Affinage

STARD7

StAR-related lipid transfer protein 7, mitochondrial · UniProt Q9NQZ5

Length
370 aa
Mass
43.1 kDa
Annotated
2026-06-10
32 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

STARD7 is a START-domain lipid transfer protein that controls mitochondrial phospholipid supply and intracellular lipid distribution, thereby governing respiratory function, cristae architecture, and redox homeostasis (PMID:20042613, PMID:27694445). Its START domain catalyzes phosphatidylcholine (PC) transfer between membranes in vitro, and this same site binds ceramide and a coenzyme Q (CoQ) variant, both of which compete with PC, establishing a single ligand pocket whose occupancy tunes transfer activity (PMID:20042613, PMID:29343537, PMID:36658222). The protein is expressed as two isoforms: StarD7-I carries an N-terminal mitochondrial-targeting sequence and a transmembrane anchor in the outer mitochondrial membrane, while StarD7-II is constitutively cytosolic (PMID:20042613, PMID:28821867). During mitochondrial import the inner-membrane rhomboid protease PARL cleaves STARD7, and an acidic sorting signal partitions the cleaved protein between the intermembrane space and the cytosol (PMID:29301859). Intramitochondrial STARD7 is necessary and sufficient to maintain inner-membrane PC, respiratory complex and supercomplex assembly, and cristae morphogenesis (PMID:29301859, PMID:27694445), whereas the cytosolic pool transports CoQ to the plasma membrane to limit lipid peroxidation and suppress ferroptosis (PMID:36658222). Loss of STARD7 impairs oxidative phosphorylation and disrupts epithelial barrier integrity through mitochondrial oxidant stress and mtDNA damage, is required for myogenic differentiation, and restrains mitophagy flux (PMID:28401922, PMID:32071354, PMID:37846201). Beyond mitochondria, the cytosolic isoform drives cell migration through an ERK1/2/connexin-43/integrin-β1 mechanism, and STARD7 supports cancer cell proliferation by linking mitochondrial lipid metabolism to metabolite-driven H3K27me3 deposition on cell-cycle gene promoters and to EGFR trafficking (PMID:36584213, PMID:40443279).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2004 Low

    Before any cellular function was known, it was unclear whether STARD7 interacts directly with lipid membranes; biophysical analysis established direct protein-lipid interaction at interfaces.

    Evidence Langmuir/Gibbs monolayer surface-pressure measurements with recombinant protein

    PMID:14715263

    Open questions at the time
    • Single biophysical method with no in-cell functional consequence demonstrated
    • Lipid preferences (PS, cholesterol, PG) at monolayers do not establish a physiological transfer substrate
    • No isoform or domain resolution
  2. 2009 High

    The molecular activity was defined by showing STARD7 is a PC-specific transfer protein, and that the StarD7-I isoform directs PC to mitochondria while StarD7-II is cytosolic.

    Evidence In vitro PC transfer assay with purified protein, fluorescent PC trafficking, protease K protection and fractionation in HEPA-1 cells

    PMID:20042613

    Open questions at the time
    • Did not resolve how the precursor is processed during import
    • Mechanistic link between PC transfer and downstream mitochondrial function not yet established
  3. 2011 Medium

    An alternative mechanism was tested: whether STARD7 acts by membrane fusion rather than monomeric lipid carriage, addressing how it moves lipid between bilayers.

    Evidence Fluorescence de-quenching, FRET lipid mixing, dynamic light scattering, multinuclear giant cell formation with recombinant protein

    PMID:22063720

    Open questions at the time
    • Fusogenic mechanism not extensively replicated and not reconciled with monomeric transfer model
    • Physiological relevance of fusion activity in cells not demonstrated
  4. 2016 High

    Causal linkage between STARD7 PC transfer and mitochondrial bioenergetics was established by genetic loss-of-function with rescue, and a parallel role in ER stress/redox homeostasis was reported.

    Evidence CRISPR/Cas9n KO and siRNA in HEPA-1 with respirometry, complex activity and rescue (idx 3); siRNA in HepG2 with ER-stress and ROS readouts (idx 12)

    PMID:27554972 PMID:27694445

    Open questions at the time
    • How reduced PC selectively destabilizes MTCO1/supercomplexes not mechanistically resolved
    • ER-stress and p53/catalase changes (idx 12) rest on single-method readouts per endpoint
  5. 2017 High

    The targeting determinants and physiological output were refined: a transmembrane anchor positions mature STARD7 on the OMM and is required for function, and epithelial loss links mitochondrial dysfunction to barrier integrity.

