Affinage

SURF4

Surfeit locus protein 4 · UniProt O15260

Length
269 aa
Mass
30.4 kDa
Annotated
2026-04-28
35 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SURF4 is a polytopic ER-resident cargo receptor that drives the selective ER-to-Golgi trafficking of a broad spectrum of soluble secretory proteins and contributes to the structural maintenance of the ERGIC and Golgi apparatus. It recognizes soluble cargoes—including PCSK9, ApoB-containing lipoproteins, EPO, proinsulin, prosaposin, SAA1, and Sonic Hedgehog—through N-terminal tripeptide motifs (ER-ESCAPE motifs) that bind co-translationally to a lumenal pocket, and it recruits specific SEC24 COPII coat paralogs (with co-receptors such as TMED10 for certain cargoes) to concentrate cargo at ER exit sites and load it into COPII vesicles or specialized tubular ERGIC carriers for expedited transport (PMID:30086131, PMID:39531033, PMID:35051356). Homozygous Surf4 knockout in mice is embryonic lethal, and tissue-specific hepatic or intestinal deletion severely impairs VLDL, chylomicron, and HDL secretion, reduces plasma lipids, and attenuates atherosclerosis and liver fibrosis (PMID:31978056, PMID:34118252, PMID:36193893, PMID:36756879). SURF4 also interacts with ERGIC-53 and p24 family members to recruit COPI and maintain ERGIC/Golgi architecture, participates in ERAD retrotranslocation of substrates such as COX-2, and negatively modulates STIM1-dependent store-operated calcium entry (PMID:18287528, PMID:37676109, PMID:22609200).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1995 High

    Establishing that SURF4 is an ER-resident integral membrane protein with multiple transmembrane domains and a C-terminal dilysine ER-retrieval motif provided the foundational topology for understanding its function as a cycling receptor in the early secretory pathway.

    Evidence In vitro translation, proteolysis protection, salt/detergent extraction, and immunofluorescence of tagged chimeras

    PMID:7540914

    Open questions at the time
    • No cargo or function identified at this stage
    • Number of transmembrane spans not fully resolved experimentally
    • Cycling between ER and Golgi not directly demonstrated
  2. 2008 High

    Demonstrating that SURF4 interacts with ERGIC-53 and p24 proteins and that combined depletion causes Golgi fragmentation and cytosolic redistribution of COPI revealed that cargo receptors collectively maintain ERGIC/Golgi architecture through COPI recruitment.

    Evidence Co-immunoprecipitation, siRNA knockdown, live imaging, brefeldin A resistance assays in HeLa cells

    PMID:18287528

    Open questions at the time
    • Whether SURF4 directly recruits COPI or acts indirectly through p24 proteins is unresolved
    • SURF4's individual contribution versus ERGIC-53 contribution not fully separated
  3. 2012 Medium

    Identifying SURF4 as a STIM1-associated negative modulator of store-operated Ca²⁺ entry expanded its known roles beyond cargo trafficking to ER calcium signaling.

    Evidence Affinity purification of STIM1 interactors, co-immunoprecipitation, SOCE measurements and STIM1 clustering in Surf4-deficient DT40 cells

    PMID:22609200

    Open questions at the time
    • Mechanism by which SURF4 restrains STIM1 clustering unknown
    • Not replicated in mammalian cells
    • Whether this reflects cargo-receptor function of SURF4 or a distinct activity is unclear
  4. 2018 High

    Convergent studies established SURF4 as a bona fide ER cargo receptor: it binds PCSK9 and ApoB to promote their ER exit, recognizes N-terminal tripeptide ER-ESCAPE motifs on soluble cargoes with specificity determined by single-residue changes, localizes to ERES, and reduces ERES number when depleted—with cross-species rescue by yeast Erv29p confirming functional conservation.

