Affinage

STOML2

Stomatin-like protein 2, mitochondrial · UniProt Q9UJZ1

Length
356 aa
Mass
38.5 kDa
Annotated
2026-04-28
44 papers in source corpus 16 papers cited in narrative 16 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

STOML2 is a mitochondrial inner membrane scaffold protein that integrates mitochondrial dynamics, quality control, calcium homeostasis, and respiratory chain maintenance. It physically interacts with prohibitins (PHB1/PHB2) to stabilize respiratory chain complex I and IV subunits, maintains long-form OPA1 (L-OPA1) levels required for stress-induced mitochondrial hyperfusion (SIMH) together with MFN1, and negatively regulates the mitochondrial Na⁺/Ca²⁺ exchanger (NCLX) to control mitochondrial calcium retention (PMID:18339324, PMID:19360003, PMID:19944461, PMID:41995387). STOML2 modulates PINK1-Parkin-dependent mitophagy through direct interactions with both Parkin (via the RING0 domain) and PINK1, and by stabilizing the rhomboid protease PARL, which controls PINK1 turnover; HIF-1α transcriptionally upregulates STOML2 under hypoxia to activate this mitophagy axis via PGAM5 cleavage (PMID:28379402, PMID:38229174, PMID:33446239, PMID:36906621, PMID:41723145). Through its interaction with PHB, STOML2 also activates the RAF1-MEK-ERK signaling cascade, a function implicated in both colorectal cancer proliferation and maintenance of pluripotency in human stem cells (PMID:34781982, PMID:41709508).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2000 Medium

    Establishing STOML2 as a novel stomatin-family member resolved its molecular identity and distinguished it from stomatin by its lack of a transmembrane domain and its peripheral membrane association via the erythrocyte cytoskeleton.

    Evidence cDNA cloning, subcellular fractionation (Triton X-100/NaOH extraction), and COS cell expression

    PMID:10713127

    Open questions at the time
    • Mitochondrial localization not yet recognized
    • Mechanism of membrane association unclear without a hydrophobic anchor
    • Function beyond structural scaffold uncharacterized
  2. 2008 High

    Demonstrating that STOML2 resides at the mitochondrial inner membrane and stabilizes prohibitins and respiratory chain complex subunits established its primary organellar context and first mechanistic function as a protein-stability scaffold.

    Evidence Proteomic identification, co-immunoprecipitation of STOML2-PHB, siRNA knockdown showing increased proteolysis of PHB and complexes I/IV subunits in HeLa cells

    PMID:18339324

    Open questions at the time
    • Whether STOML2 directly inhibits a protease or acts via prohibitin ring assembly is unknown
    • No structural data on the STOML2-PHB interface
  3. 2009 High

    Identifying STOML2 as essential for stress-induced mitochondrial hyperfusion (SIMH) and for maintaining L-OPA1 levels revealed its role in adaptive mitochondrial dynamics, placing it in a genetic pathway with MFN1 and OPA1 but independent of prohibitins.

    Evidence siRNA epistasis analysis with OPA1/MFN1/MFN2/BAX/BAK/PHB knockdowns, live-cell imaging of mitochondrial morphology, ATP measurement under UV/actinomycin D stress

    PMID:19360003

    Open questions at the time
    • How STOML2 prevents L-OPA1 processing is not determined
    • Whether STOML2 directly contacts OPA1 or acts through an intermediate protease is unresolved
  4. 2009 High

    Showing that STOML2 negatively regulates the mitochondrial Na⁺/Ca²⁺ exchanger (mNCX) established a distinct ion-homeostasis function, with STOML2 depletion accelerating Ca²⁺ extrusion and STOML2 overexpression prolonging mitochondrial Ca²⁺ retention.

    Evidence Gain- and loss-of-function Ca²⁺ imaging in permeabilized cells, pharmacological dissection with CGP-37157 and Na⁺ removal

    PMID:19944461

    Open questions at the time
    • Whether STOML2 directly binds the exchanger was not shown until later work
    • The stoichiometry and membrane topology of the STOML2-mNCX complex are unknown
  5. 2013 Medium

    Conservation of STOML2 function in C. elegans, where the ortholog STL-1 is induced by the stress-responsive factor SKN-1/Nrf and promotes mitochondrial fusion during reoxygenation, extended the stress-adaptive role across species and linked STOML2 to oxidative stress transcriptional programs.

