Kindlin-1's central mechanism is beta-integrin-tail binding at focal adhesions, with cooperation in integrin activation and cell-matrix attachment. The core uses integrin binding (GO:0005178), focal adhesion (GO:0005925), positive regulation of integrin activation (GO:0033625), and cell-matrix adhesion (GO:0007160). The two process terms have no ancestor/descendant relationship under the inspected strict is_a/part_of hierarchy. Focal adhesion is a cellular anatomical entity, not a protein-containing complex.
The original human evidence in PMID:14634021(../../../publications/PMID_14634021.md) supports endogenous focal-adhesion/conditional ruffle localization and beta-integrin-tail association. The association assay uses cell lysate, so it is not described as a two-purified-protein affinity measurement. Its kindlin-alone activation result is distinguished from talin cooperation in PMID:19804783(../../../publications/PMID_19804783.md). The latter source separates human functional constructs from mouse purified structural domains. Human keratinocyte evidence in PMID:21356350(../../../publications/PMID_21356350.md) supports overlapping kindlin-1/kindlin-2 contributions to integrin activation and attachment; overlapping functions do not imply interchangeability.
The direct source guide records the actual original Methods/Results recovered for the three direct publication groups, including limitations of cached full-text flags. The database source guide records eleven mouse donor chains, the three literal PAINT joins, InterPro/rule provenance and the additional original evidence. Full manual reference objects are preserved as whole objects in the integrated review. No abstract is silently rewritten into full text.
The direct decision table and database decision table retain complete source keys and zero-based indices. All 31 approved review successors are preserved. Broad migration row 14 is TOO_GENERAL because the separately retained positive row 29 carries its verified strict descendant GO:1903691. The latter remains non-core, not withdrawn. TGF-beta production row 24 is refined to the already present signaling-regulation term GO:0030511; it does not create a new annotation.
Contextual Wnt/TGF-beta signaling, hair cycling, stem-cell behavior, basement-membrane organization, polarity and migration are kept outside the narrow core. The donor experiments and human corroboration remain distinguished. Nuclear import and direct actin-filament binding remain UNDECIDED where the recovered source does not isolate those specific mechanisms; neither uncertainty negates positive observed localization or signaling.
The phylogeny evidence preserves actual family labels and positive IBD strings without pretending that the failed tree/MSA requests verified ancestry. The donor-chain evidence exposes exact orthology sources. Target self-WITH is expected and donor count is not used as a quality metric.
The product map preserves all four natural splice products and exact sequence-reconstruction facts. Artificial deletion constructs, phosphorylation-state bands and the historical mouse construct are not assigned to natural human isoforms. No new processed product or common activity for every splice form is inferred.
All 21 normal sources are retained byte-for-byte: the 19 accepted intake files, exact main PMID24681597 and genuinely fetched PMID16876785. Ten are current reference/family dependencies and eleven preserve the intake discovery record. The existing cached GO-CAM index had no FERMT1/Q9BQL6 entry at inspection; that absence is not interpreted as a missing-process annotation.
The appended literature journal gives source-linked biological synthesis and experimental questions. Nuclear-import row 19 remains explicitly UNDECIDED after full-text access: the authors describe nuclear translocation, but the relative contributions of import, export, retention and beta-catenin stability are unresolved. GO:0042308 does not require direct pore binding or a particular kinetic assay. This uncertainty is not a rejection of the donor experiment or of the independently supported Wnt-signaling role. Actin-binding row 21 also remains unresolved on its own source evidence.
Cell-junction row 13 retains the resolution of the human tissue immunogold assay; it does not replace the independently demonstrated focal-adhesion location. For TGF-beta row 24, official QuickGO marks GO:0036363 and GO:1901390 obsolete because their activation concepts represent molecular functions. The current signaling-regulation replacement is retained. PH-domain lipid specificity is an explicit question, with no new lipid-binding assertion or core function. Four proposed experiments address direct actin binding, nuclear transport/turnover, natural splice-product activity and lipid recognition.