Affinage

EXOC5

Exocyst complex component 5 · UniProt O00471

Length
708 aa
Mass
81.9 kDa
Annotated
2026-04-28
26 papers in source corpus 22 papers cited in narrative 22 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

EXOC5 (Sec10) is a core subunit of the octameric exocyst complex that mediates polarized vesicle trafficking, primary ciliogenesis, and innate immune regulation across diverse cell types. Structurally a tandem antiparallel helix-bundle rod, EXOC5 bridges the exocyst to cargo via its N-terminal interaction with Sec15p and engages the ER translocon subunit Sec61β, facilitating basolateral protein translocation and polarized delivery of apical cargoes such as uroplakins and ciliary proteins including polycystin-2, IFT88, and IFT20 (PMID:9658167, PMID:23037926, PMID:26046524, PMID:21490950). Conditional knockouts in mice demonstrate essential roles in primary ciliogenesis in renal epithelia, cochlear hair cell survival, retinal pigment epithelium integrity, folliculogenesis, and urothelial differentiation (PMID:19297529, PMID:29327200, PMID:34064901, PMID:39037927). In myeloid cells, EXOC5 suppresses antiviral type I interferon responses through three convergent mechanisms: promoting STUB1-mediated K6-linked polyubiquitination and proteasomal degradation of STAT1, facilitating TRIM56-mediated K63-linked polyubiquitination and autophagic degradation of STING1 via SQSTM1/p62, and inhibiting the NRF2–ATF4 transcriptional axis that drives RIG-I expression (PMID:40920886, PMID:41968661, PMID:41079927).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1997 Medium

    Establishing that EXOC5 is the mammalian exocyst subunit answered whether the yeast Sec10p-based secretory machinery is conserved in humans and placed EXOC5 in the post-Golgi trafficking pathway.

    Evidence Cloning of human SEC10 and co-localization with Sec8p by immunofluorescence in mammalian cells

    PMID:9119050

    Open questions at the time
    • No direct biochemical demonstration of complex membership in mammalian cells
    • Functional requirement not yet tested
  2. 1998 High

    Domain dissection of yeast Sec10p revealed that its N-terminus binds Sec15p to anchor the complex while its C-terminus independently directs polarized morphogenesis, establishing EXOC5 as a bifunctional scaffold within the exocyst.

    Evidence Dominant-negative overexpression of Sec10p domains, biochemical fractionation, and genetic analysis in S. cerevisiae

    PMID:9658167

    Open questions at the time
    • Whether mammalian EXOC5 retains the same domain-function separation
    • Identity of C-terminal binding partners
  3. 2002 High

    Tissue-specific knockdown in Drosophila demonstrated that EXOC5 is selectively essential for endocrine secretion (steroid hormone release from the ring gland) rather than being universally required for all polarized exocytosis, revealing cell-type-specific dependence.

    Evidence Tissue-specific transgenic RNAi in Drosophila with ecdysone rescue

    PMID:12453153

    Open questions at the time
    • Whether tissue-selective requirement reflects redundancy with other exocyst subunits or cargo specificity
  4. 2009 High

    The discovery that EXOC5 knockdown abolishes primary cilium axoneme formation while overexpression enhances ciliogenesis fundamentally expanded the exocyst's role beyond plasma-membrane-directed exocytosis to ciliary biogenesis.

    Evidence shRNA knockdown and overexpression in MDCK cells with electron microscopy, co-IP with Par3, 3D cyst assays, and rescue with human Sec10

    PMID:19297529

    Open questions at the time
    • Which specific ciliary cargoes require exocyst-mediated delivery
    • How Par3 interaction recruits the exocyst to the cilium base
  5. 2011 High

    Identifying EXOC5 as a physical interactor of polycystin-2, IFT88, and IFT20, and showing genetic epistasis with pkd2 in zebrafish, established a molecular mechanism linking the exocyst to ciliopathy-relevant cargo trafficking and left-right body axis patterning.