    Evidence Truncation mutants, N-terminal cleavage-site sequencing and rescue (idx 4); BEAS-2B knockdown and epithelial-specific KO mice with antioxidant rescue (idx 5)

    PMID:28401922 PMID:28821867

    Open questions at the time
    • Protease responsible for the TM-domain cleavage not identified in idx 4
    • Whether barrier defects are fully attributable to PC transfer versus secondary oxidant stress not separated
  6. 2018 High

    The import/sorting logic and the ligand-binding basis of regulation were resolved: PARL cleavage plus an acidic sorting signal partitions STARD7 between IMS and cytosol, and the START domain uses a shared PC/ceramide site where ceramide inhibits PC transfer.

    Evidence PARL KO cells, import assays, sorting-signal mutagenesis and rescue (idx 1); pacCer photoaffinity labeling, START-domain mutagenesis and ceramide-competition transfer assay (idx 2)

    PMID:29301859 PMID:29343537

    Open questions at the time
    • Whether ceramide regulation of PC transfer operates in cells, not only in vitro
    • Structural model of the shared binding pocket not determined
  7. 2020 Medium

    Tissue-context dependence and a developmental requirement were established: PARL is dispensable for STARD7 processing in myoblasts, and STARD7 is required for myogenic differentiation via mitochondrial PC/respiration and PGC-1α.

    Evidence siRNA, CRISPR KO and rescue in C2C12, immuno-EM, respirometry, differentiation-marker analysis

    PMID:32071354

    Open questions at the time
    • Alternative processing protease in C2C12 not identified
    • Single lab; cell-type specificity of PARL independence not generalized
  8. 2021 Medium

    A regulatory connection to mitochondrial dynamics was tested, showing isoform-specific STARD7-I overexpression drives Drp1-dependent fragmentation and alters fusion proteins.

    Evidence Isoform-specific stable overexpression and siRNA in HTR-8/SVneo, Drp1 mutant epistasis, fluorescent PC transport and live-cell imaging

    PMID:34416390

    Open questions at the time
    • Whether fission changes are a direct lipid effect or secondary to bioenergetic stress not resolved
    • Single cell type, overexpression-based
  9. 2022 Medium

    A mitochondria-independent function was defined: cytosolic StarD7.II drives cell migration through ERK1/2/Cx43/integrin-β1 signaling and MTOC/Golgi reorientation.

    Evidence siRNA with isoform-specific re-expression (StarD7.I vs II), migration assays, immunofluorescence and signaling Western blots in HTR-8/SVneo

    PMID:36584213

    Open questions at the time
    • How cytosolic STARD7 lipid handling connects mechanistically to ERK1/2 activation not established
    • Single lab, single cell type
  10. 2023 High

    The cytosolic pool was assigned a distinct cargo and physiological output—CoQ transport to the plasma membrane to suppress ferroptosis—while additional studies linked STARD7 to mitophagy control and to transcriptional regulation by TCF4.

    Evidence PARL/STARD7 KO-rescue, in vitro CoQ/PC competitive binding, ferroptosis and lipidomics assays (idx 6); mKeima mitophagy imaging in C2C12 (idx 11); CRISPR screen and TCF4 deSUMOylation in colon cancer (idx 13)

    PMID:36658222 PMID:37191369 PMID:37846201

    Open questions at the time
    • How a single START pocket coordinates PC, ceramide and CoQ binding in vivo not structurally resolved
    • Mitophagy and TCF4-transcription findings (Medium) are single-lab
  11. 2025 Medium

    STARD7 was linked to cancer cell proliferation through metabolic-epigenetic coupling and receptor trafficking, broadening its role beyond bioenergetics.

    Evidence STARD7 KO in breast cancer cells with metabolomics, H3K27me3 ChIP-seq, cell-cycle analysis and EGFR trafficking assays

    PMID:40443279

    Open questions at the time
    • Causal chain from carnitine/SAM accumulation to H3K27me3 not fully dissected
    • Single lab; relationship between EGFR trafficking defect and lipid transfer unclear
  12. 2026 Medium

    An in vivo muscle requirement and a substrate-specificity refinement were established: STARD7 preferentially transfers linoleic-acid-containing PC supporting cardiolipin remodeling and endurance capacity.

