| 2006 |
ROMO1 (Reactive oxygen species modulator 1) is a novel protein localized in the mitochondria that increases cellular ROS levels when overexpressed. |
Subcellular fractionation/localization; overexpression with ROS measurement |
Biochemical and biophysical research communications |
Medium |
16842742
|
| 2010 |
In response to TNF-alpha, TNF complex II (comprising RIP1, TRADD, TRAF2, FADD, and pro-caspase-8) binds to the C-terminus of mitochondrial ROMO1. ROMO1 then recruits BCL-XL to reduce mitochondrial membrane potential, resulting in ROS production and apoptotic cell death, establishing ROMO1 as a molecular bridge between TNF-alpha signaling and mitochondrial ROS production. |
Co-immunoprecipitation, binding domain mapping, siRNA knockdown with apoptosis and ROS readouts |
Cell death and differentiation |
Medium |
20203691
|
| 2010 |
ROMO1 knockdown by siRNA blocks mitochondrial ROS production caused by serum deprivation (originating in the mitochondrial electron transport chain) and inhibits serum deprivation-induced apoptosis. |
siRNA knockdown, mitochondrial ROS measurement, apoptosis assay |
Apoptosis |
Medium |
19904609
|
| 2008 |
ROMO1-derived ROS are required for normal cell proliferation; ROMO1 knockdown reduces ROS and inhibits cell growth via the ERK pathway, which can be rescued by exogenous hydrogen peroxide. |
siRNA knockdown, ERK pathway inhibition, exogenous H2O2 rescue experiment |
Biochemical and biophysical research communications |
Medium |
18313394
|
| 2008 |
Enforced ROMO1 expression triggers premature senescence and DNA damage via ROS production originating in the mitochondrial electron transport chain; endogenous ROMO1 expression increases with replicative age in IMR-90 fibroblasts and ROMO1 knockdown inhibits replicative senescence progression. |
Overexpression, siRNA knockdown, ROS measurement, senescence assays (SA-β-gal), DNA damage markers |
The Journal of biological chemistry |
Medium |
18836179
|
| 2009 |
Endogenous ROMO1-derived mitochondrial ROS are required for G1-to-S cell cycle transition in normal WI-38 fibroblasts; ROMO1 knockdown reduces ROS and causes G1 arrest associated with increased p27(Kip1) levels. |
siRNA knockdown, flow cytometry cell cycle analysis, p27(Kip1) western blot, ROS measurement |
Free radical research |
Medium |
19513905
|
| 2011 |
Upregulated MYC induces ROMO1 expression; in a negative-feedback loop, ROMO1-derived ROS stimulate SKP2-mediated ubiquitylation and proteasomal degradation of MYC in normal lung fibroblasts. Additionally, pre-existing ROMO1-derived ROS are required for MYC induction and quiescent cell cycle re-entry. |
Overexpression, siRNA knockdown, ubiquitylation assay, western blot for Myc/Skp2, cell cycle analysis |
Journal of cell science |
Medium |
21558421
|
| 2011 |
BCL-XL expression blocks serum deprivation-induced and ROMO1-triggered ROS generation and apoptotic cell death, indicating BCL-XL acts downstream of or in parallel to ROMO1 to suppress oxidative stress. |
BCL-XL overexpression, ROS measurement, apoptosis assay, epistasis with ROMO1 |
Oncology reports |
Low |
21399876
|
| 2013 |
ROMO1 mediates mitochondrial ROS production through complex III of the mitochondrial electron transport chain and is required for apoptosis induced by oxidative stress (H2O2) in lung epithelial cells; ROMO1 knockdown suppresses cellular ROS and H2O2-induced cell death. |
siRNA knockdown, complex III identification, ROS measurement, cell death assay |
Biochemical and biophysical research communications |
Medium |
23867822
|
| 2014 |
ROMO1 is required for mitochondrial fusion and normal cristae morphology; oxidative stress promotes formation of high-molecular-weight ROMO1 complexes; ROMO1 is essential for oligomerization of the inner membrane GTPase OPA1, which maintains cristae junction integrity. ROMO1 knockdown causes mitochondrial fragmentation, loss of cristae, impaired mitochondrial respiration, and increased sensitivity to cell death stimuli. |
