PELO — Pelota mRNA surveillance and ribosome rescue factor
PELO belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.
PELO's module in each cell type
| Cell type | Module | Shares the module with | |
|---|---|---|---|
| CD4⁺ T cells | Th17/MAIT type-17 Th17 fate | AKT1S1, CA10, CA2, CCL20, CEBPD, GFPT2, IL22, IL4I1 +9 more | View in SCUBA |
| Endothelial | Glucocorticoid Response Inflammation | CCM2L, CFAP20, DUSP6, INAFM2, INHBB, MIER2, MYLIP, NUAK1 +6 more | View in SCUBA |
| Gamma-delta T cells | Gut-homing Residence Tissue residence | ADAM28, ASB2, ATP8B4, CAPG, CCR9, CD101, CD9, DAPK2 +8 more | |
| Pericytes | Basement Membrane Assembly ECM production | F2R, FARP1, ITGB1, JAK1, LAMA4, LAMC1, LIMS1, NID1 +1 more | View in SCUBA |
About the gene
| Chromosome | 5: 52787916-52804044 |
|---|---|
| Predicted location | Intracellular |
| Essential gene | Yes |
| Protein class | Essential proteins, Predicted intracellular proteins |
| Biological process | Cell cycle, Cell division, Translation regulation |
Function
Component of the Pelota-HBS1L complex, a complex that recognizes stalled ribosomes and triggers the No-Go Decay (NGD) pathway. In the Pelota-HBS1L complex, PELO recognizes ribosomes stalled at the 3' end of an mRNA and engages stalled ribosomes by destabilizing mRNA in the mRNA channel. Following mRNA extraction from stalled ribosomes by the SKI complex, the Pelota-HBS1L complex promotes recruitment of ABCE1, which drives the disassembly of stalled ribosomes, followed by degradation of damaged mRNAs as part of the NGD pathway. As part of the PINK1-regulated signaling, upon mitochondrial damage is recruited to the ribosome/mRNA-ribonucleoprotein complex associated to mitochondrial outer membrane thereby enabling the recruitment of autophagy receptors and induction of mitophagy.
Human Protein Atlas · Open Targets · UniProt
Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.