    Evidence BioID proteomics, genome-scale CRISPR screen, co-immunoprecipitation in human and C. elegans systems, systematic tripeptide mutagenesis, Surf4-null and rescue cell lines, ERES quantification

    PMID:29643117 PMID:30086131 PMID:30251625

    Open questions at the time
    • Structural basis of the lumenal cargo-binding pocket not determined
    • Whether all cargoes use the same motif-dependent mechanism or alternative recognition modes exist
    • Relationship between SURF4 and COPII coat subunit selection not yet addressed
  5. 2020 High

    Extension of SURF4's cargo repertoire to EPO and demonstration that murine Surf4 knockout is embryonic lethal established the receptor's essentiality and breadth beyond lipoproteins.

    Evidence Genome-scale CRISPR screen with Co-IP and rescue for EPO in Hep3B cells; CRISPR germline knockout mice with embryonic staging

    PMID:31978056 PMID:32989016

    Open questions at the time
    • Cause of embryonic lethality not defined at the molecular level
    • Whether lethality reflects loss of a single critical cargo or cumulative secretory failure is unknown
  6. 2021 High

    Resolving the in vivo hepatic function of SURF4 showed it is the principal cargo receptor for VLDL/ApoB100 secretion, and identifying prosaposin as a SURF4 cargo that in turn escorts progranulin revealed a layered cargo-receptor relay for lysosomal protein delivery.

    Evidence Liver-specific Surf4 knockout mice with plasma lipid and atherosclerosis phenotyping; Co-IP epistasis between SURF4, prosaposin, and progranulin with lysosomal delivery assays

    PMID:34118252 PMID:34919127

    Open questions at the time
    • Whether SURF4 directly contacts progranulin or acts exclusively through prosaposin is unclear
    • Discrepancy between in vitro and in vivo PCSK9 dependence on SURF4 remains unresolved across studies
  7. 2022 High

    Discovery that SURF4 induces formation of a tubular ERGIC (t-ERGIC) that is ERGIC-53-negative but Rab1-positive revealed a specialized transport carrier that expedites ER-to-Golgi transit of SURF4-bound cargoes, distinct from classical vesicular COPII transport.

    Evidence Super-resolution live-cell TIRF/SIM microscopy, SURF4 KO, cargo kinetics, Rab1 and ERGIC-53 marker analysis

    PMID:35051356

    Open questions at the time
    • Mechanism of t-ERGIC tubule formation and whether SURF4 directly deforms membranes is unknown
    • Whether t-ERGIC exists in all cell types or is context-dependent not addressed
  8. 2022 High

    Demonstrating that SURF4 physically interacts with proinsulin and Sec12, oligomerizes, and is glucose-regulated positioned it as a metabolically responsive cargo receptor that coordinates ERES assembly for insulin biosynthesis.

    Evidence Co-immunoprecipitation of Surf4–proinsulin and Surf4–Sec12, siRNA knockdown in INS-1 β-cells, insulin secretion assays

    PMID:35562580

    Open questions at the time
    • Whether Surf4 oligomerization is required for function is untested
    • Direct Sec12 binding site on SURF4 not mapped
  9. 2022 High

    Hepatic Surf4 inactivation in vivo reduced plasma PCSK9 by ~60% and increased hepatic LDLR ~50%, resolving an earlier discrepancy and confirming SURF4 as a physiological PCSK9 secretion receptor alongside its role in ApoB-lipoprotein export; SURF4 was also shown to facilitate Shh ER export via a proteoglycan-dependent relay in the Golgi.

    Evidence Hepatic conditional KO, acute CRISPR/Cas9, liver-targeted siRNA for PCSK9/LDLR; Co-IP and mutational analysis for Shh ER export signal

    PMID:35271396 PMID:36193893

    Open questions at the time
    • Molecular basis of SURF4–Shh dissociation by proteoglycans not structurally defined
    • Whether PCSK9 and ApoB compete for the same SURF4 binding site is unknown
  10. 2023 Medium

    Identifying SURF4 as a downstream component of the derlin-mediated ERAD retrotranslocation pathway for COX-2 extended its functional repertoire beyond anterograde cargo sorting to ER quality control and protein degradation.

