| 2018 |
TMEM41B is an ER-localized multispanning membrane protein required for autophagosome formation at an early step; its deletion causes accumulation of ATG proteins and small vesicles but no elongating autophagosome-like structures, and also causes lipid droplet accumulation. |
Genome-wide CRISPR screen with GFP-LC3-RFP reporter, knockout cell analysis, fluorescence microscopy |
The Journal of cell biology |
High |
30093494
|
| 2018 |
TMEM41B physically interacts with VMP1 (another ER multispanning membrane protein essential for autophagy) both in vivo (co-immunoprecipitation) and in vitro, and overexpression of VMP1 can restore autophagic flux in TMEM41B-KO cells. |
Co-immunoprecipitation, in vitro binding assay, rescue experiment by VMP1 overexpression in TMEM41B-KO cells |
The Journal of cell biology |
High |
30093494 30773971
|
| 2018 |
TMEM41B localizes to the endoplasmic reticulum (ER) as a multi-spanning membrane protein; its absence causes stalled autophagosome biogenesis with LC3 accumulating at WIPI2- and DFCP1-positive isolation membranes, and results in enlarged lipid droplets and reduced fatty acid mobilization and β-oxidation. |
Pooled CRISPR screens, immunostaining, interaction proteomics, lipid droplet assays, β-oxidation assay |
EMBO reports |
High |
30126924
|
| 2018 |
TMEM41B (Stasimon) localizes to mitochondria-associated ER membranes (MAM), as determined by subcellular fractionation and super-resolution microscopy, and its interactome (identified by immunoprecipitation-mass spectrometry) includes components of the ER, mitochondria, and COPI vesicle trafficking machinery. |
Immunoprecipitation-mass spectrometry, subcellular fractionation, super-resolution microscopy |
Biochemical and biophysical research communications |
Medium |
30352685
|
| 2019 |
TMEM41B is an integral ER membrane protein required for phagophore maturation; it plays related but not fully overlapping roles with VMP1 in autophagosome biogenesis. |
Genome-wide CRISPR screen, quantitative microscopy, biochemical analyses, genetic complementation |
PLoS biology |
High |
30933966
|
| 2020 |
TMEM41B is required for infection by all tested members of the Flaviviridae family and by SARS-CoV-2 (Coronaviridae); it associates with viral proteins and is proposed to facilitate membrane curvature to create flavivirus RNA replication complexes. SNPs in TMEM41B present at ~20% in East Asian populations reduce flavivirus infection. |
Genome-wide loss-of-function CRISPR-Cas9 screens, infection assays, mechanistic studies with viral protein co-association |
Cell |
High |
33338421
|
| 2021 |
TMEM41B is an ER-resident host factor required at an early, post-receptor-engagement stage of coronavirus (HCoV-229E, SARS-CoV-2) replication; mechanistic studies suggest it contributes to viral replication complex formation via mobilization of cholesterol and other lipids to facilitate membrane expansion and curvature, though the protein was not enriched at replication complexes. |
Genome-wide loss-of-function CRISPR screen, infection stage assays, lipid mobilization experiments, KO cell analysis |
PLoS pathogens |
Medium |
34043740
|
| 2021 |
TMEM41B-KO cells are unable to form double-membrane vesicles (DMVs) required for coronavirus (TGEV) replication, establishing that TMEM41B contributes to formation of CoV replication organelles. |
Genome-scale CRISPR KO screen, electron microscopy of DMV formation, mouse infection model |
PLoS pathogens |
Medium |
34871328
|
| 2022 |
TMEM41B and VMP1 are required for DMV biogenesis during β-coronavirus infection, but function at distinct steps: TMEM41B facilitates the nsp3-nsp4 interaction and ER zippering, while VMP1 is required for closing the paired ER into DMVs. |
KO cell analysis, expression of viral nsp3/nsp4, co-immunoprecipitation of nsp3-nsp4, electron microscopy of DMV formation |
The Journal of cell biology |
High |
35536318 35900889
|
| 2022 |
TMEM41B and VMP1 possess lipid scramblase activity, demonstrated by in vitro fluorescent liposome-based phospholipid scrambling assays and in vivo metabolic labeling with alkyne-choline in living cells. |
In vitro liposome-based phospholipid scrambling assay, in vivo metabolic labeling with alkyne-choline |
STAR protocols |
Medium |
35496801
|
| 2022 |
VMP1 and TMEM41B contain a DedA domain predicted to adopt a structure with two reentrant loops, and both proteins have experimentally demonstrated lipid scrambling activity; they regulate formation of multiple ER-derived structures including autophagosomes, lipid droplets, lipoproteins, and viral DMVs. |