    Evidence Genetic epistasis in C. elegans (egl-9, hif-1, skn-1, stl-1 mutants), GFP reporter assays, live mitochondrial imaging

    PMID:24385935

    Open questions at the time
    • Ortholog inference; direct mammalian Nrf2-STOML2 regulation not demonstrated
    • Molecular mechanism of fusion promotion in worms not defined
  6. 2017 High

    Demonstrating that STOML2 physically interacts with Parkin at mitochondria and that STOML2 overexpression rescues Parkin-deficiency phenotypes in neurons and Drosophila established STOML2 as a functional partner in the Parkin-dependent mitochondrial quality-control pathway.

    Evidence Endogenous co-immunoprecipitation and proximity ligation assay, genetic rescue in iPSC-derived neurons and Drosophila, complex I activity measurement

    PMID:28379402

    Open questions at the time
    • The Parkin binding domain on STOML2 was not mapped
    • Whether STOML2 modulates Parkin's E3 ubiquitin ligase activity is unknown
  7. 2021 High

    Two parallel studies revealed that STOML2 interacts with PINK1 to amplify PINK1-Parkin mitophagy under HIF-1α-driven transcriptional induction, and that STOML2 activates MAPK/ERK signaling through PHB in colorectal cancer, broadening its role from mitochondrial scaffold to signaling modulator.

    Evidence STOML2-PINK1 co-immunoprecipitation, ChIP and luciferase reporter for HIF-1α regulation; yeast two-hybrid, co-immunoprecipitation and phospho-ERK Western blots for STOML2-PHB-MAPK axis; orthotopic tumor model

    PMID:33446239 PMID:34781982

    Open questions at the time
    • Whether PHB-ERK signaling depends on STOML2's mitochondrial localization or a distinct pool is unclear
    • The structural basis of STOML2-PINK1 interaction is not defined
  8. 2023 Medium

    Identifying STOML2 as a stabilizer of the rhomboid protease PARL, which degrades PINK1, provided a mechanistic link between STOML2 and PINK1 accumulation: STOML2 restrains PINK1-dependent mitophagy by preserving PARL activity under basal conditions.

    Evidence Co-immunoprecipitation of STOML2-PARL, PINK1 protein level changes upon STOML2 manipulation, xenograft chemosensitivity model in pancreatic cancer

    PMID:36906621

    Open questions at the time
    • Apparent contradiction with the 2021 finding that STOML2 amplifies PINK1-Parkin mitophagy; context-dependent regulation not reconciled
    • PARL enzymatic activity not measured directly
    • Single lab, awaits independent replication
  9. 2024 High

    Mapping the Parkin-STOML2 interface to the Parkin RING0 domain, and showing that PD-associated PRKN mutations at this interface disrupt binding and that RING0 delivery rescues mitochondrial function, provided the first structural-level insight into the interaction and a potential therapeutic strategy.

    Evidence Domain truncation mapping, proximity ligation assay quantification, computational modeling from crystal structure, high-resolution respirometry in iPSC-derived neurons

    PMID:38229174

    Open questions at the time
    • No co-crystal structure of STOML2-Parkin
    • Whether the RING0 mini-peptide acts solely through STOML2 or engages other partners is untested
  10. 2024 Medium

    Discovery that STOML2 binds TRADD and activates NF-κB signaling to upregulate CCND1, VEGF, and PD-L1 expanded STOML2's signaling repertoire beyond MAPK into inflammatory and immune-evasion pathways in colorectal cancer.

    Evidence Co-immunoprecipitation of STOML2-TRADD, siRNA/overexpression, Western blot, in vivo tumor models

    PMID:38214751

    Open questions at the time
    • Whether STOML2-TRADD interaction occurs at mitochondria or another compartment is not defined
    • Awaits independent replication
    • Mechanism by which a mitochondrial scaffold engages cytoplasmic TRADD unclear
  11. 2025 Medium

    Demonstrating that HIF-1α-induced STOML2 translocates to the outer mitochondrial membrane under hypoxia and promotes PGAM5 cleavage to initiate PINK1-dependent mitophagy refined the mechanistic pathway linking hypoxia sensing to mitophagy execution.

