| 2020 |
RBM26 (along with RBM27, ZC3H3, and PABPN1) is a component of the PAXT (Poly(A) Tail eXosome Targeting) connection required for nuclear RNA exosome-mediated degradation of polyadenylated RNA. Loss of RBM26 results in accumulation of PAXT substrates, establishing it as a limiting factor for PAXT activity. |
Characterization of nuclear pA+-RNA bound proteomes, MTR4-ZFC3H1 co-complex purification, knockdown/loss-of-function with substrate accumulation readout |
Nucleic acids research |
High |
31950173
|
| 2024 |
ZFC3H1 (core PAXT component) adopts a 'closed' conformation when initially loaded co-transcriptionally, blocking exosome recruitment. Short RNAs with fewer exons preferentially recruit transient PAXT components ZC3H3 and RBM26/27 to the 3' end, which triggers ZFC3H1 'opening' and subsequent exosomal degradation, thereby determining RNA fate between export and decay. |
Functional dissection of ZFC3H1 conformational states, depletion of RBM26/27 and ZC3H3 with RNA fate readouts, co-transcriptional loading assays |
Molecular cell |
High |
39461342
|
| 2023 |
PABPN1 recruits RBM26 and RBM27 to promote splicing of last introns with weak 3' splice sites; this interaction involves the coiled-coil and RRM domain of RBM27 (and by extension RBM26), and tethering PABPN1 to non-polyadenylated transcripts is sufficient to promote splicing, indicating a direct role. |
PABPN1 depletion with intron retention readout, TurboID-MS interactome, tethering assay, domain interaction mapping |
EMBO reports |
Medium |
37661812
|
| 2024 |
In C. elegans, rbm-26 (ortholog of human RBM26/RBM27) encodes an RNA-binding protein that negatively regulates expression of the MALS-1 (MALSU1) mitoribosomal assembly factor by binding its mRNA. Loss of rbm-26 causes dramatic overexpression of mals-1 mRNA and MALS-1 protein, leading to mitochondrial dysfunction and axon degeneration during larval neurodevelopment; genetic epistasis shows MALS-1 overexpression is responsible for these defects. |
Biochemical mRNA-binding screen, C. elegans loss-of-function genetics, genetic epistasis (double mutant rescue), protein and mRNA quantification |
PLoS biology |
High |
39480871
|
| 2024 |
Autism-associated missense variants in C. elegans rbm-26 (RBM26/27 ortholog) cause a sharp decrease in RBM-26 protein expression and produce axon overlap and axon degeneration phenotypes during larval development, mechanistically linking disease-associated variants to loss of RBM-26 protein stability and downstream MALS-1 dysregulation. |
Missense variant introduction in C. elegans, protein expression quantification, axon morphology phenotyping |
PLoS biology |
Medium |
39480871
|
| 2024 |
Preprint version confirms rbm-26 (C. elegans RBM26/27 ortholog) binds mals-1 mRNA and negatively regulates its expression; loss of rbm-26 overexpresses MALS-1 and causes mitochondrial and axon degeneration defects reversed by reducing mals-1, consistent with the published peer-reviewed findings. |
Biochemical screen, genetics, mRNA/protein quantification in C. elegans |
bioRxivpreprint |
Medium |
37873356
|
| 2025 |
In fission yeast S. japonicus, the RBM26/27 ortholog Rmn1 interacts with Pab2/PABPN1 and participates in constitutive heterochromatin formation at centromeres; Rmn1 can also interact with the H3K9 methyltransferase Clr4, placing it in a complex required for heterochromatin assembly. |
Co-immunoprecipitation, genetic deletion analysis (Pab2 N-terminal deletion disrupting interaction), chromatin/histone methylation assays at centromeres |
PLoS genetics |
Medium |
40163528
|
| 2017 |
RBM26 was identified as a mono-methylated arginine (MMA)-containing protein in EBV-transformed B-cells, co-immunoprecipitated using an MMA-RG-repeat-specific antibody and confirmed by immunoprecipitation and/or Western blot, indicating RBM26 harbors MMA post-translational modifications on its RG repeat sequences. |
Immunoprecipitation with MMA-specific monoclonal antibody, mass spectrometry, Western blot confirmation |
The Journal of general virology |
Low |
28758620
|