| 2012 |
TRIM67 interacts with PRG-1 and 80K-H (a Ras-mediated signaling pathway component); ectopic TRIM67 expression causes ubiquitin-dependent degradation of endogenous 80K-H, attenuates cell proliferation, and enhances neuritogenesis in N1E-115 neuroblastoma cells, suggesting TRIM67 negatively regulates Ras signaling via 80K-H degradation. |
Co-immunoprecipitation, ectopic overexpression, knockdown of 80K-H, morphological assays in neuroblastoma cells |
The Journal of biological chemistry |
Medium |
22337885
|
| 2018 |
TRIM67 interacts with its closest paralog TRIM9 and with the netrin receptor DCC; deletion of murine Trim67 results in hypotrophy of specific brain regions (hippocampus, striatum, amygdala, thalamus) and thinning of forebrain commissures, demonstrating a necessary role in brain development. |
Co-immunoprecipitation, Trim67 knockout mouse model, neuroanatomical analysis, behavioral testing |
eNeuro |
Medium |
29911180
|
| 2019 |
TRIM67 directly interacts with the C-terminus of p53, inhibiting MDM2-mediated ubiquitination and degradation of p53; TRIM67 is also a transcriptional target of p53, forming a TRIM67/p53 self-amplifying loop that boosts p53-induced cell growth inhibition and apoptosis; Trim67 knockout in mice accelerates colorectal tumor formation and dampens p53 responses. |
Co-immunoprecipitation, ubiquitination assay, RNA sequencing, Trim67 knockout mouse models, chromatin immunoprecipitation, in vitro and in vivo rescue experiments |
Cancer research |
High |
31239268
|
| 2020 |
Proximity-dependent biotin identification (BioID) in developing cortical neurons defined the TRIM67 neuronal interactome; validated interaction partners include Myo16, Coro1A, MAP1B, ExoC1, GRIP1, PRG-1, and KIF1A; TIRF microscopy demonstrated dynamic colocalization of TRIM67 with these candidates at the axonal periphery including filopodial tips; Myo16 knockdown altered growth cone filopodia density and axonal branching in a TRIM9- and netrin-1-dependent manner. |
BioID proximity labeling, mass spectrometry, co-immunoprecipitation validation, TIRF microscopy, RNAi knockdown in cortical neurons |
Molecular biology of the cell |
Medium |
33378226
|
| 2020 |
TRIM67 inhibits colorectal cancer cell proliferation and metastasis by negatively regulating MAPK11; RNA sequencing identified MAPK11 as a downstream target of TRIM67, and reversing MAPK11 expression rescued the anti-proliferative and anti-metastatic effects of TRIM67. |
RNA sequencing, TRIM67 overexpression/knockdown in CRC cells, MAPK11 rescue experiments, CCK-8, colony formation, transwell assays |
Journal of Cancer |
Low |
32922543
|
| 2021 |
TRIM67 promotes full-vesicle fusion (FVF)-like exocytic mode in developing cortical neurons, in part by limiting incorporation of the Qb/Qc SNARE SNAP47 into SNARE complexes, thereby controlling plasma membrane expansion during neuronal morphogenesis. |
TIRF microscopy of individual exocytic events, classification algorithms, RNAi knockdown of TRIM67, co-immunoprecipitation to assess SNARE complex composition, simulation modeling |
Cell reports |
High |
33567284
|
| 2022 |
TRIM67 negatively regulates TNFα-triggered NF-κB activation by competitively binding β-TrCP (beta-transducin repeat-containing protein), thereby preventing β-TrCP-mediated K48-linked ubiquitination and degradation of IκBα and sustaining IκBα stability. |
Ectopic expression and knockdown in MEFs, NF-κB luciferase reporter assay, Co-immunoprecipitation to demonstrate TRIM67–β-TrCP and TRIM67–IκBα interactions, cytokine expression assays |
Frontiers in immunology |
Medium |
35273593
|
| 2023 |
TRIM67 binds IκBα and modulates its ubiquitination: it reduces K48-linked (degradative) ubiquitination and increases K63-linked ubiquitination of IκBα, thereby stabilizing IκBα and inhibiting NF-κB activity after cerebral ischemia–reperfusion injury. |
Co-immunoprecipitation, ubiquitination assays (K48 vs K63 linkage-specific), TRIM67 overexpression in MCAO/R mouse model and OGD/R microglia, infarct size measurement |
Cell & bioscience |
Medium |
37248543
|
| 2024 |
TRIM67 ubiquitinates DLK1 via its RING domain, targeting DLK1 for degradation; because DLK1 normally inhibits Notch1 receptor activation, TRIM67-mediated DLK1 ubiquitination results in Notch pathway activation and promotes NSCLC cell invasion, migration, and proliferation. |
Co-immunoprecipitation, ubiquitination assay with RING domain mutant, TRIM67 and DLK1 overexpression/knockdown in NSCLC cell lines, Notch pathway reporter assays |