    Evidence Triple knockdown of HIF-1α/STOML2/PGAM5, immunofluorescence for OMM localization, mitophagy and neuronal injury assays, in vivo mouse model

    PMID:41723145

    Open questions at the time
    • Mechanism of STOML2 translocation from IMM to OMM unknown
    • PGAM5 cleavage protease not identified
    • Single lab study
  12. 2026 Medium

    Confirming a direct STOML2-NCLX interaction and linking STOML2 loss to impaired oxidative phosphorylation, elevated ROS, chondrocyte senescence, and ferroptosis extended the calcium-homeostasis function to degenerative disease contexts.

    Evidence Co-immunoprecipitation of STOML2-NCLX, mitochondrial Ca²⁺ and OCR measurement, ROS assay, rat osteoarthritis intra-articular delivery model

    PMID:41995387

    Open questions at the time
    • STOML2-NCLX binding interface not mapped
    • Whether STOML2 regulates NCLX channel gating or membrane stability is unresolved
    • Single lab
  13. 2026 Medium

    Showing that STOML2-PHB sustains ERK signaling and pluripotency factor expression in human pluripotent stem cells generalized the STOML2-PHB-ERK axis beyond cancer to normal stem cell biology.

    Evidence shRNA knockdown, RNA-seq, phospho-ERK Western blot, flow cytometry for pluripotency markers in hPSCs

    PMID:41709508

    Open questions at the time
    • Whether STOML2 is required for in vivo embryonic development is untested
    • PHB ring complex stoichiometry with STOML2 in stem cells unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: (1) the structural basis of STOML2 interactions with PHB, PINK1, PARL, and NCLX; (2) how STOML2 reconciles apparently opposing roles in promoting versus restraining PINK1-dependent mitophagy in different contexts; (3) the mechanism by which STOML2 translocates from the inner to outer mitochondrial membrane under hypoxia; and (4) whether STOML2 plays a non-redundant role in neurodegeneration in vivo.
  • No co-crystal or cryo-EM structure for any STOML2 complex
  • Context-dependent mitophagy regulation (PARL-mediated restraint vs. PINK1 amplification) not mechanistically reconciled
  • In vivo mammalian knockout phenotype not reported

