Mir127

Summary: Rfam2GO annotation placing the mature miRNA in RISC.

Reason: Mature miR-127 is loaded into Argonaute/RISC; this is core to how the gene product works.

Summary: Rfam2GO annotation of the generic microRNA process.

Reason: Correct and core: miR-127 silences Rtl1 transcripts through the trans-homologue interaction that defines its known biology.

Summary: The functionally established role of mir-127, from a paper devoted to it.

Reason: Mutant-phenotype evidence from a study whose entire subject is the miR-127-Rtl1 trans-homologue interaction and its effect on the placenta. This is the core specific biology of mir-127 and the correct contrast with the two batch-derived IEP rows below.

Summary: The specific placental compartment affected by loss of the miR-127-Rtl1 interaction.

Reason: A more precise statement of the same well-supported placental phenotype, from the same mutant analysis.

Summary: Reflects the imprinted, allele-specific nature of the miR-127-Rtl1 pair.

Reason: Defensible - miR-127 acts from the maternal allele on the paternally expressed Rtl1, so allele-specific regulation is genuinely part of the mechanism. Kept as non-core because the imprinting is a property of the locus rather than an activity of the mature miRNA, whose own action is ordinary RISC-mediated repression.

Summary: Batch expression annotation from an embryonic-stem-cell screen in which mir-127 was not among the tested miRNAs.

Reason: One of 291 IEP annotations to this term from a single paper. The study induced ESC differentiation by withdrawing LIF and recorded which miRNAs rose; only miR-34a, miR-100 and miR-137 were then functionally tested, and mir-127 is not among them. A miRNA rising when a cytokine is removed is also a poor fit for "cellular response to leukemia inhibitory factor", which describes a reaction to the presence of LIF. Marked over-annotated rather than removed because only the abstract is cached, so the underlying expression measurement cannot be inspected directly.

Summary: mir-127 is not discussed anywhere in the cited paper; the row reflects membership of the detected-miRNA set.

Reason: The bottom tier of the 130-member IEP batch from this study. The paper detected 372 miRNAs, found 12 that changed during LTP, and functionally validated three; miR-127 is in none of those groups and the PMC full text does not mention it. The sole fact behind this annotation is that mir-127 was detectable in hippocampal slices. Note also that the same batch omits let-7a, one of the three miRNAs the paper does establish as required, so the cohort is not merely over-inclusive but poorly aligned with the paper's findings.

Summary: Direct-assay support from a study of imprinted miR-127 reprogramming in cloned embryos.

Reason: The cited paper is specifically about aberrant epigenetic reprogramming of imprinted miR-127 and Rtl1, so the term is well matched to the source. Kept as non-core for the same reason as the IMP duplicate above: imprinting is a property of the locus rather than an activity of the mature miRNA.

Summary: Cannot be adjudicated from the cached record.

Reason: The cached publication is abstract-only and concerns miR-29 in cardiac fibrosis after myocardial infarction, with no mention of miR-127 in the abstract. Post-infarction miRNA surveys are exactly the kind of source that produces expression-derived process annotations, but the curator saw the full text, so this is left undecided rather than challenged.