No CSRP3 GO-CAM target occurs in the selected index.
The two compact core entries distinguish structural support of muscle from directly measured actin-filament binding. PMID:24934443 used tag-cleaved recombinant human MLP with purified actin, high-speed binding assays, low-speed sedimentation and imaging of bundles (Methods and Results, DOI:10.1128/MCB.00651-14). Its direct-binding core does not duplicate the sarcomere process list or imply equivalent activity of the short product. No NEW molecular-function row is added because the current typed closure places GO:0051015 below the already retained cytoskeletal-binding coverage, GO:0008092. Direct bundling is positive evidence, not a necessity-only inference, but a separate NEW bundle-assembly process is not required to express the reviewed structural role and directly measured core activity. The contradictory cofilin assay outcomes remain explicit; no untested tag-based explanation is asserted.
Both former directed-localization uncertainties are refined to GO:0072595, maintenance of protein localization in organelle. This supersedes the earlier unresolved term-scoping conclusion in this journal. The full PMID:12507422 Results and Discussion show telethonin redistribution into the soluble fraction in MLP-null mouse myocardium, preservation in the MLP/PLN double knockout, and physical interaction; the precise stabilizing mechanism can remain unknown while maintenance is supported. Human W4R observations are kept separate. The reviewer's proposed GO:0032507 was considered and its organelle-specific child selected for the Z disc. Directed delivery is not established (original article; indexed author-uploaded Results/Discussion locators remain in the evidence index).
All nine pre-existing binding refinements now contain short exact selected-cache anchors. The alpha-actinin transfer rows use PMID:15205937 as independent class corroboration while retaining the original mouse/PAINT provenance; its quote is not presented as a reinspection of every donor experiment. PMID:24860983's extract associations remain distinct from purified binary binding, and the CFL2 annotation classifies an actin-associated regulatory protein rather than an actin subunit. For cytosol, the uncertain-reliability HPA evidence is supplemented by the full-length human MLP-Venus signal in mouse C2C12 cells from PMID:24934443; native human muscle localization and short-product equivalence are not inferred.
Reviewer access flags describe the original text actually accessed, while the protected publication cache flags describe what that cache contains. Genuine external full-text reading is retained for the four access-limited caches, without editing or refetching machine files merely to synchronize these different fields. The authored evidence index remains public provenance. Earlier notes and history remain exact; this append records the corrected conclusions. ClinGen completion bookkeeping follows verified merge, and no checklist count is changed for this open PR.