    Evidence Co-immunoprecipitation, zebrafish morpholino epistasis, and MAPK activation assays

    PMID:21490950

    Open questions at the time
    • Whether EXOC5 directly loads ciliary cargoes or acts indirectly through vesicle tethering
    • Structural basis of EXOC5–IFT interaction
  6. 2010 Medium

    Demonstrating that EXOC5 overexpression activates MAPK/ERK signaling and protects epithelial barriers from oxidative injury placed the exocyst upstream of a major pro-survival kinase cascade in renal cells.

    Evidence MDCK overexpression with U0126 pharmacological inhibition, transepithelial resistance after H₂O₂ treatment

    PMID:20053792

    Open questions at the time
    • Whether MAPK activation is direct or secondary to enhanced receptor trafficking
    • Mechanism connecting vesicle trafficking to ERK phosphorylation
  7. 2012 Medium

    The finding that EXOC5 binds the ER translocon subunit Sec61β and is preferentially recruited to ER membranes during basolateral protein translation extended the exocyst's function upstream from the Golgi to the ER, suggesting a role in co-translational sorting.

    Evidence GST pulldown and cell-free translation/translocation assay with ³²P-labeling

    PMID:23037926

    Open questions at the time
    • Whether ER recruitment is physiologically rate-limiting for basolateral sorting in vivo
    • Structural basis of EXOC5–Sec61β interaction
  8. 2014 High

    Two studies in 2014 defined EXOC5's role in endosomal recycling and EGFR signaling: in C. elegans, SEC-10 maintains endosomal tubular networks for basolateral recycling of clathrin-independent cargoes, while in mammalian cells, the exocyst-EGFR interaction drives EGFR endocytosis and downstream MAPK activation that protects against kidney injury.

    Evidence C. elegans RNAi with live imaging and epistasis analysis; mammalian co-IP with pharmacological inhibition (gefitinib, Dynasore, U0126) and zebrafish AKI model

    PMID:25298525 PMID:25301900

    Open questions at the time
    • Whether EXOC5 directly tethers EGFR-containing endosomes or acts through adaptor proteins
    • Conservation of endosomal tubule role in mammalian cells
  9. 2015 High

    Conditional knockout of Exoc5 in mouse ureteric bud-derived cells, combined with MDCK cyst analyses, demonstrated that EXOC5 is essential for apical uroplakin delivery, mitotic spindle orientation, and ciliogenesis in vivo, consolidating its role in multiple axes of epithelial polarity.

    Evidence Conditional KO mouse (Ksp1.3-Cre), shRNA knockdown with rescue, EM for uroplakin plaques, spindle angle measurements, 3D cyst culture

    PMID:26040895 PMID:26046524

    Open questions at the time
    • Molecular basis for spindle orientation defect
    • Whether polarity and ciliogenesis defects are independent or sequential consequences of trafficking failure
  10. 2017 High

    The crystal structure of near-full-length zebrafish Sec10 at 2.73 Å confirmed the tandem antiparallel helix-bundle rod architecture conserved among exocyst subunits, providing the first atomic model for this subunit.

    Evidence X-ray crystallography of zebrafish Sec10

    PMID:28098232

    Open questions at the time
    • No structure of EXOC5 in complex with other exocyst subunits or cargo adaptors
    • Human EXOC5 structure not yet determined
  11. 2018 High

    Hair cell-specific Exoc5 deletion causing stereociliary disorganization and progressive cochlear cell death, along with the EXOC5–DGKγ axis controlling cell migration, demonstrated that EXOC5 has non-redundant roles in sensory cell survival and wound-healing migration.

    Evidence Conditional KO mouse (Gfi1Cre) with ABR testing; MDCK wound assay with DGK inhibitor rescue

    PMID:29326040 PMID:29327200

    Open questions at the time
    • Whether stereociliary defect is secondary to ciliogenesis failure or a distinct trafficking defect
    • Direct mechanism linking EXOC5 to DGKγ localization
  12. 2021 High

    RPE-specific Exoc5 knockout causing photoreceptor degeneration in both mice and zebrafish established EXOC5 as essential for retinal pigment epithelium function and visual cycle maintenance.