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 2
Localization
GO:0005739 mitochondrion 9
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-9612973 Autophagy 4 R-HSA-162582 Signal Transduction 3 R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-5357801 Programmed Cell Death 2
Partners
NCLXOPA1PARLPHBPHB2PINK1PRKNTRADD
Complex memberships
PHB1/PHB2 prohibitin complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 SLP-2 (STOML2) was cloned and characterized as a novel stomatin homologue present in erythrocytes and other tissues. It partitions into both Triton X-100-soluble and -insoluble pools, is fully extractable by NaOH (unlike stomatin, indicating no direct membrane bilayer insertion), and interacts with the peripheral erythrocyte cytoskeleton. It lacks the N-terminal hydrophobic domain found in other stomatin family members. cDNA cloning, Northern/Western blot, subcellular fractionation (Triton X-100, NaOH extraction), SDS-PAGE, expression in COS cells The Journal of biological chemistry Medium 10713127
2008 SLP-2 is strongly associated with the mitochondrial inner membrane and physically interacts with prohibitins (PHB1/PHB2). Depletion of SLP-2 in HeLa cells leads to increased proteolysis of prohibitins and subunits of respiratory chain complexes I and IV, indicating SLP-2 regulates the stability of these mitochondrial proteins. Proteomic approaches, co-immunoprecipitation, siRNA knockdown, subcellular fractionation, Western blot Biochimica et biophysica acta High 18339324
2009 SLP-2 is required for stress-induced mitochondrial hyperfusion (SIMH). In the absence of SLP-2, long-form OPA1 (L-OPA1) is lost and SIMH is prevented. SIMH requires L-OPA1, MFN1, and SLP-2 but is independent of MFN2, BAX/BAK, and prohibitins. SIMH is accompanied by increased mitochondrial ATP production and represents a pro-survival adaptive response. siRNA knockdown, live-cell imaging of mitochondrial morphology, epistasis analysis (double knockdown/knockout), ATP measurement, UV/actinomycin D stress models The EMBO journal High 19360003
2009 SLP-2 modulates mitochondrial sodium-calcium exchange. SLP-2 depletion increases rates of Ca2+ extrusion from mitochondria via the mitochondrial Na+/Ca2+ exchanger (mNCX); this effect is abolished by Na+ removal or CGP-37157 (mNCX inhibitor). SLP-2 overexpression prolongs mitochondrial Ca2+ retention, and SLP-2 depletion increases cytosolic Ca2+ elevations, demonstrating SLP-2 negatively regulates mNCX activity. siRNA knockdown, SLP-2 overexpression, mitochondrial and cytosolic Ca2+ imaging, pharmacological inhibition (CGP-37157, Na+ removal), permeabilized cell assays Cell calcium High 19944461
2009 SLP-2 localizes to mitochondria, maintains mitochondrial membrane potential (MMP) and ATP production, and its knockdown inhibits cell motility and proliferation and enhances chemosensitivity in tumor cells. siRNA knockdown, immunofluorescence (mitochondrial localization), MMP assay, ATP measurement, cell motility assays, cell proliferation assays Cancer biology & therapy Medium 19597348
2013 In C. elegans, the STOML2 ortholog STL-1 (Stomatin-like 1) is transcriptionally induced by SKN-1/Nrf in response to anoxia and facilitates mitochondrial fusion dynamics during reoxygenation. This places STOML2 downstream of the oxidative stress response factor SKN-1 in controlling mitochondrial fission/fusion balance. Genetic epistasis in C. elegans, live imaging of mitochondrial morphology, GFP reporter assays, mutant analysis (egl-9, hif-1, skn-1, stl-1) PLoS genetics Medium 24385935
2017 SLP-2 physically interacts with Parkin at mitochondria. Co-immunoprecipitation and proximity ligation assays demonstrated endogenous interaction. SLP-2 and Parkin genetically interact: SLP-2 overexpression rescues Parkin-deficiency phenotypes (reduced complex I activity, abnormal mitochondrial morphology, loss of dopaminergic neurons, reduced ATP, motor dysfunction) in iPSC-derived neurons and Drosophila. SLP-2 is placed epistatic to Parkin in maintaining mitochondrial respiratory chain function. Co-immunoprecipitation, proximity ligation assay (endogenous proteins), siRNA knockdown, iPSC-derived neuron models, Drosophila genetic rescue experiments, respiratory chain complex I activity assay, mitochondrial network imaging Human molecular genetics High 28379402
2021 STOML2 interacts with and stabilizes PINK1 under cellular stress conditions, amplifying PINK1-Parkin-mediated mitophagy. HIF-1α transcriptionally upregulates STOML2 expression. The STOML2-PINK1 interaction was demonstrated by co-immunoprecipitation. Co-immunoprecipitation, laser confocal microscopy, flow cytometry, transmission electron microscopy, Western blot, ChIP assay, luciferase reporter assay Journal of hematology & oncology High 33446239