Genome-wide RNAi screen, ROMO1 KD, native PAGE for OPA1 oligomers, electron microscopy of cristae, mitochondrial respiration assay, redox stress treatment |
Science signaling |
High |
24473195
|
| 2014 |
ROMO1 expression is required to maintain constitutive NF-κB nuclear DNA-binding activity and transcriptional activity via constitutive IκBα phosphorylation in hepatocellular carcinoma cells; ROMO1 overexpression promotes p65 nuclear translocation. |
siRNA knockdown, overexpression, NF-κB reporter assay, IκBα phosphorylation western blot, p65 nuclear translocation assay |
Biochemical and biophysical research communications |
Medium |
25044121
|
| 2015 |
ROMO1-induced increase in invasive activity is blocked by an IKK inhibitor, demonstrating that ROMO1-driven tumor cell invasion is mediated through the NF-κB signaling pathway. |
siRNA knockdown, IKK inhibitor treatment, invasion assay |
International journal of oncology |
Medium |
25673177
|
| 2018 |
ROMO1 is a constituent of the human TIM23 presequence translocase complex with an exceptionally short half-life. ROMO1 is not required for general presequence import but is specifically required for import of the inner membrane protease YME1L; in ROMO1 knockout cells, YME1L is lost from the inner membrane, leading to aberrant OPA1 processing and altered inner membrane structure. ROMO1 also participates in the dynamics of TIM21 during respiratory chain biogenesis. |
Mass spectrometry identification of TIM23 complex constituents, ROMO1 KO cell line analysis, import assays, OPA1 processing western blot, TIM21 dynamics analysis |
The Journal of cell biology |
High |
30598479
|
| 2018 |
ROMO1 forms a nonselective cation channel with its amphipathic helical transmembrane domain necessary for pore-forming activity; structurally resembles class II viroporins; channel activity is specifically inhibited by Fe2+ ions. A hexameric structural model was constructed by experimental data-guided structural bioinformatics. |
Electrophysiology (channel recording), transmembrane domain mutagenesis, structural bioinformatics/modeling, Fe2+ inhibition assay |
The Journal of cell biology |
High |
29545371
|
| 2019 |
SRA receptor stimulation activates ERK phosphorylation, which upregulates and activates ROMO1 to enhance mitochondrial ROS production and promote NETs formation in neutrophils; inhibition of ROMO1 dampens SRA-stimulated NET release. |
Pharmacological inhibition, siRNA knockdown, ERK inhibition, ROS measurement, NET assay |
Biochemical and biophysical research communications |
Medium |
30850160
|
| 2020 |
ROMO1 overexpression in bone marrow cells results in M2 polarization of bone marrow-derived macrophages through the mTORC1 signaling pathway. |
Overexpression in bone marrow cells, glioblastoma mouse model, macrophage polarization assay, mTORC1 pathway analysis |
Aging |
Low |
31945745
|
| 2020 |
ROMO1 inhibition elevates BAX protein levels by downregulating the ubiquitin-proteasome system and downregulates the interaction between BAX and Parkin, thereby sensitizing colorectal cancer cells to TRAIL-mediated mitochondrial apoptosis. |
siRNA knockdown, western blot for BAX and ubiquitin-proteasome components, Co-IP for BAX-Parkin interaction, TRAIL apoptosis assay, xenograft model |
Cancers |
Medium |
32825500
|
| 2021 |
ROMO1 knockdown in porcine preimplantation embryos disrupts OPA1 isoform balance, leading to cytochrome c release, reduced ATP, mitochondrial fragmentation, decreased mitochondrial membrane potential, increased ROS production, and induction of apoptosis; ROMO1 overexpression rescues these defects. |
siRNA knockdown, overexpression rescue, OPA1 western blot, cytochrome c release assay, ATP measurement, mitochondrial morphology imaging |
Cell division |
Medium |
34915903
|
| 2023 |
TRAF2 deficiency increases ROMO1 expression, which activates the NAD+/SIRT3/SOD2 pathway to promote ROS production, cause mitochondrial dysfunction, and trigger DNA damage response leading to hepatocellular carcinoma senescence. |