    Evidence RPE-specific conditional KO mouse, electroretinography, zebrafish exoc5 mutants with histology

    PMID:34064901

    Open questions at the time
    • Which RPE cargoes require EXOC5 for trafficking
    • Relationship between RPE EXOC5 loss and photoreceptor outer segment maintenance
  13. 2024 High

    Oocyte-specific deletion showed that EXOC5 is required for folliculogenesis beyond the secondary follicle stage and for oocyte developmental competence, extending the gene's essential trafficking roles to female germ cells.

    Evidence Zp3-Cre conditional KO mouse, IVF, superovulation, histology

    PMID:39037927

    Open questions at the time
    • Identity of oocyte cargoes requiring EXOC5-dependent secretion
    • Whether the folliculogenesis block reflects paracrine signaling failure or cell-autonomous defect
  14. 2025 High

    The identification of three convergent mechanisms by which EXOC5 suppresses antiviral IFN-I signaling—STUB1-mediated proteasomal degradation of STAT1 via K6-linked ubiquitination, TRIM56/p62-mediated autophagic degradation of STING1 via K63-linked ubiquitination, and NRF2–ATF4 axis inhibition reducing RIG-I transcription—revealed an unexpected immunomodulatory function for this trafficking subunit.

    Evidence Co-IP with ubiquitination site-specific mutants, autophagy flux assays, ChIP/promoter analysis, myeloid-specific conditional KO mice with viral challenge

    PMID:40920886 PMID:41079927 PMID:41968661

    Open questions at the time
    • Whether EXOC5's immune role depends on its exocyst complex membership or is an independent moonlighting function
    • Physiological context where immune suppression by EXOC5 is beneficial versus detrimental
  15. 2026 Medium

    Two studies extended EXOC5's functions to exosome-regulated macrophage migration (via formin1 retention) and negative regulation of YAP signaling in renal fibrosis, broadening its role to intercellular communication and mechanotransduction pathways.

    Evidence LysM-Cre and PEPCK-Cre conditional KO mice, exosome quantification, pharmacological inhibition of formin1/Rac1, UUO fibrosis model, siRNA in HK-2 cells

    PMID:41604889 PMID:41781492

    Open questions at the time
    • Molecular mechanism connecting EXOC5 to YAP expression levels
    • Whether exosome release defect is a direct consequence of exocyst dysfunction at multivesicular bodies
    • Independent replication needed for both formin1 and YAP pathways

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major open questions include whether EXOC5's immunomodulatory functions are exocyst-dependent or represent moonlighting roles, the structural basis for EXOC5's interaction with diverse cargo adaptors (IFTs, EGFR, STUB1, TRIM56), and how tissue-specific trafficking requirements explain the diverse conditional knockout phenotypes across epithelia, sensory cells, immune cells, and germ cells.
  • No cryo-EM or crystal structure of EXOC5 in assembled exocyst complex with cargo
  • Exocyst-independent versus exocyst-dependent functions not dissected
  • No human genetic disease directly linked to EXOC5 mutations in the timeline