2021 STOML2 interacts with prohibitin (PHB) and activates the MAPK signaling pathway (RAF1, MEK1/2, ERK1/2 phosphorylation) to promote colorectal cancer proliferation. The STOML2-PHB interaction was confirmed by co-immunoprecipitation and immunofluorescence co-localization. Knockdown of STOML2 downregulates MAPK pathway phosphorylation. Yeast two-hybrid screening, co-immunoprecipitation, immunofluorescence, Western blot (phospho-RAF1/MEK/ERK), siRNA knockdown, organoid culture, orthotopic tumor model Journal of experimental & clinical cancer research : CR Medium 34781982
2023 STOML2 stabilizes PARL (presenilin-associated rhomboid-like protease) at the mitochondrial inner membrane, preventing PARL-mediated PINK1 degradation and thereby restricting PINK1-dependent mitophagy. In pancreatic cancer, this STOML2-PARL-PINK1 axis controls mitochondrial mass and chemosensitivity. Tissue microarray, siRNA/overexpression, Western blot, co-immunoprecipitation (STOML2-PARL interaction), flow cytometry, mitochondrial mass measurement, xenograft model Cell death & disease Medium 36906621
2024 STOML2 physically binds TRADD protein and activates NF-κB signaling, resulting in upregulation of CCND1, VEGF, and PD-L1 in colorectal cancer, thereby promoting proliferation, angiogenesis, and immune escape. Co-immunoprecipitation (STOML2-TRADD binding), siRNA/overexpression, Western blot, in vitro and in vivo tumor models Cellular and molecular life sciences : CMLS Medium 38214751
2024 The Parkin-SLP-2 interaction is mediated primarily through the Parkin RING0 domain. PD-associated PRKN missense mutations that overlap with SLP-2 binding sites reduce the Parkin-SLP-2 interaction. Delivery of the isolated Parkin RING0 domain or a derived mini-peptide rescues mitochondrial dysfunction in Parkin-deficient neuroblastoma cells and iPSC-derived neurons. Proximity ligation assay (quantitative), domain mapping (truncation constructs), computational structural modeling (crystal structure-based), high-resolution respirometry, immunofluorescence, live imaging, iPSC-derived neurons Journal of translational medicine High 38229174
2025 Under hypoxia, HIF-1α transcriptionally induces STOML2 expression. STOML2 then translocates to the outer mitochondrial membrane and participates in PGAM5 cleavage, initiating PINK1-dependent mitophagy as a neuroprotective response. Knockdown of HIF-1α, STOML2, or PGAM5 inhibits this mitophagy and worsens neuronal injury. siRNA knockdown of HIF-1α/STOML2/PGAM5, overexpression, immunofluorescence (mitochondrial localization), mitophagy assays, neuronal injury assays, in vivo mouse model Cell death discovery Medium 41723145
2026 STOML2 interacts with the mitochondrial Na+/Ca2+ exchanger NCLX to support mitochondrial Ca2+ efflux and metabolic stability. STOML2 depletion impairs oxidative phosphorylation, elevates mitochondrial ROS, and promotes chondrocyte senescence and ferroptotic cell death in osteoarthritis models. Co-immunoprecipitation (STOML2-NCLX), siRNA knockdown, STOML2 overexpression, mitochondrial Ca2+ measurement, OCR measurement, ROS assay, intra-articular delivery in rat OA model Genetics research Medium 41995387
2026 STOML2 and PHB form a functional axis that maintains ERK/MAPK signaling activity and pluripotency in human pluripotent stem cells. STOML2 knockdown reduces OCT4, NANOG, PHB, and phosphorylated ERK while increasing differentiation markers, demonstrating STOML2 is required for hPSC self-renewal through the PHB-ERK pathway. shRNA knockdown, transcriptomic profiling (RNA-seq), Western blot (phospho-ERK), immunofluorescence, flow cytometry International journal of stem cells Medium 41709508
2025 SLP-2 overexpression protects against alpha-synuclein-induced mitochondrial dysfunction and dopaminergic neuron loss. SLP-2 levels are reduced in human PD brains and in an A53T alpha-synuclein mouse model. SLP-2 overexpression in iPSC-derived neurons improves mitochondrial function, reduces oxidative stress, and prevents alpha-synuclein-mitochondria interactions. SLP-2 depletion exacerbates degeneration in mouse and Drosophila models. Human PD brain analysis (Western blot), A53T αSyn mouse model, iPSC-derived neuron overexpression, mitochondrial function assays, oxidative stress assays, proximity/co-localization assays for αSyn-mitochondria interaction, Drosophila depletion model bioRxivpreprint Medium bio_10.1101_2025.06.13.659577

