| 1999 |
SEC24C (KIAA0079) is a mammalian homologue of yeast Sec24p: it co-elutes with mammalian Sec23p on gel filtration, its C-terminal region binds the N-terminal region of Sec23p in vitro, and overexpression causes a defect in protein export from the ER. |
Gel filtration co-elution, in vitro binding assay, overexpression ER-export assay |
FEBS letters |
Medium |
10214955
|
| 2009 |
SEC24C is required for docking of the prechylomicron transport vesicle (PCTV) with the Golgi; immunodepletion of SEC24C from cytosol nearly completely abolished PCTV-Golgi docking activity, which was restored by adding back recombinant SEC24C. |
Immunodepletion of cytosolic SEC24C, reconstitution with recombinant SEC24C, PCTV-Golgi docking assay |
Journal of lipid research |
High |
19965600
|
| 2011 |
SERT exclusively requires SEC24C (not SEC24A, B, or D) for ER export: mass spectrometry showed SERT C-terminal peptide recruits SEC24C-containing COPII complexes from brain lysates; siRNA depletion of SEC24C (but not other isoforms) trapped SERT in the ER; a dominant-negative SEC24C-D796V/D797N reduced SERT surface levels; and a SERT-607RI608-AA mutant lacking the SEC24C-binding motif was insensitive to SEC24C knockdown. |
Mass spectrometry pulldown from brain lysates, isoform-selective siRNA knockdown, dominant-negative SEC24C overexpression, surface biotinylation |
The Journal of biological chemistry |
High |
21454670
|
| 2012 |
The triple Arg (3R) motif in the third intracellular loop of α2B-adrenergic receptor mediates direct interaction with Sec24C/D and is required for ER export; mutation or deletion of the 3R motif reduced co-immunoprecipitation with Sec24C/D and impaired cell surface transport. |
Co-immunoprecipitation, mutagenesis, surface expression assay, CD8 chimera transfer assay |
Traffic (Copenhagen, Denmark) |
Medium |
22404651
|
| 2013 |
A single residue at position +2 downstream of the ER export motif (RI) in SERT determines SEC24C vs. SEC24D isoform specificity: hydrophilic residues (Lys, Asn, Gln) recruit SEC24C, whereas hydrophobic residues (Tyr, Val) recruit SEC24D. Substituting Lys610 with Tyr switched SERT from SEC24C- to SEC24D-dependence. |
siRNA depletion of individual SEC24 isoforms, dominant-negative SEC24C/D overexpression, mutagenesis of SERT and other SLC6 transporters, surface biotinylation |
The Journal of biological chemistry |
High |
23288844
|
| 2013 |
A novel ER export signal motif ΦXΦXΦ (hydrophobic-X-hydrophobic-X-hydrophobic) in the N-terminus of bovine AE1 anion exchanger selectively interacts with SEC24C (via the Sec23A-Sec24C complex); mutation of the SEC24C IxM cargo-binding site (895LIL897→AAA) caused ER retention of ΦXΦXΦ-containing chimeric proteins. |
Synthetic peptide pulldown with Sec23A-Sec24C complex, chimeric protein mutagenesis, cell surface expression assay, N-glycan processing analysis, co-transfection with SEC24C-AAA dominant negative |
The Journal of biological chemistry |
High |
23658022
|
| 2014 |
SEC24C-dependent ER export determines axonal targeting of SERT in dorsal raphe neurons: disruption of the SEC24C-binding motif (RI→AA) or overexpression of dominant-negative SEC24C-D796V/D797N redirected SERT from axons to the somatodendritic compartment, while VMAT2 axonal targeting was unaffected by either dominant-negative SEC24C or SEC24D. |
Dominant-negative SEC24C/D overexpression in cultured neurons, fluorescence imaging of endogenous and heterologous SERT distribution, mutagenesis |
The Journal of neuroscience |
High |
24790205
|
| 2014 |
SEC24C is essential for early mammalian embryonic development; homozygous Sec24c null mice die at ~E7.5, whereas tissue-specific deletion in hepatocytes, pancreatic cells, smooth muscle cells, and intestinal epithelial cells produces no phenotype, indicating functional compensation by other SEC24 paralogs in those tissues. |
Conventional and conditional knockout mice, embryonic phenotype analysis |
The Journal of biological chemistry |
High |
24876386
|
| 2016 |
SEC24C directly interacts with Syntaxin5 in its 'open' conformation and is required for ER export of the preassembled Q-SNARE complex (Syntaxin5, GS27, Bet1); mutation of the IxM cargo-binding site in SEC24C drastically reduced incorporation of all three Q-SNAREs into COPII vesicles, while R-SNARE Sec22b is recruited by other isoforms. |
Co-immunoprecipitation, dominant-negative/mutation of IxM site in SEC24C, immunoisolation of COPII vesicles, confocal co-localization |
Molecular biology of the cell |
High |
27413010
|
| 2017 |
Claudin-1 interacts with SEC24C through its C-terminal YV motif for ER export and cell surface delivery; this interaction is required for HCV entry, as blocking COPII transport reduces claudin-1 surface levels. |
Co-immunoprecipitation, mutagenesis of YV motif, surface expression assay, HCV entry assay |
Journal of virology |
Medium |
28679754
|
| 2018 |
SEC24C is essential for postmitotic neuron survival: conditional KO of Sec24c in neural progenitors caused perinatal mortality, microcephaly, unfolded protein response activation, and apoptosis of cortical neurons; this neuronal cell death was rescued by knock-in expression of SEC24D in place of SEC24C. |
Conditional Sec24c KO mice, SEC24D knock-in rescue, iPSC-derived neuron KD, UPR marker analysis, TUNEL apoptosis assay |
The Journal of clinical investigation |
High |
29939162
|
| 2018 |