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0005886 plasma membrane 3 GO:0005929 cilium 2 GO:0031410 cytoplasmic vesicle 2 GO:0005768 endosome 1 GO:0005783 endoplasmic reticulum 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-5653656 Vesicle-mediated transport 5 R-HSA-1852241 Organelle biogenesis and maintenance 4 R-HSA-168256 Immune System 3 R-HSA-9609507 Protein localization 3 R-HSA-392499 Metabolism of proteins 2 R-HSA-9612973 Autophagy 1
Partners
EGFRIFT20IFT88PKD2SEC15SEC61BSTUB1TRIM56
Complex memberships
Exocyst complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Human SEC10 (hSec10p) was identified as the human homologue of yeast Sec10p, a component of the exocyst complex. Co-transfection and immunofluorescence showed that hSec10p and mammalian Sec8p have identical subcellular distribution including peripheral cytoplasm localization, consistent with hSec10p being part of the mammalian exocyst complex involved in post-Golgi traffic. Cloning, co-transfection, immunofluorescence, Northern/Western blot FEBS letters Medium 9119050
1998 Yeast Sec10p has two functional domains: an N-terminal two-thirds that directly interacts with Sec15p (another exocyst component), whose overexpression displaces Sec10p from the exocyst and blocks exocytosis causing vesicle accumulation; and a C-terminal domain that does not interact with other exocyst components but is required for cell morphogenesis (reorientation of secretory pathway during cell cycle). Dominant-negative overexpression, biochemical fractionation, genetic analysis in yeast (S. cerevisiae) Molecular biology of the cell High 9658167
2002 Drosophila Sec10 (dSec10) is essential for endocrine (steroid hormone) secretion from the ring gland but is not required for neurotransmission, polarized secretion in nervous system, musculature, gut, or epidermis. Developmental arrest from dSec10 RNAi was partially rescued by feeding ecdysone, placing dSec10 upstream of steroid hormone secretion. Tissue-specific transgenic RNAi, ecdysone rescue assay, phenotypic characterization in Drosophila Traffic High 12453153
2009 Exocyst component Sec10 regulates primary ciliogenesis in renal epithelial cells: shRNA knockdown of Sec10 in MDCK cells results in cilia containing only basal bodies (no axoneme), while overexpression increases ciliogenesis. Sec10 knockdown prevents cyst morphogenesis in collagen matrix, overexpression increases cystogenesis. Par3 co-localizes and co-immunoprecipitates with the exocyst, suggesting the exocyst targets vesicles carrying proteins necessary for primary ciliogenesis. shRNA knockdown, stable overexpression, immunofluorescence, scanning/transmission electron microscopy, co-immunoprecipitation, 3D collagen cyst assay, rescue with human Sec10 Molecular biology of the cell High 19297529
2011 Sec10 biochemically interacts with the ciliary proteins polycystin-2 (PKD2), IFT88, and IFT20, and co-localizes with polycystin-2 at the primary cilium. Sec10 knockdown in zebrafish phenocopies polycystin-2 knockdown (curly tail, left-right patterning defects, glomerular expansion, MAPK activation), and synergistic genetic interaction between sec10 and pkd2 morpholinos supports a model where the exocyst is required for ciliary localization of polycystin-2. Co-immunoprecipitation, immunofluorescence, zebrafish morpholino knockdown, genetic epistasis (synergistic interaction), MAPK activation assays PLoS genetics High 21490950
2010 Sec10 overexpression in renal tubule cells activates the MAPK pathway (elevated basal ERK phosphorylation), which protects epithelial barrier integrity and accelerates recovery following oxidative stress. MAPK inhibitor U0126 blocked the protective effect of Sec10 overexpression, placing Sec10 upstream of ERK in this pathway. Sec10 overexpression in MDCK cells, transepithelial electrical resistance measurements, H2O2 treatment, pharmacological inhibition of MAPK (U0126), Western blot for p-ERK American journal of physiology. Renal physiology Medium 20053792