Journal of Cancer |
Medium |
38434968
|
| 2025 |
TRIM67 promotes ubiquitinated degradation of ARSD through its RING domain; TRIM67 overexpression suppresses GBM cell glycolysis and increases temozolomide sensitivity by decreasing ARSD expression, which inactivates the β-catenin pathway. |
Co-immunoprecipitation, ubiquitination assay, TRIM67 overexpression/knockdown, rescue with ARSD overexpression, xenograft mouse model |
FASEB journal |
Medium |
41396160
|
| 2025 |
Coro1A physically interacts with TRIM67; a Coro1A mutant deficient in TRIM67 binding cannot rescue loss-of-Coro1A phenotypes (netrin-dependent axon turning, branching, corpus callosum development), establishing that the Coro1A–TRIM67 interaction is required for netrin-mediated neuronal morphogenesis. |
Co-immunoprecipitation, Coro1A binding-deficient mutant rescue experiments in cortical neurons, axon turning and branching assays, Trim67/Coro1A knockout mice |
The Journal of cell biology |
High |
41085995
|
| 2025 |
TRIM67 promotes ubiquitination and proteasomal degradation of VDAC1 through K63-linked polyubiquitination; propofol upregulates TRIM67 expression, leading to VDAC1 degradation, suppression of ferroptosis, and cerebroprotection against ischemia–reperfusion injury. |
Co-immunoprecipitation, ubiquitination assay (K63-linkage specific), TRIM67 knockdown and overexpression, OGD/R cell model and MCAO rat model |
Chemical biology & drug design |
Medium |
42136259
|
| 2026 |
TRIM67 directly interacts with NFS1 and promotes its ubiquitination and proteasomal degradation; TRIM67 overexpression suppresses CRC cell proliferation, migration, and stemness, and these effects are rescued by concurrent NFS1 overexpression. |
Co-immunoprecipitation, ubiquitination assay, cycloheximide chase, TRIM67 overexpression/knockdown, rescue experiments, xenograft model |
Cellular signalling |
Medium |
42069097
|
| 2026 |
TRIM67 directly interacts with ACSL4 and promotes its ubiquitination and degradation; TRIM67-mediated ACSL4 downregulation alleviates OGD/R-induced neuronal apoptosis, inflammation, and ferroptosis; remimazolam enhances TRIM67 expression to achieve these neuroprotective effects. |
Co-immunoprecipitation, ubiquitination assay, TRIM67 knockdown and overexpression, OGD/R cell model and MCAO rat model, Western blot |
Journal of biochemical and molecular toxicology |
Medium |
41587377
|
| 2025 |
PCK2 (PEPCK-M) competitively binds TRIM67 to block TRIM67-mediated ubiquitination of SMAD3, thereby stabilizing SMAD3 protein, promoting its nuclear translocation and autoregulation, and activating TGF-β/SMAD3-driven EMT in triple-negative breast cancer. |
Co-immunoprecipitation, ubiquitination assay, PCK2 knockdown and overexpression, SMAD3 knockdown rescue experiments, Western blot for phospho-SMAD3 |
Cancer biology & therapy |
Medium |
40081967
|
| 2024 |
TRIM67 interacts with ENAH protein (as shown by Co-IP and GST pull-down); TRIM67 knockdown promotes apoptosis and autophagy in lung cancer cells, and ENAH overexpression reverses these effects, placing TRIM67–ENAH interaction upstream of apoptosis/autophagy regulation. |
Co-immunoprecipitation, GST pull-down, siRNA knockdown, immunofluorescence localization, flow cytometry, Western blot, TEM |
General physiology and biophysics |
Medium |
38477606
|
| 2023 |
TRIM67 is abundantly expressed in the mitral cell layer of the olfactory bulb; genetic deletion of TRIM67 in mice leads to excessive proliferation of mitral cells and defects in synaptic development, resulting in reduced olfactory function; TRIM67 may regulate mitral cells via the Semaphorin 7A/Plexin C1 (Sema7A/PlxnC1) signaling pathway. |
Trim67 knockout mouse model, immunohistochemistry, neuroanatomical analysis, olfactory behavioral tests, Western blot/pathway analysis |
International journal of molecular sciences |
Low |
37686246
|
| 2026 |
miR-8085 (delivered via astrocyte-derived extracellular vesicles) targets and downregulates TRIM67 in NSCLC tumor cells; loss of TRIM67 stabilizes the transcription factor ELK1 by reducing its ubiquitin-mediated degradation, thereby promoting tumor stemness and brain metastasis. |
miRNA target validation (luciferase reporter), TRIM67 knockdown/overexpression, ubiquitination assay for ELK1, extracellular vesicle isolation and transfer assays, in vivo models |
Cellular & molecular biology letters |
Medium |
42226139
|