ALR performs the MIA40 redox-regeneration step rather than merely being imported cargo PMID:21383138(https://pubmed.ncbi.nlm.nih.gov/21383138/). Its terminal-acceptor breadth and engineered-reagent limits are recorded in the selected evidence.
The short natural product is sequence-supported but its reported secreted pool is distinct from a demonstrated human regenerative mechanism. Rat donor evidence and the legitimate liver-regeneration/development relationship remain positive while the specific assay-participation question is unresolved PMID:24880092(https://pubmed.ncbi.nlm.nih.gov/24880092/), PMID:8058770(https://pubmed.ncbi.nlm.nih.gov/8058770/).
Mitochondrial occurrence is retained at the granularity of each experimental or ancestral assertion; the separate IMS annotation still identifies the core subcompartment. The electron relay can use cytochrome c as well as oxygen, so the direction-neutral protein-disulfide activity remains informative PMID:22224850(https://pubmed.ncbi.nlm.nih.gov/22224850/).
The two additional primary supports and their assay limits are centralized in selected evidence. Reported secretion remains unresolved without primary human assay support. The liver-development judgment continues to preserve positive rat evidence and valid ancestry while distinguishing regenerative participation from general survival dependence. The archive retains the old review and historical quote associations.