2012 Sec10 interacts with the ER translocon subunit Sec61β via GST pulldown, and the exocyst is preferentially recruited to ER membranes during basolateral protein (VSV-G) translation compared to apical protein (hemagglutinin) translation in cell-free assays. Sec10 overexpression increases Sec61β phosphorylation, suggesting a regulatory role for the exocyst in basolateral protein translation/translocation. GST pulldown, cell-free translation/translocation assay, 32P-orthophosphate labeling, immunoprecipitation Nephron. Experimental nephrology Medium 23037926
2014 SEC-10 (C. elegans ortholog) operates at an intermediate step between early endosomes and recycling endosomes, forming an endosomal tubular network required for basolateral recycling of clathrin-independent endocytic (CIE) cargoes. SEC-10 coordinates with RAB-10 and microtubules to maintain endosomal tubule structure; depletion converts tubules to ring-like structures. RNAi depletion, epistasis analysis, live imaging in C. elegans intestine PNAS High 25301900
2014 The exocyst biochemically interacts with EGFR (co-immunoprecipitation), and Sec10 overexpression enhances EGFR endocytosis and MAPK/ERK activation in response to EGF. Gefitinib (EGFR inhibitor) reverses the protective effect of Sec10 overexpression following renal cell injury, establishing an exocyst–EGFR–endocytosis–MAPK axis in protection from kidney injury. Co-immunoprecipitation, EGFR endocytosis assays, pharmacological inhibition (gefitinib, Dynasore, U0126), in vivo zebrafish AKI model with sec10 morpholino knockdown American journal of physiology. Renal physiology Medium 25298525
2015 Conditional knockout of Sec10 in ureteric bud-derived cells in mice (first conditional allele for any exocyst gene) causes loss of uroplakin-3 at the urothelial apical surface and subsequent urothelial degeneration, demonstrating Sec10 is required for polarized apical delivery of uroplakin proteins to form luminal plaques in urothelium. Conditional knockout mouse (Ksp1.3-Cre × Sec10 floxed), immunofluorescence for uroplakin-3, histology, electron microscopy PloS one High 26046524
2015 Sec10 knockdown MDCK cells show abnormal mitotic spindle angles (planar cell polarity defect) and increased basal apoptotic cell extrusion; primary cilia assembly is disrupted in both Sec10 KD cysts and kidney-specific Sec10 KO mouse renal tubules. Restoring Sec10 with shRNA-resistant human Sec10 reverses these phenotypes, confirming specificity. shRNA knockdown, 3D collagen cyst culture, kidney-specific conditional KO mouse, immunofluorescence for mitotic spindle angles, apoptosis assays, rescue with shRNA-resistant Sec10 American journal of physiology. Cell physiology High 26040895
2015 Zebrafish cdc42 and sec10 act in the same genetic pathway (synergistic interaction upon suboptimal morpholino co-injection) to regulate outer segment development of retinal photoreceptors through trafficking proteins necessary for ciliogenesis. Sec10 knockdown additionally causes intracellular transport defects affecting retrograde melanosome transport. Zebrafish morpholino knockdown, genetic epistasis (synergistic morpholino interaction), histology, immunohistology, TEM, melanosome transport assay Investigative ophthalmology & visual science Medium 26024121
2017 Crystal structure of near-full-length zebrafish Sec10 was solved at 2.73 Å resolution, revealing tandem antiparallel helix bundles forming a straight rod, consistent with the helical architecture of other exocyst subunits. X-ray crystallography Scientific reports High 28098232
2018 Sec10 downregulation in MDCK cells accelerates wound healing and ruffle formation by reducing DGK-gamma at the leading edge. Sec10 overexpression inhibits cell migration by increasing DGKγ at the leading edge; a DGK inhibitor reverses this inhibition, placing Sec10 upstream of DGKγ in the regulation of cell migration. Sec10 overexpression/knockdown in MDCK cells, wound scratch assay, DGK inhibitor treatment, immunofluorescence for DGKγ localization, in vivo I/R mouse model Biochemical and biophysical research communications Medium 29326040