    Evidence CRISPR library screen, siRNA epistasis ordering derlin-2 → derlin-1 → Surf4, Co-IP of Surf4–COX-2, ubiquitylation and p97 interaction assays

    PMID:37676109

    Open questions at the time
    • Whether SURF4's ERAD role extends to substrates beyond COX-2 is untested
    • Structural basis for SURF4 participation in retrotranslocation versus anterograde transport is undefined
    • Single-lab finding awaiting independent confirmation
  11. 2023 High

    Intestinal Surf4 was shown to be essential for chylomicron and HDL secretion, with tissue-specific knockout causing fat malabsorption, enterocyte lipid accumulation, and hypolipidemia, broadening the physiological relevance of SURF4 beyond the liver.

    Evidence Intestinal-specific Surf4 KO mice, Co-IP of Surf4–ApoB48, electron microscopy, proteomics, radiolabeled lipid absorption assays

    PMID:36756879 PMID:38042368

    Open questions at the time
    • Whether intestinal SURF4 loss affects non-lipid cargoes in vivo is not characterized
    • Compensatory mechanisms for lipid absorption in Surf4-deficient intestine not explored
  12. 2024 High

    Mechanistic dissection revealed that SURF4 recruits distinct SEC24 COPII coat paralogs in a cargo-dependent manner (SEC24A for PCSK9 with co-receptor TMED10; SEC24C/D for Cab45/NUCB1), and that ER-exit signals bind co-translationally to a lumenal SURF4 pocket, establishing the molecular logic of cargo-coat coupling.

    Evidence Genetic perturbation of individual SEC24 paralogs, TMED10 co-receptor analysis, biochemical co-translational binding assays

    PMID:39531033

    Open questions at the time
    • No high-resolution structure of the SURF4 lumenal pocket or its cargo complexes
    • How SURF4 cytoplasmic tail engages different SEC24 paralogs is structurally unresolved
    • Whether additional co-receptors beyond TMED10 exist for other cargoes is unknown
  13. 2024 High

    Identification of SAA1 as a hepatic SURF4 cargo linked SURF4-mediated secretion to liver fibrosis pathogenesis, as reduced SAA1 secretion from Surf4-deficient hepatocytes attenuated hepatic stellate cell activation.

    Evidence Hepatic Surf4 KO mice in CCl4 fibrosis model, Co-IP of Surf4–SAA1, conditioned medium with SAA1 rescue, LX-2 stellate cell activation assays

    PMID:39105051

    Open questions at the time
    • Whether SURF4 regulation of fibrosis operates through SAA1 alone or additional inflammatory cargoes is unclear
    • Therapeutic potential of targeting SURF4 in fibrosis not assessed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the atomic structure of SURF4 and its lumenal cargo-binding pocket, how a single receptor accommodates dozens of structurally diverse cargoes (motif-dependent versus motif-independent recognition), the mechanism by which SURF4 participates in both anterograde transport and ERAD retrotranslocation, and the physiological significance of SURF4's modulation of store-operated Ca²⁺ entry.
  • No high-resolution structure of SURF4
  • Unified model for cargo selectivity versus promiscuity lacking
  • ERAD role mechanistically unexplained relative to anterograde trafficking
  • STIM1 modulation not replicated in mammalian systems

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 10 GO:0060090 molecular adaptor activity 2
Localization
GO:0005783 endoplasmic reticulum 6 GO:0043226 organelle 2 GO:0005829 cytosol 1
Pathway
R-HSA-9609507 Protein localization 9 R-HSA-1430728 Metabolism 4 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-392499 Metabolism of proteins 1
Partners
APOBERGIC53PCSK9PSAPSAA1SEC12STIM1TMED10