    Evidence Muscle-specific KO mice with targeted lipidomics, in vitro binding/transfer assay, EM and respirometry

    PMID:41989333

    Open questions at the time
    • Mechanism connecting PC species selectivity to cardiolipin remodeling enzymes not defined
    • Respiratory complexes intact despite cristae defects—uncoupling of phenotypes not explained

Open questions

Synthesis pass · forward-looking unresolved questions
  • A unified structural and regulatory model for how one START pocket selects among PC species, ceramide, and CoQ in different subcellular pools—and how isoform partitioning is controlled in a tissue-specific manner—remains open.
  • No high-resolution structure of the START domain with bound ligands
  • In vivo regulation of cytosol-versus-IMS partitioning beyond PARL not defined
  • No human Mendelian disease link established in the corpus

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008289 lipid binding 4 GO:0140104 molecular carrier activity 2
Localization
GO:0005739 mitochondrion 4 GO:0005829 cytosol 3
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-5357801 Programmed Cell Death 1 R-HSA-9612973 Autophagy 1
Partners
PARL

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 StarD7 specifically catalyzes the transfer of phosphatidylcholine (PC) between lipid vesicles in vitro, and overexpression of StarD7-I (the isoform containing a mitochondrial-targeting sequence) increases intracellular transport of fluorescent PC to mitochondria. StarD7-I localizes to mitochondria (associated with the outer mitochondrial membrane by protease K protection assay) while StarD7-II is constitutively cytoplasmic. In vitro PC transfer assay with purified recombinant protein, fluorescent PC trafficking assay in HEPA-1 cells, protease K protection assay, overexpression and subcellular fractionation The Journal of biological chemistry High 20042613
2018 The mitochondrial inner membrane rhomboid protease PARL cleaves STARD7 during mitochondrial import, partitioning it between the cytosol and the mitochondrial intermembrane space (IMS). Negatively charged amino acids in STARD7 serve as a sorting signal for cytosolic release after PARL cleavage, while TIM23-mediated membrane insertion promotes mitochondrial IMS retention. Mitochondrial STARD7 is necessary and sufficient for PC accumulation in the inner membrane and for maintenance of respiration and cristae morphogenesis. PARL knockout cells, co-immunoprecipitation, subcellular fractionation, mitochondrial import assays, site-directed mutagenesis of sorting signal, rescue experiments with STARD7 variants The EMBO journal High 29301859
2018 StarD7's START domain harbors a shared binding site for both phosphatidylcholine (PC) and ceramide, as demonstrated by photoaffinity labeling with a clickable ceramide analog (pacCer) and site-directed mutagenesis. StarD7 lacks robust ceramide transfer activity in vitro, but ceramide specifically inhibits StarD7's ability to shuttle PC between model membranes. Photoaffinity labeling with bifunctional ceramide analog (pacCer), site-directed mutagenesis of START domain, in vitro PC transfer assay with ceramide competition Journal of lipid research High 29343537
2016 StarD7 knockout (via CRISPR/Cas9n) and knockdown in HEPA-1 cells reduces mitochondrial PC content, impairs oxygen consumption rate and mitochondrial complex activities, lowers ATP levels, reduces MTCO1 (complex IV subunit) protein without affecting its mRNA, disrupts mitochondrial supercomplex formation, and causes disorganized cristae structure. Re-expression of StarD7-I rescues MTCO1 levels and mitochondrial abnormalities. siRNA knockdown, CRISPR/Cas9n knockout, real-time respirometry (Seahorse), mitochondrial complex activity assay, phospholipid analysis, rescue by overexpression The Journal of biological chemistry High 27694445