2018 Hair cell-specific deletion of Exoc5 in mice (Gfi1Cre/+;Exoc5f/f) results in progressive hair cell apoptosis with disorganized stereociliary bundles and hearing loss; deletion throughout the otic epithelium additionally causes abnormal spiral ganglion neuron neurite morphology and subsequent SGN apoptosis, demonstrating Exoc5 is required for survival of cochlear hair cells and SGNs. Conditional knockout mouse (Gfi1Cre and rAAV-iCre), auditory brainstem response, histology, immunofluorescence, apoptosis assays Molecular neurobiology High 29327200
2021 RPE-specific conditional knockout of Exoc5 in mice causes RPE dysfunction (abnormal RPE65 levels, reduced c-wave amplitude), retinal thinning, and loss of visual pigments with progressive photoreceptor degeneration. In exoc5 zebrafish mutants, shorter photoreceptor outer segments and loss of melanocytes in RPE were observed, demonstrating Exoc5 is required for RPE structure and function. Conditional KO mouse (RPE-specific), electroretinography, zebrafish exoc5 mutants, histology, immunofluorescence for visual pigments International journal of molecular sciences High 34064901
2025 Sec10 attenuates antiviral JAK-STAT signaling by interacting with E3 ligase STUB1, promoting STUB1-STAT1 interaction, and accelerating proteasomal degradation of STAT1 via K6-linked polyubiquitination at Lys240 and Lys652. Myeloid-specific Exoc5 knockout mice show enhanced IFN-I response and improved viral infection survival. Co-immunoprecipitation, ubiquitination assays with site-specific mutants (K240R, K652R), myeloid-specific conditional KO mice, IFN signaling assays PLoS pathogens High 40920886
2025 Sec10 negatively regulates antiviral innate immunity by inhibiting the NRF2-ATF4 axis during RNA viral infection, which suppresses ATF4-driven transcription of the RIG-I promoter, thereby reducing RIG-I expression and IFN-I response. Sec10 deficiency enhances innate immunity and reduces viral load in mice. ChIP/promoter analysis showing ATF4 binding to RIG-I promoter, Sec10 KO cells and mice, IFN signaling assays, RNA viral infection models International journal of biological sciences Medium 41079927
2024 Oocyte-specific deletion of Exoc5 (Zp3-Exoc5-cKO) blocks folliculogenesis past the secondary follicle stage in adult waves (subsequent waves undergo apoptosis at preantral stage), while first-wave folliculogenesis proceeds to antral stage but produces developmentally incompetent oocytes. This demonstrates EXOC5 is required for follicular development and oocyte developmental competence. Conditional knockout mouse (Zp3-Cre × Exoc5 floxed), IVF, histology, superovulation Molecular human reproduction High 39037927
2026 EXOC5 facilitates autophagic degradation of STING1 via K63-linked polyubiquitination at Lys224 and Lys338 by E3 ligase TRIM56, with SQSTM1/p62 serving as cargo receptor, thereby suppressing cGAS-STING1-driven IFN-I antiviral signaling. Myeloid-specific Exoc5 KO mice show improved survival and reduced viral load. Co-immunoprecipitation, ubiquitination assays with K63R mutants and site-specific mutations, autophagy flux assays, myeloid-specific conditional KO mice Autophagy High 41968661
2026 Myeloid-specific Exoc5 deficiency reduces exosome release from macrophages, leading to intracellular accumulation of formin1, which enhances macrophage migration into the kidney. An actin disruptor and formin1 inhibitor reversed the enhanced migration phenotype, placing Exoc5-mediated exosome secretion upstream of formin1-dependent macrophage motility. LysM-Cre × Exoc5 floxed conditional KO mice, exosome quantification, formin1 localization, pharmacological inhibition (actin disruptor, formin1 inhibitor, Rac1 inhibitor), macrophage migration assays, adoptive transfer Biomedicine & pharmacotherapy Medium 41604889
2026 Exoc5 deficiency in renal proximal tubule cells increases YAP expression and activation, and augments TGF-β-induced YAP activation and epithelial-to-mesenchymal transition, worsening kidney fibrosis following ureteral obstruction. This places Exoc5 as a negative regulator of YAP signaling in the context of renal fibrosis. Proximal tubule-specific conditional KO mouse (PEPCK-Cre), unilateral ureteral obstruction model, siRNA knockdown in HK-2 cells, Western blot for YAP/CTGF/CYR61/Pax2 Experimental & molecular medicine Medium 41781492