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 SURF4 is an integral membrane protein with seven predicted transmembrane domains and a double lysine ER retrieval motif on its carboxyl terminus, localizing to the ER and tightly associating with microsomal membranes; proteolysis protection experiments confirmed at least two membrane-spanning domains consistent with the proposed topology. In vitro translation, salt/detergent extraction, proteolysis protection, immunofluorescence of myc-tagged chimeras Molecular membrane biology High 7540914
2008 SURF4 interacts with ERGIC-53 and p24 family proteins; combined silencing of SURF4 and ERGIC-53 (or silencing of the p24 member p25) causes fragmentation of the Golgi apparatus, reduced ERGIC cluster number and stability, partial redistribution of COPI (but not Golgi matrix proteins) to the cytosol, and partial resistance of cis-Golgi to brefeldin A, revealing a role for cargo receptors in maintaining ERGIC/Golgi architecture via COPI recruitment. Co-immunoprecipitation, siRNA knockdown, live imaging, immunofluorescence, brefeldin A treatment Molecular biology of the cell High 18287528
2018 SURF4 functions as an ER cargo receptor that physically interacts with PCSK9 in the early secretory pathway; SURF4 deletion causes ER accumulation and decreased extracellular secretion of PCSK9, and SURF4 cDNA rescues the secretion defect. Proximity-dependent biotinylation (BioID) combined with proteomics, genome-scale CRISPR screen, multiple independent sgRNAs, clonal knockout cell lines, co-immunoprecipitation, functional rescue with SURF4 cDNA eLife High 30251625
2018 SURF4 (Erv29p ortholog) acts as an ER cargo receptor that binds amino-terminal tripeptide motifs (ER-ESCAPE motifs) exposed after signal sequence cleavage of soluble cargo proteins; binding affinity for these tripeptides determines steady-state ER concentrations of cargoes and prevents aggregation. Changing a single amino acid in the tripeptide abolishes efficient ER exit. Surf4-null human cells lose preferential trafficking of cargoes with strong ER-ESCAPE motifs, and this is rescued by re-expression of SURF4 or yeast Erv29p. Systematic tripeptide variant screen, Surf4-null cell lines, functional rescue with SURF4 or Erv29p cDNA, ER localization assays PLoS biology High 30086131
2018 SFT-4 (C. elegans SURF4 ortholog) localizes predominantly to ER exit sites (ERES) and physically interacts with the yolk lipoprotein VIT-2 in vivo; SFT-4 loss strongly inhibits ER exit of yolk proteins and other soluble cargoes. Mammalian SURF4 physically interacts with apolipoprotein B (ApoB) and its loss causes ER accumulation of ApoB in HepG2 cells. Loss of SFT-4/SURF4 reduces the number of COPII-positive ERES. Co-immunoprecipitation (in vivo in C. elegans and in HepG2 cells), RNAi/siRNA knockdown, fluorescence microscopy of ERES markers The Journal of cell biology High 29643117
2020 SURF4 functions as an ER cargo receptor mediating efficient secretion of erythropoietin (EPO); SURF4 disruption causes ER accumulation and extracellular depletion of EPO, SURF4 and EPO physically interact, and SURF4 overexpression increases EPO secretion. Genome-scale CRISPR screen, multiple independent sgRNAs, co-immunoprecipitation, immunofluorescence (ER localization), functional rescue with SURF4 cDNA, endogenous EPO secretion in Hep3B cells under hypoxia Molecular and cellular biology High 32989016