2017 StarD7-I contains a transmembrane (TM) domain C-terminal to its mitochondrial-targeting signal that anchors the mature protein to the outer leaflet of the outer mitochondrial membrane (OMM). The precursor is cleaved between Met76–Ala77 and Ala77–Ala78 in the TM domain. A truncated StarD7 lacking the TM domain localizes to the mitochondrial matrix and cannot rescue mitochondrial complex formation or PC content defects in StarD7-KO cells, unlike full-length StarD7-I. Truncation mutants, immunofluorescence and subcellular fractionation in HEPA-1 and HepG2 cells, N-terminal sequencing of cleavage site, rescue of StarD7-KO cells with wild-type vs. truncated forms Scientific reports High 28821867
2017 Stard7 deficiency in lung bronchiolar epithelial cells (BEAS-2B knockdown and Stard7epi∆/∆ mice) causes altered mitochondrial size and membrane organization, decreased aerobic respiration, increased oxidant stress, and mitochondrial DNA damage, which in turn disrupts epithelial barrier integrity and function. These defects are rescued by targeting Stard7 to mitochondria or treating cells with a mitochondrial-targeted antioxidant. siRNA knockdown in BEAS-2B, conditional epithelial-specific KO mice, respirometry, ROS assays, mtDNA damage assay, barrier permeability assay, rescue with mitochondria-targeted Stard7 and MitoTEMPO Scientific reports High 28401922
2023 STARD7 is a critical factor for intracellular coenzyme Q (CoQ) transport from mitochondria to the plasma membrane and suppressor of ferroptosis. PARL-mediated cleavage of STARD7 partitions it between the mitochondrial IMS (where it supports CoQ synthesis and cristae morphogenesis) and the cytosol (where it transports CoQ to the plasma membrane to limit lipid peroxidation). A CoQ variant competes with PC for binding to purified STARD7 in vitro. Overexpression of cytosolic STARD7 increases ferroptosis resistance but reduces mitochondrial CoQ and respiratory growth. PARL and STARD7 KO/rescue cells, in vitro competitive binding assay with purified STARD7 and CoQ/PC, ferroptosis assays (lipid peroxidation, cell viability), lipidomics, respirometry, STARD7 isoform overexpression Nature cell biology High 36658222
2011 Recombinant StarD7 functions as a fusogenic protein: it accelerates lipid dilution between donor and acceptor liposomes via bilayer fusion (not monomeric lipid transport), as demonstrated by fluorescence de-quenching, FRET between labeled lipids, dynamic light scattering, and induction of multinuclear giant cell formation. Fusogenic activity depends on electrostatic interactions with the lipid-water interface and is favored by phosphatidylethanolamine. Fluorescence de-quenching assay, FRET-based lipid mixing assay, dynamic light scattering, multinuclear giant cell formation with recombinant protein, pH and salt modulation experiments Biochimica et biophysica acta Medium 22063720
2021 StarD7.I overexpression in HTR-8/SVneo cells increases PC transport to mitochondria, alters mitochondrial morphology (increased fragmentation), and modulates fission/fusion proteins: Drp1 and Mfn2 are increased while Mfn1 is decreased. Mitochondrial fragmentation in StarD7.I-overexpressing cells occurs in a fission-dependent manner via Drp1 (established by dominant-negative Drp1-K38A, and phosphomimetic/non-phosphorylatable Drp1 mutants). StarD7 silencing decreases Mfn1 and Mfn2 without changing Drp1 and induces donut-shaped mitochondria. Stable overexpression of StarD7.I and StarD7.II isoforms, siRNA knockdown, transfection with Drp1 mutants (K38A, S637D, S637A), fluorescent PC analog transport assay, live-cell imaging, ROS measurement, mitochondrial membrane potential assay Biochimica et biophysica acta. Molecular and cell biology of lipids Medium 34416390
2022 StarD7 silencing in HTR-8/SVneo cells decreases connexin 43 (Cx43), integrin β1, and p-ERK1/2 expression, causes Golgi disruption and reduced ability to reorient the microtubule-organizing center, and impairs cell migration. Re-expression specifically of the cytosolic StarD7.II isoform (not the mitochondria-targeted StarD7.I) restores cell migration, ERK1/2, Cx43, and integrin β1 expression, defining a mitochondria-independent, ERK1/2/Cx43-dependent mechanism for StarD7 in cell motility. siRNA knockdown, stable isoform-specific re-expression (StarD7.I vs StarD7.II), wound healing and transwell migration assays, immunofluorescence for Golgi and MTOC, Western blot for signaling proteins PloS one Medium 36584213