Amino acid transporter SLC6A14 (ATB0,+) exclusively co-precipitates with SEC24C (not with SEC24A, B, or D) for ER export; a dominant-negative SEC24C mutant reduced ATB0,+ plasma membrane expression and increased its proteolytic degradation; a Lys at position +2 of the RI export motif is required for SEC24C binding. |
Co-immunoprecipitation, proximity ligation assay, dominant-negative SEC24C, surface biotinylation, immunofluorescence co-localization |
Biochimica et biophysica acta. Molecular cell research |
Medium |
30445147
|
| 2021 |
SEC24C is an HIV-1 host dependency factor: it directly and specifically interacts with hexameric HIV-1 capsid lattices via an FG-motif (residues 228-242); a 2.3-Å crystal structure showed the FG-motif binds a pocket comprising two adjoining capsid subunits; deletion of SEC24C reduced core stability, reverse transcription, nuclear import, and infectivity; live-cell microscopy showed SEC24C co-trafficked with HIV-1 cores in the cytoplasm during ingress. |
Crystal structure at 2.3-Å resolution, biochemical binding assays, Sec24C gene deletion and complementation in Jurkat cells, siRNA knockdown in HeLa cells, live-cell microscopy, reverse transcription and nuclear import assays |
Nature microbiology |
High |
33649557
|
| 2021 |
AKT kinase phosphorylates SEC24C, and AKT inhibition decreases SEC24C phosphoserine levels (detected by proximity ligation assay and 2D electrophoresis), which correlates with transient increase of SLC6A14 transporter at the plasma membrane, suggesting AKT-mediated phosphorylation of SEC24C regulates ER export of SLC6A14. |
2D electrophoresis, proximity ligation assay with phospho-specific antibodies, AKT inhibitor (MK-2206) treatment, surface biotinylation |
Cells |
Low |
34359969
|
| 2021 |
Murine SEC24D can functionally substitute for SEC24C during embryonic development: Sec24cc-d/c-d knock-in mice (C-terminal 90% of SEC24C replaced by SEC24D sequence) survive to term whereas Sec24c null mice die at E7.5, indicating the early embryonic requirement for SEC24C reflects tissue/stage-specific expression rather than unique cargo specificity. |
Dual recombinase-mediated cassette exchange knock-in mice, embryonic lethality rescue analysis, pathological evaluation |
Scientific reports |
High |
34702932
|
| 2024 |
SEC24C and p24-family members TMP21 and TMED9 facilitate clearance of misfolded alpha-1-antitrypsin Z (ATZ) from the ER to lysosomes via ERLAD: ATZ co-immunoprecipitates with TMP21, TMED9, SEC24C, FAM134B, and calnexin; live-cell imaging showed ATZ and p24-family members co-trafficking to lysosomes; depletion of SEC24C inhibited lysosomal trafficking of ATZ and increased intracellular ATZ levels; p24-family members co-immunoprecipitate with both ATZ and SEC24C, placing SEC24C at ER-exit sites for ERLAD. |
Co-immunoprecipitation, live-cell imaging, chemical inhibitors of ER exit/autophagy, siRNA depletion, overexpression of p24 proteins |
Molecular biology of the cell |
High |
38294851
|
| 2024 |
SEC24C interacts with PERK (EIF2AK3) and activates downstream UPR-related apoptosis; under normal conditions SEC24C is nuclear-localized but translocates to the ER upon ER stress, and SEC24C overexpression augments bortezomib-induced apoptosis in hepatocellular carcinoma cells. |
Co-immunoprecipitation, subcellular fractionation/localization, overexpression + drug treatment apoptosis assay |
Bioscience trends |
Low |
39085101
|
| 2025 |
SEC24C is dynamically regulated by O-GlcNAcylation (present in interphase) and phosphorylation (enriched in specific cell cycle phases); O-GlcNAc is rapidly removed upon mitotic entry and its removal influences the timing of SEC24C dispersal from juxtanuclear ER exit sites to a diffuse cytosolic pool; novel phosphosites were identified that regulate SEC24C stability and localization during mitosis. |
Mass spectrometry phosphoproteomics, O-GlcNAc modification analysis, cell cycle synchronization, live-cell imaging of SEC24C localization, mutagenesis of phosphosites |
The Journal of biological chemistry |
Medium |
40617351
|
| 2025 |
Tanshinone IIA inhibits STING transport from the ER to the Golgi by weakening the interaction between STING and SEC24C, thereby preventing cGAS-STING pathway activation. |
Co-immunoprecipitation of STING and SEC24C with/without Tanshinone IIA, STING localization assay, downstream signaling readouts |
International immunopharmacology |
Low |
40252465
|
| 2025 |
Kremen1 (dependence receptor) induces autophagic cell death requiring SEC24C: biotin proximity labeling identified SEC24C as a critical effector; Kremen1 is in proximity with SEC24C and ATG9A after vesicular trafficking, and SEC24C is brought into proximity with ATG8, ERGIC, and ATG9A, increasing autophagosome formation leading to cell death. |
Biotin proximity labeling (BioID/TurboID), genetic silencing of autophagy effectors, pharmacological inhibition of autophagy, proximity ligation assay |
Cell communication and signaling |
Low |
41807954
|
| 2025 |
Acute glucose starvation impairs ER-to-Golgi export of specific cargoes (e.g., E-cadherin) in a SEC24C-dependent manner; AMPK and ULK1 signaling (independent of autophagy) orchestrate this process, with ULK1-mediated phosphorylation of SEC31A driving SEC24C-dependent COPII reorganization. |
SEC24C knockout cells, quantitative cell surface proteomics, nutrient deprivation experiments, ULK1 kinase assay, AMPK/ULK1 inhibitor experiments |
bioRxivpreprint |
Medium |
|