2020 Murine Surf4 is essential for early embryonic development; homozygous Surf4-/- mice die between embryonic days 3.5 and 9.5, while heterozygous mice are grossly normal but show detectable intrahepatic ApoB accumulation. CRISPR/Cas9 germline knockout, embryonic staging, intrahepatic protein analysis PloS one High 31978056
2021 SURF4 mediates ER export of prosaposin, which in turn is required for efficient ER exit of progranulin; prosaposin physically interacts with SURF4, and Surf4 depletion impairs ER export of both progranulin and prosaposin, reducing their lysosomal delivery. Co-immunoprecipitation, siRNA knockdown, immunofluorescence (ER/lysosome localization), epistasis between prosaposin-progranulin interaction and SURF4 The Journal of cell biology High 34919127
2021 Hepatic Surf4 specifically mediates VLDL secretion (via ApoB100) but not PCSK9 secretion in vivo; liver-specific Surf4 knockout in mice significantly reduced plasma cholesterol, triglycerides, and ApoB levels without causing hepatic lipid accumulation. Surf4 co-immunoprecipitated and colocalized with ApoB100 in human hepatocytes. Knockdown in Ldlr-/- mice significantly reduced atherosclerosis. Liver-specific knockout mice, co-immunoprecipitation, immunofluorescence co-localization, siRNA knockdown in Ldlr-/- mice, plasma lipid measurements Journal of lipid research High 34118252
2012 SURF4 associates with STIM1 in the endoplasmic reticulum; deletion of Surf4 in DT40 B cells results in markedly increased store-operated Ca2+ entry (SOCE) and facilitated STIM1 clustering upon store depletion, indicating SURF4 is a negative modulator of STIM1-mediated SOCE. Affinity purification of STIM1-binding proteins, co-immunoprecipitation, Surf4-deficient DT40 cells, Ca2+ entry measurements, STIM1 clustering assay Biochemical and biophysical research communications Medium 22609200
2022 SURF4 induces formation of a highly elongated tubular ERGIC (t-ERGIC) that is ERGIC-53-negative but Rab1A/B-positive; the t-ERGIC selectively expedites ER-to-Golgi transport of SURF4-bound cargoes due to its large surface-to-volume ratio and high intracellular speed. SURF4 recognizes the N-terminus of soluble cargoes and co-clusters with them to expand the ER exit site. t-ERGIC-mediated fast transport is antagonized by KDEL-mediated ER retrieval. Super-resolution live-cell microscopy (TIRF/SIM), SURF4 knockdown/knockout, cargo trafficking kinetics, Rab1A/B and ERGIC-53 marker analysis Developmental cell High 35051356
2022 Surf4 regulates ER export of proinsulin via recruitment to ER exit sites (ERES); Surf4 expression is upregulated under high-glucose conditions. Surf4 forms oligomers, physically interacts with proinsulin and with Sec12 (essential for COPII vesicle formation), and its knockdown causes proinsulin ER retention and decreased mature insulin in secretory granules. siRNA knockdown in INS-1 cells, co-immunoprecipitation (Surf4–proinsulin and Surf4–Sec12), immunofluorescence (ERES localization), insulin secretion assay Communications biology High 35562580
2022 Hepatic inactivation of Surf4 in mice reduces plasma PCSK9 by ~60% with a corresponding ~50% increase in hepatic LDLR abundance, confirming SURF4 as a cargo receptor for PCSK9 in vivo. Additionally, Surf4-deficient mice show a severe defect in hepatic APOB-containing lipoprotein secretion, causing marked reduction in plasma cholesterol and triglycerides. Hepatic-specific Surf4 knockout mice (Surf4 Alb-Cre), acute CRISPR/Cas9 and liver-targeted siRNA depletion, PCSK9 and LDLR protein quantification, lipoprotein metabolism characterization eLife High 36193893