Review of experimental data; DedA domain structural prediction; scramblase activity assays referenced |
EMBO reports |
Medium |
35044051
|
| 2022 |
TMEM41B deficiency impairs DENV replication organelle formation; the inhibitory effect of TMEM41B deficiency on DENV replication (but not HCoV-OC43) can be partially reversed by exogenous fatty acid supplementation, linking TMEM41B's lipid mobilization function to flavivirus replication. |
KO cell infection assays, fatty acid supplementation rescue, metabolomic/lipidomic profiling, mitochondrial function assays |
PLoS pathogens |
Medium |
35939522
|
| 2023 |
Loss of TMEM41B (an ER-localized lipid scramblase) delays ER-to-Golgi transport of GPI-anchored proteins and transmembrane proteins, slows PGAP1 turnover via ER-associated degradation, and thereby promotes PGAP1-dependent GPI-inositol deacylation through PGAP1 stabilization. |
KO cell analysis, PI-PLC sensitivity assay, protein transport assays, PGAP1 turnover assays |
Journal of biochemistry |
Medium |
37279648
|
| 2023 |
TMEM41B is an interferon-stimulated gene (ISG); its knockdown blocks PRV entry by affecting lipid synthesis via downregulation of key lipid synthesis enzymes and by altering clathrin-coated pit (CCP) dynamics; lipid replenishment restores CCP dynamics and PRV entry in TMEM41B knockdown cells. |
IFN induction experiments, KO/knockdown/overexpression cell assays, PRV life cycle stage assays, CCP dynamics analysis, lipid replenishment rescue |
Journal of virology |
Medium |
37255475
|
| 2024 |
VMP1 and TMEM41B (as lipid scramblases) are required for primitive endoderm specification; mechanistically, their loss reduces FZD2 (WNT receptor) at the plasma membrane, impairing WNT signaling, and transgenic FZD2 expression rescues XEN differentiation. |
ESC knockout generation, differentiation assays, cell surface proteome profiling, transgenic rescue experiment |
Cell death and differentiation |
Medium |
39695329
|
| 2024 |
miR-660-5p directly targets TMEM41B; inhibition of miR-660-5p increases TMEM41B protein levels in breast cancer cells, and TMEM41B was validated as a direct miR-660-5p target by dual-luciferase reporter assay and Western blot. |
Dual-luciferase reporter assay, Western blot, miRNA inhibitor experiments |
Hereditas |
Low |
39709500
|
| 2025 |
Purified recombinant TMEM41B forms a concentration-dependent Ca2+ channel in single-channel electrophysiology assays; TMEM41B deficiency causes ER Ca2+ overload while overexpression depletes ER Ca2+, establishing TMEM41B as an ER Ca2+ release channel. ER Ca2+ overload in TMEM41B-deficient naive T cells upregulates IL-2/IL-7 receptors and activates JAK-STAT, AKT-mTOR, and MAPK pathways, lowering the T cell activation threshold. |
Single-channel electrophysiology with purified recombinant protein, ER Ca2+ measurement in KO and overexpression cells, T cell signaling pathway analysis |
Cell discovery |
Medium |
40038246
|
| 2025 |
TMEM41B stabilizes fatty acid synthase (FASN) in vascular smooth muscle cells by inhibiting its ubiquitination and degradation, thereby promoting lipid synthesis and intracellular lipid storage; this TMEM41B-FASN axis drives foam cell-like features in VSMCs. |
TMEM41B silencing/overexpression in VSMCs, ubiquitination assay, lipidomics, FASN protein stability assays |
Metabolism: clinical and experimental |
Medium |
41297878
|
| 2025 |
TMEM41B and VMP1 localize at mitochondria-associated membranes (MAM) in hepatocytes; loss of hepatic TMEM41B impairs VLDL secretion and reduces phospholipid (PC and PE) levels; TMEM41B and VMP1 have overlapping but distinct roles in hepatic lipoprotein secretion and autophagy. |
Liver-specific KO and KI mouse models, lipidomics, metabolomics, VLDL secretion assay, EM ultrastructural analysis, MAM fractionation |
bioRxivpreprint |
Medium |
40291711
|
| 2025 |
VMP1 and TMEM41B scramblase activity is required for the maturation and stability of FZD2/FRIZZLED2 (a WNT receptor), linking ER lipid metabolism to protein trafficking and WNT signaling during primitive endoderm development. |
ESC knockout analysis, protein trafficking assays, FZD2 maturation/stability assays |
Autophagy |
Medium |
39968886
|
| 2025 |
The antibiotic carrimycin directly binds TMEM41B and induces its K48-ubiquitination and proteasomal degradation, thereby inhibiting coronavirus (including SARS-CoV-2) replication by disrupting DMV formation; TMEM41B overexpression partially reverses carrimycin's antiviral effect. |
Direct binding assay, ubiquitination assay, overexpression rescue experiment, viral replication assays, DMV formation analysis |
Acta pharmacologica Sinica |
Medium |
40374896
|