2020 In C2C12 myoblasts, PARL is not involved in StarD7 processing or maturation (unlike in HEK293 cells). StarD7 localizes to the cytosol, inner mitochondrial space, and outer leaflet of the OMM. siRNA knockdown of StarD7 impairs myogenic differentiation and reduces expression of myomaker, myomerger, and PGC-1α; these defects (including reduced mitochondrial PC and oxygen consumption) are fully rescued by re-expression of StarD7 in knockout C2C12 cells. siRNA knockdown, CRISPR KO, rescue by re-expression, immunofluorescence, immuno-electron microscopy, oxygen consumption assay, differentiation markers by Western blot/qPCR Scientific reports Medium 32071354
2023 StarD7 deficiency in C2C12 myoblasts increases mitophagy flux: knockdown cells accumulate LC3B-II and BNIP3 in mitochondria-enriched fractions, accumulate autophagolysosomal vesicles, and show enhanced mitochondria delivery to lysosomes (by live-cell imaging with mitochondria-targeted mKeima). StarD7 reconstitution restores LC3B-II levels in mitochondrial fractions. siRNA knockdown, live-cell imaging with mitochondria-targeted mKeima, mitochondrial fractionation, LC3B-II and BNIP3 Western blot, lysosomal vesicle quantification, StarD7 rescue The FEBS journal Medium 37846201
2016 StarD7 knockdown in HepG2 cells induces ER stress (increased IRE1α, calnexin, GRP78/BiP, PERK, p-eIF2α), alters mitochondria and ER morphology, increases ROS generation, and reduces cell viability after H2O2 exposure. Knockdown also causes p53 protein degradation and increases heme oxygenase-1 and catalase expression and catalase enzymatic activity. siRNA knockdown in HepG2 cells, Western blot for ER stress markers, ROS assay, cell viability assay, electron microscopy of organelle morphology, catalase activity assay Free radical biology & medicine Medium 27554972
2023 SUMO1 degrader HB007 reduces StarD7 mRNA and protein in colon cancer cells through deSUMOylation and degradation of the transcription factor TCF4, which transcriptionally activates StarD7. StarD7 knockout identified as critical for HB007 anticancer activity by genome-wide CRISPR screen. Genome-wide CRISPR-Cas9 KO screen, SUMO1 degrader treatment, TCF4 deSUMOylation assay, mRNA and protein quantification in 3D organoids and PDX models Molecular carcinogenesis Medium 37191369
2004 Recombinant StarD7 protein forms stable Gibbs and Langmuir monolayers at the air-buffer interface and penetrates phospholipid monolayers, showing preference for phosphatidylserine, cholesterol, and phosphatidylglycerol, demonstrating direct protein-lipid interaction at membrane interfaces. Langmuir monolayer technique, surface pressure measurements, Gibbs film analysis with recombinant StarD7 Biochemical and biophysical research communications Low 14715263
2025 Loss of STARD7 in breast cancer cells leads to accumulation of carnitine derivatives and S-Adenosyl-L-methionine (SAM), which increases H3K27 trimethylation on promoters of cell cycle genes, causing cell cycle arrest. STARD7 deficiency also impairs EGFR trafficking to lysosomes, disrupting EGFR signaling in triple-negative breast cancer cells. STARD7 KO in breast cancer cell lines, metabolomics, ChIP-seq for H3K27me3, cell cycle analysis, EGFR trafficking assay, ERα-dependent proliferation assay Advanced science Medium 40443279
2026 Muscle-specific STARD7 knockout mice show reduced endurance exercise capacity and decreased mitochondrial PC, cardiolipin, and coenzyme Q in soleus muscle, with disorganized cristae but intact respiratory chain complexes. An in vitro binding assay indicates STARD7 preferentially transfers linoleic acid-containing PC species required for cardiolipin remodeling. Muscle-specific knockout mice, targeted lipidomics, in vitro lipid binding/transfer assay, electron microscopy, respirometry, RNA-seq, fiber-type analysis FASEB journal Medium 41989333