2022 SURF4 facilitates ER export of Sonic Hedgehog (Shh) via an ER export signal; proteoglycans in the Golgi promote dissociation of SURF4 from Shh, suggesting a SURF4-to-proteoglycan relay mechanism for cargo transfer from ER to Golgi. Co-immunoprecipitation, mutational analysis of ER export signal, localization studies Proceedings of the National Academy of Sciences of the United States of America Medium 35271396
2023 Surf4 collaborates with derlin-2 and derlin-1 in ERAD: derlin-2 acts upstream, then derlin-1, then Surf4 downstream, to mediate retrotranslocation of COX-2 from the ER lumen to the cytosol for degradation. Surf4 knockdown impedes COX-2 ubiquitylation and its interaction with caveolin-1 and p97 in the cytosol. CRISPR library screening, siRNA knockdown epistasis, co-immunoprecipitation (Surf4–COX-2, derlin–COX-2), ubiquitylation assays, N-glycosylation analysis Journal of cell science Medium 37676109
2023 SURF4 traffics a broad range of secretory cargoes in hepatic cells; mass spectrometry of conditioned media and cell lysates from SURF4-knockout HuH7 cells revealed that cargo recognition is governed by complex mechanisms rather than a single universal binding motif. CRISPR-targeted gene inactivation, quantitative mass spectrometry of secretome and proteome Journal of proteome research Medium 37844105
2023 Intestinal Surf4 is essential for chylomicron secretion; it co-localizes and co-immunoprecipitates with ApoB48 in Caco-2 cells, and intestinal-specific Surf4 knockout mice show lipid accumulation in enterocytes, impaired fat absorption and secretion, reduced serum lipids. Intestinal-specific conditional knockout mice, co-immunoprecipitation, transmission electron microscopy, radiolabeled oleic acid absorption assay Arteriosclerosis, thrombosis, and vascular biology High 36756879
2023 Intestinal SURF4 is required for transport of ApoA1, PRAP1, and ApoB48 and for assembly and secretion of chylomicrons and HDL; intestine-specific Surf4 knockout mice show ectopic lipid deposition and hypolipidemia. Intestine-specific Surf4 knockout mice, proteomics, cellular models Molecular metabolism High 38042368
2024 SURF4 recruits distinct SEC24 COPII coat paralogs depending on cargo: PCSK9 export requires both SURF4 and co-receptor TMED10 via SEC24A, whereas Cab45 and NUCB1 export requires SEC24C/D. ER export signals of Cab45 and NUCB1 bind co-translationally to a lumenal pocket of SURF4. Genetic perturbation of SEC24 paralogs, TMED10 co-receptor studies, biochemical co-translational binding assays, bioinformatics of ER-exit signal motifs The Journal of cell biology High 39531033
2024 Hepatic Surf4 deficiency reduces SAA1 secretion from hepatocytes; Surf4 co-immunoprecipitates and co-localizes with SAA1, and reduced SAA1 secretion leads to decreased hepatic stellate cell activation and attenuated liver fibrosis in a CCl4 model. Hepatic Surf4 knockout mice, CCl4 fibrosis model, co-immunoprecipitation, conditioned medium experiments with recombinant SAA1 rescue, SAA1 knockdown epistasis, LX-2 cell activation assays Research (Washington, D.C.) High 39105051
2025 YIPF5 directly interacts with SURF4 and negatively regulates SURF4-mediated ER export; YIPF5 knockout alters SURF4 localization, causing elongated Rab1-positive tubules from COPII-labeled ER exit sites, and kinetic analysis shows enhanced SURF4-mediated export in YIPF5-depleted cells. Co-immunoprecipitation, YIPF5 knockout cells, live-cell fluorescence imaging of ERGIC/COPII structures, kinetic trafficking assays bioRxivpreprint Medium bio_10.1101_2025.06.11.659036