TRAF2 knockdown/KO, ROMO1 western blot, NAD+/SIRT3/SOD2 pathway analysis, mitochondrial function assays, DNA damage markers |
Free radical biology & medicine |
Medium |
38043870
|
| 2023 |
PKLR undergoes nuclear translocation under androgen-deprivation conditions and binds to the MYCN/MAX complex to upregulate ROMO1 expression; elevated ROMO1 alters mitochondrial function and promotes neuroendocrine differentiation of prostate cancer cells. |
Nuclear fractionation, Co-IP for PKLR-MYCN/MAX complex, ROMO1 western blot, mitochondrial function assays, NE differentiation markers |
Redox biology |
Medium |
36963289
|
| 2025 |
ROMO1 overexpression causes a reductive shift in the mitochondrial cysteinome, protecting mitochondrial proteinaceous thiols from oxidation; this promotes energy metabolism and Ca2+ uniport while inhibiting mitochondrial permeability transition. ROMO1 overexpression reverses cysteinome oxidations in aged mice and slows functional decline. |
Redox proteomics of mitochondrial cysteinome, ROMO1 overexpression in cells and aged mice, mitochondrial respiration assay, Ca2+ uniport measurement, mPTP assay |
Nature communications |
High |
40461459
|
| 2026 |
ROMO1 is essential for embryonic development (Romo1-null mice die before embryonic day 8.5); conditional ROMO1 knockout in pancreatic beta cells impairs glucose-stimulated insulin secretion and reduces spare respiratory capacity by specifically decreasing complex II/succinate dehydrogenase activity; human islets lacking ROMO1 also show reduced spare respiratory capacity. |
Whole-body and conditional (beta cell) Romo1 knockout mice, glucose tolerance test, insulin secretion assay, mitochondrial respiratory analysis (Seahorse), isolated human islets with ROMO1 KO |
Diabetologia |
High |
41995846
|
| 2026 |
ROMO1 silencing in airway epithelial cells suppresses cigarette smoke extract-induced mitochondrial ROS production, STAT6 phosphorylation, and MUC5AC (mucin) expression, placing ROMO1 upstream of a mitochondrial ROS-STAT6 pathway that drives airway mucus hypersecretion. |
siRNA knockdown, mitochondrial ROS measurement, STAT6 phosphorylation western blot, MUC5AC expression assay, mitochondrial targeted antioxidant and STAT6 inhibitor epistasis |
Respiratory research |
Medium |
41673839
|
| 2025 |
Selective depletion of ROMO1 in cholinergic neurons in mice causes adult-onset progressive locomotor deficits resembling ALS, with age-dependent motor neuron loss, axon degeneration, disrupted cholinergic transmission, neuromuscular junction denervation, and muscle atrophy; early mitochondrial cristae deformation precedes onset of ALS-like symptoms. |
Conditional KO in cholinergic neurons, behavioral locomotor assays, motor neuron counting, axon morphology, neuromuscular junction staining, electron microscopy of cristae |
bioRxivpreprint |
Medium |
|
| 2024 |
Structural modelling predicts ROMO1 forms a channel within the TIM23 core complex together with TIM17, providing an alternative import channel for PINK1 translocation into the matrix; ROMO1/TIM17 and PARL/TIM17 interactions are mutually exclusive, with PINK1 TMD structural plasticity (α-helix vs α/β-hybrid) determining whether it is translocated through the ROMO1/TIM17 channel or cleaved by PARL. |
Structural modelling, PINK1 import analysis in intact cells, transmembrane domain structural prediction |
bioRxivpreprint |
Low |
|
| 2026 |
ROMO1 is the most significantly downregulated mitochondrial protein at 24 hours post-high-dose irradiation in keratinocytes; ROMO1 overexpression increases mtROS and mitochondrial membrane potential but suppresses cell viability after radiation; skin-specific Romo1 knockout mice show accelerated wound healing and enhanced tissue regeneration after radiation injury. |
Mitochondrial proteomics, ROMO1 overexpression, Romo1 skin-specific KO mice, ROS and membrane potential measurement, wound healing and skin injury scoring |
Journal of Sichuan University. Medical science edition |
Medium |
42021879
|