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2023 Mitochondria regulate intracellular coenzyme Q transport and ferroptotic resistance via STARD7. Nature cell biology 131 36658222
2019 Intronic ATTTC repeat expansions in STARD7 in familial adult myoclonic epilepsy linked to chromosome 2. Nature communications 110 31664034
2009 StarD7 mediates the intracellular trafficking of phosphatidylcholine to mitochondria. The Journal of biological chemistry 90 20042613
2018 PARL partitions the lipid transfer protein STARD7 between the cytosol and mitochondria. The EMBO journal 83 29301859
2018 A search for ceramide binding proteins using bifunctional lipid analogs yields CERT-related protein StarD7. Journal of lipid research 48 29343537
2017 The Phosphatidylcholine Transfer Protein Stard7 is Required for Mitochondrial and Epithelial Cell Homeostasis. Scientific reports 45 28401922
2016 StarD7 Protein Deficiency Adversely Affects the Phosphatidylcholine Composition, Respiratory Activity, and Cristae Structure of Mitochondria. The Journal of biological chemistry 42 27694445
2013 The Lipid Transfer Protein StarD7: Structure, Function, and Regulation. International journal of molecular sciences 31 23507753
2004 GTT1/StarD7, a novel phosphatidylcholine transfer protein-like highly expressed in gestational trophoblastic tumour: cloning and characterization. Placenta 31 15013637
2003 Glucose uptake in Trichoderma harzianum: role of gtt1. Eukaryotic cell 30 12912890
2008 Expression and localization of StarD7 in trophoblast cells. Placenta 27 18378304
2017 Identification of the N-terminal transmembrane domain of StarD7 and its importance for mitochondrial outer membrane localization and phosphatidylcholine transfer. Scientific reports 26 28821867
2016 Suppression of StarD7 promotes endoplasmic reticulum stress and induces ROS production. Free radical biology & medicine 26 27554972
2015 Haploinsufficiency for Stard7 is associated with enhanced allergic responses in lung and skin. Journal of immunology (Baltimore, Md. : 1950) 23 25980009
2012 StarD7 knockdown modulates ABCG2 expression, cell migration, proliferation, and differentiation of human choriocarcinoma JEG-3 cells. PloS one 21 22952907
2004 Surface activity and interaction of StarD7 with phospholipid monolayers. Biochemical and biophysical research communications 18 14715263
2021 Role of the lipid transport protein StarD7 in mitochondrial dynamics. Biochimica et biophysica acta. Molecular and cell biology of lipids 16 34416390
2020 The phosphatidylcholine transfer protein StarD7 is important for myogenic differentiation in mouse myoblast C2C12 cells and human primary skeletal myoblasts. Scientific reports 16 32071354
2023 SUMO1 degrader induces ER stress and ROS accumulation through deSUMOylation of TCF4 and inhibition of its transcription of StarD7 in colon cancer. Molecular carcinogenesis 13 37191369
2024 STARD7 maintains intestinal epithelial mitochondria architecture, barrier integrity, and protection from colitis. JCI insight 11 39576011
2024 LncRNA STARD7-AS1 suppresses cervical cancer cell proliferation while promoting autophagy by regulating miR-31-5p/TXNIP axis to inactivate the mTOR signaling. Journal of gynecologic oncology 10 38670562
2011 StarD7 behaves as a fusogenic protein in model and cell membrane bilayers. Biochimica et biophysica acta 6 22063720
2023 StarD7 deficiency switches on glycolysis and promotes mitophagy flux in C2C12 myoblasts. The FEBS journal 5 37846201
2025 Loss of STARD7 Triggers Metabolic Reprogramming and Cell Cycle Arrest in Breast Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 4 40443279
2022 StarD7 deficiency hinders cell motility through p-ERK1/2/Cx43 reduction. PloS one 2 36584213
2018 Hexosamine pathway regulates StarD7 expression in JEG-3 cells. Molecular biology reports 2 30315445
2012 [Effect of StarD7 and Wnt/β-catenin signal pathway on the testosterone secretion stimulated by Annexin 5 in rat Leydig cells]. Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences 2 22898837
2026 The lipid transfer protein STARD7 controls intestinal tumor development in a context-dependent manner. EMBO molecular medicine 0 41912870
2026 Loss of STARD7 Impairs Mitochondrial Phospholipid Homeostasis and Contributes to Mitochondrial Myopathy. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 41989333
2026 The Wnt/StarD7 axis protects retinal ganglion cells from glutamate excitotoxicity by inhibiting ferroptosis. Biology direct 0 42157244
2025 CircEGLN1 alleviates calcium oxalate-induced renal injury via miR-212-5p/STARD7 axis, offering a potential strategy for kidney stone prevention. International journal of biological macromolecules 0 40685053
2025 A novel function of STARD7: its tumor-promoting role involves the activation of NF-κB signaling pathway in ovarian cancer. Human cell 0 41398485

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