Source papers

Stage 0 corpus · 35 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 The cargo receptors Surf4, endoplasmic reticulum-Golgi intermediate compartment (ERGIC)-53, and p25 are required to maintain the architecture of ERGIC and Golgi. Molecular biology of the cell 98 18287528
2018 The cargo receptor SURF4 promotes the efficient cellular secretion of PCSK9. eLife 79 30251625
2018 Surf4 (Erv29p) binds amino-terminal tripeptide motifs of soluble cargo proteins with different affinities, enabling prioritization of their exit from the endoplasmic reticulum. PLoS biology 57 30086131
2018 SFT-4/Surf4 control ER export of soluble cargo proteins and participate in ER exit site organization. The Journal of cell biology 51 29643117
2022 SURF4-induced tubular ERGIC selectively expedites ER-to-Golgi transport. Developmental cell 35 35051356
1995 The surf-4 gene encodes a novel 30 kDa integral membrane protein. Molecular membrane biology 34 7540914
2012 Surf4 modulates STIM1-dependent calcium entry. Biochemical and biophysical research communications 33 22609200
2022 A SURF4-to-proteoglycan relay mechanism that mediates the sorting and secretion of a tagged variant of sonic hedgehog. Proceedings of the National Academy of Sciences of the United States of America 31 35271396
2020 The Endoplasmic Reticulum Cargo Receptor SURF4 Facilitates Efficient Erythropoietin Secretion. Molecular and cellular biology 29 32989016
2022 Hepatic inactivation of murine Surf4 results in marked reduction in plasma cholesterol. eLife 26 36193893
2021 Atherosclerosis-associated hepatic secretion of VLDL but not PCSK9 is dependent on cargo receptor protein Surf4. Journal of lipid research 25 34118252
2022 Cargo receptor Surf4 regulates endoplasmic reticulum export of proinsulin in pancreatic β-cells. Communications biology 24 35562580
2020 Murine Surf4 is essential for early embryonic development. PloS one 24 31978056
2023 Surf4, cargo trafficking, lipid metabolism, and therapeutic implications. Journal of molecular cell biology 23 36574593
2021 Efficient progranulin exit from the ER requires its interaction with prosaposin, a Surf4 cargo. The Journal of cell biology 19 34919127
2023 Surf4 (Surfeit Locus Protein 4) Deficiency Reduces Intestinal Lipid Absorption and Secretion and Decreases Metabolism in Mice. Arteriosclerosis, thrombosis, and vascular biology 14 36756879
2020 SURF4 maintains stem-like properties via BIRC3 in ovarian cancer cells. Journal of gynecologic oncology 14 32026660
2022 The role of hepatic Surf4 in lipoprotein metabolism and the development of atherosclerosis in apoE-/- mice. Biochimica et biophysica acta. Molecular and cell biology of lipids 11 35803528
2021 Surf4 facilitates reprogramming by activating the cellular response to endoplasmic reticulum stress. Cell proliferation 10 34585448
2018 SURF4 has oncogenic potential in NIH3T3 cells. Biochemical and biophysical research communications 10 29777698
2023 Intestinal SURF4 is essential for apolipoprotein transport and lipoprotein secretion. Molecular metabolism 9 38042368
2024 Hepatic Surf4 Deficiency Impairs Serum Amyloid A1 Secretion and Attenuates Liver Fibrosis in Mice. Research (Washington, D.C.) 8 39105051
2024 ER export via SURF4 uses diverse mechanisms of both client and coat engagement. The Journal of cell biology 7 39531033
2021 Loss of Hepatic Surf4 Depletes Lipid Droplets in the Adrenal Cortex but Does Not Impair Adrenal Hormone Production. Frontiers in cardiovascular medicine 7 34859075
2023 Identification of LMAN1- and SURF4-Dependent Secretory Cargoes. Journal of proteome research 6 37844105
2012 Positive diversifying selection on the Plasmodium falciparum surf4.1 gene in Thailand. Tropical medicine and health 5 23264727
1996 Tissue-specific processing of the Surf-5 and Surf-4 mRNAs. Gene expression 5 9196076
2025 Distinct but Redundant Roles of ER Cargo Receptors p24 and Erv29 in Facilitating Proper Secretion of Cellulases in Trichoderma reesei. Molecular microbiology 2 39895577
2023 Surf4 collaborates with derlin-2 and derlin-1 to mediate cyclooxygenase-2 translocation to the cytosol for degradation. Journal of cell science 2 37676109
2023 Identification of LMAN1 and SURF4 dependent secretory cargoes. bioRxiv : the preprint server for biology 1 37066360
2026 SURF4 inhibits autophagy to enhance lung adenocarcinoma progression and stemness through Hedgehog pathway regulation. Tissue & cell 0 41637921
2025 [High expression of SURF4 promotes migration, invasion and proliferation of gastric cancer cells by inhibiting tight junction proteins]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 40916534
2025 Intestinal SURF4 in dyslipidaemia and female-specific metabolic disorders: insights from rats with polycystic ovary syndrome. Frontiers in nutrition 0 41041130
2024 Plasmodium falciparum surf4.1 in clinical isolates: From genetic variation and variant diversity to in silico design immunopeptides for vaccine development. PloS one 0 39775228
2023 Corrigendum: Loss of hepatic Surf4 depletes lipid droplets in the adrenal cortex but does not impair adrenal hormone production. Frontiers in cardiovascular medicine 0 37234368