In human CEM-C7 cells, GSDME-dependent mitochondrial permeabilization amplifies apoptosis; the mouse Apaf1 experiment is a separate test. PMID:30976076(https://pubmed.ncbi.nlm.nih.gov/30976076/).
Granzyme B can directly activate the human protein; lytic outcome and total cell death are distinct readouts. PMID:32188940(https://pubmed.ncbi.nlm.nih.gov/32188940/).
The familial deafness mutation alters splicing, whereas the physiological N-terminal product is released proteolytically. PMID:9771715(https://pubmed.ncbi.nlm.nih.gov/9771715/).
The mutation-associated MAPK and cell-death observations remain contextual. They are not assigned to the basal precursor. PMID:26236191(https://pubmed.ncbi.nlm.nih.gov/26236191/).
All 35 incoming records remain represented. The helper omitted one extension; the restored BFO:0000050/GO:0070269 atom is explicit in the raw-to-stored map. No incoming qualifier, gene-product identifier, partner, reference or evidence code was changed.
The cardiolipin decisions distinguish source provenance, and the programmed-cell-death decisions distinguish physiological inference from the original mutant assay. These differences are retained for validation instead of changing biology to obtain a status.
Primary originals and official source records were inspected manually. No provider report was generated or impersonated. Normal missing-source acquisition, genuine history, native status and rendering remain pending.
Genuine native helpers completed the 22 missing source records, preserving all 17 inherited source records byte-for-byte. Actual inputs match the frozen 35-context projection and official product declarations; the one omitted extension was restored as documented. Normal-cache titles and access flags were reconciled separately from independently read originals. History, validation and rendering results follow after execution.
Gene, reference, genuine CREATE-history and family checks passed. The reference validator checked one excerpt and 29 titles with no issues. The actual 951-family corpus at the native base had zero conflicts; unrelated unresolved entries remain reported. Computed review status stays DRAFT with six advisory warnings: three explicit consistency exceptions are marked stale by the table checker, while the legacy same-term checker reports the corresponding three mismatches. The source-specific and relation-specific distinctions remain intentional; no action was changed to obtain a status. The final HTML was regenerated, and source files and original contexts were preserved. Publication and later exact-head gates remain separate.
This entry supersedes the earlier action/status commentary; the earlier journal entries remain intact. Source access was investigated manually, using the original URLs and section locators in the source-evidence record. No provider report was generated.
HEK293T mutant-versus-wild-type comparisons show JNK/ERK activation and partial rescue by SP600125. The signaling response belongs to this disease-construct experiment; the experiment does not establish a normal MAPK-regulator role. PMID:26236191(https://pubmed.ncbi.nlm.nih.gov/26236191/).
Mitochondrial targeting is supported by human CEM-C7 knockout experiments and isolated-organelle assays. The active fragment can therefore act at the mitochondrial outer membrane as well as the plasma membrane. PMID:30976076(https://pubmed.ncbi.nlm.nih.gov/30976076/).
Familial segregation and aberrant splicing establish pathogenic hearing loss. They do not by themselves identify GSDME as a physiological participant in sound perception. PMID:9771715(https://pubmed.ncbi.nlm.nih.gov/9771715/).
The existing-lane follow-up passed gene validation, strict GOA matching, all 29 reference titles and five supporting snippets, history validation and the computed-status check. The stale consistency-exception metadata was removed without changing its annotation decision; the original diagnostics remain in the execution record. Status remains DRAFT with the legacy membrane-action comparison and the core-location coverage advisory. No NEW annotation was added. All 39 normal sources and the existing ontology cache remain byte-exact. Rendering and the final sorted-cache check complete this preparation.
Three retained HuRI records support human GSDME–TIFA association in yeast two-hybrid assays; its physiological role remains unresolved [PMID:32296183; GSDME-source-evidence.json, HuRI.current_rows].
Following the standing ClinGen project instruction, the supported generic-binding row is retained as KEEP_AS_NON_CORE. No evidence-backed specific replacement has been established.
Direct schema, ontology-term, reference, strict GOA and history checks passed. Five excerpts and 29 titles passed reference validation. Status remains DRAFT with three advisories: the binding-policy exception and the two pre-existing membrane/location advisories. HTML was regenerated.