Source papers

Stage 0 corpus · 26 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 The exocyst protein Sec10 is necessary for primary ciliogenesis and cystogenesis in vitro. Molecular biology of the cell 151 19297529
2011 The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes. PLoS genetics 78 21490950
2002 Drosophila sec10 is required for hormone secretion but not general exocytosis or neurotransmission. Traffic (Copenhagen, Denmark) 40 12453153
2015 Urothelial Defects from Targeted Inactivation of Exocyst Sec10 in Mice Cause Ureteropelvic Junction Obstructions. PloS one 39 26046524
1998 Dominant negative alleles of SEC10 reveal distinct domains involved in secretion and morphogenesis in yeast. Molecular biology of the cell 37 9658167
1997 Identification and characterization of homologues of the Exocyst component Sec10p. FEBS letters 36 9119050
2014 SEC-10 and RAB-10 coordinate basolateral recycling of clathrin-independent cargo through endosomal tubules in Caenorhabditis elegans. Proceedings of the National Academy of Sciences of the United States of America 32 25301900
2014 Dissecting a hidden gene duplication: the Arabidopsis thaliana SEC10 locus. PloS one 25 24728280
2010 Exocyst Sec10 protects epithelial barrier integrity and enhances recovery following oxidative stress, by activation of the MAPK pathway. American journal of physiology. Renal physiology 25 20053792
2015 Cdc42 and sec10 Are Required for Normal Retinal Development in Zebrafish. Investigative ophthalmology & visual science 24 26024121
2014 Exocyst Sec10 protects renal tubule cells from injury by EGFR/MAPK activation and effects on endocytosis. American journal of physiology. Renal physiology 20 25298525
2018 An ancient Sec10-formin fusion provides insights into actin-mediated regulation of exocytosis. The Journal of cell biology 19 29374070
2015 The exocyst gene Sec10 regulates renal epithelial monolayer homeostasis and apoptotic sensitivity. American journal of physiology. Cell physiology 19 26040895
2017 Crystal structure of Sec10, a subunit of the exocyst complex. Scientific reports 16 28098232
2018 Exocyst Complex Member EXOC5 Is Required for Survival of Hair Cells and Spiral Ganglion Neurons and Maintenance of Hearing. Molecular neurobiology 9 29327200
2018 Downregulation of exocyst Sec10 accelerates kidney tubule cell recovery through enhanced cell migration. Biochemical and biophysical research communications 7 29326040
2021 Conditional Loss of the Exocyst Component Exoc5 in Retinal Pigment Epithelium (RPE) Results in RPE Dysfunction, Photoreceptor Cell Degeneration, and Decreased Visual Function. International journal of molecular sciences 6 34064901
2012 Exocyst Sec10 is involved in basolateral protein translation and translocation in the endoplasmic reticulum. Nephron. Experimental nephrology 5 23037926
2024 Oocyte-specific EXOC5 expression is required for mouse oogenesis and folliculogenesis. Molecular human reproduction 3 39037927
2025 Sec10 suppresses antiviral innate immune response by facilitating STUB1-mediated STAT1 degradation. PLoS pathogens 2 40920886
2025 Sec10 negatively regulates antiviral immunity by downregulating NRF2-ATF4-RIG-I axis. International journal of biological sciences 1 41079927
2026 Myeloid-specific Exoc5 deficiency develops renal inflammation and hypertension. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 0 41604889
2026 Deficiency of exocyst complex component Exoc5 exacerbates the progression of kidney fibrosis. Experimental & molecular medicine 0 41781492
2026 SEC10 suppresses KLF15-mediated transcriptional activation of JAK1 and promotes BoHV-1 replication. Veterinary microbiology 0 41903488
2026 EXOC5/SEC10 attenuates antiviral IFN-I signaling by targeting STING1 for autophagic degradation. Autophagy 0 41968661
2025 The C-terminal domain of SEC-10 is fundamental for exocyst function, apical organization, and cell morphogenesis in Neurospora crassa. Molecular biology of the cell 0 40632529