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 SLP-2 is required for stress-induced mitochondrial hyperfusion. The EMBO journal 628 19360003
2021 STOML2 potentiates metastasis of hepatocellular carcinoma by promoting PINK1-mediated mitophagy and regulates sensitivity to lenvatinib. Journal of hematology & oncology 135 33446239
2000 Identification and characterization of human SLP-2, a novel homologue of stomatin (band 7.2b) present in erythrocytes and other tissues. The Journal of biological chemistry 99 10713127
2008 SLP-2 interacts with prohibitins in the mitochondrial inner membrane and contributes to their stability. Biochimica et biophysica acta 74 18339324
2017 SLP-2 interacts with Parkin in mitochondria and prevents mitochondrial dysfunction in Parkin-deficient human iPSC-derived neurons and Drosophila. Human molecular genetics 49 28379402
2013 Anoxia-reoxygenation regulates mitochondrial dynamics through the hypoxia response pathway, SKN-1/Nrf, and stomatin-like protein STL-1/SLP-2. PLoS genetics 48 24385935
2009 Downregulation of a mitochondria associated protein SLP-2 inhibits tumor cell motility, proliferation and enhances cell sensitivity to chemotherapeutic reagents. Cancer biology & therapy 40 19597348
2023 STOML2 restricts mitophagy and increases chemosensitivity in pancreatic cancer through stabilizing PARL-induced PINK1 degradation. Cell death & disease 39 36906621
2011 Knockdown of stomatin-like protein 2 (STOML2) reduces the invasive ability of glioma cells through inhibition of the NF-κB/MMP-9 pathway. The Journal of pathology 30 21960069
2009 SLP-2 negatively modulates mitochondrial sodium-calcium exchange. Cell calcium 28 19944461
2019 Alginate oligosaccharide (AOS) improves immuno-metabolic systems by inhibiting STOML2 overexpression in high-fat-diet-induced obese zebrafish. Food & function 22 31290903
2001 A novel member of the STOMATIN/EPB72/mec-2 family, stomatin-like 2 (STOML2), is ubiquitously expressed and localizes to HSA chromosome 9p13.1. Cytogenetics and cell genetics 22 11435687
2018 The diagnostic value of TROP-2, SLP-2 and CD56 expression in papillary thyroid carcinoma. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery 19 29951933
2022 Cytochrome B5 type A alleviates HCC metastasis via regulating STOML2 related autophagy and promoting sensitivity to ruxolitinib. Cell death & disease 18 35851063
2021 STOML2 interacts with PHB through activating MAPK signaling pathway to promote colorectal Cancer proliferation. Journal of experimental & clinical cancer research : CR 17 34781982
2013 Expression of SLP-2 was associated with invasion of esophageal squamous cell carcinoma. PloS one 17 23667687
2013 Clinicopathological significance of SLP-2 overexpression in human gallbladder cancer. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 12 23918306
2019 Expression and clinical significance of SLP-2 in ovarian tumors. Oncology letters 11 30944651
2013 Increased expression of stomatin-like protein 2 (STOML2) predicts decreased survival in gastric adenocarcinoma: a retrospective study. Medical oncology (Northwood, London, England) 11 24258357
2005 [Effect of stomatin-like protein 2 (SLP-2) gene on growth and proliferation of esophageal squamous carcinoma cell line TE12]. Ai zheng = Aizheng = Chinese journal of cancer 11 15694024
2023 Resveratrol augments paclitaxel sensitivity by modulating miR-671-5p/STOML2/PINK1/Parkin-mediated autophagy signaling in A549 cell. Journal of biochemical and molecular toxicology 10 37840424
2020 Clinical significance of SLP-2 in epithelial ovarian cancer and its regulatory effect on the Notch signaling pathway. European review for medical and pharmacological sciences 8 32141532
2006 Mass spectrometrical verification of stomatin-like protein 2 (SLP-2) primary structure. Proteins 8 16671055
2024 Overexpressing lipid raft protein STOML2 modulates the tumor microenvironment via NF-κB signaling in colorectal cancer. Cellular and molecular life sciences : CMLS 7 38214751
2020 Coexisting overexpression of STOML1 and STOML2 proteins may be associated with pathology of oral squamous cell carcinoma. Oral surgery, oral medicine, oral pathology and oral radiology 7 32402568
2017 Clinical significance of SLP-2 in hepatocellular carcinoma tissues and its regulation in cancer cell proliferation, migration, and EMT. OncoTargets and therapy 7 29033585
2016 Identification of STOML2 as a putative novel asthma risk gene associated with IL6R. Allergy 7 26932604
2021 Effect and mechanism of action of SLP-2 on the apoptosis and autophagy of gastric cancer cells. Oncology letters 5 34457062
2025 STOML2 inhibits sorafenib-induced ferroptosis in hepatocellular carcinoma via p-AKT signaling pathway. American journal of cancer research 4 40371153
2022 SLP-2 regulates the generation of reactive oxygen species and the ERK pathway to promote papillary thyroid carcinoma motility and angiogenesis. Tissue & cell 4 36527788
2021 Expression of STOML2 promotes proliferation and glycolysis of multiple myeloma cells via upregulating PAI-1. Journal of orthopaedic surgery and research 4 34774067
2024 Intracellular delivery of Parkin-RING0-based fragments corrects Parkin-induced mitochondrial dysfunction through interaction with SLP-2. Journal of translational medicine 2 38229174
2005 [Expression of SLP-2 mRNA in endometrial cancer and its significance]. Zhonghua fu chan ke za zhi 2 16202296
2025 STOML2 knockdown inhibits inflammation and airway remodeling of PDGF-BB-induced airway smooth-muscle cells by the MAPK pathway. The Journal of asthma : official journal of the Association for the Care of Asthma 1 40787720
2025 STOML2 interacts with PHB to activate the MEK/ERK signaling pathway and mediates autophagy‑related proteins in the progression of hepatocellular carcinoma. International journal of molecular medicine 1 41347828
2015 [Overexpression of STOML-2 inhibits apoptosis of human cervical squamous carcinoma Siha cells in vitro]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 1 26403741
2026 STOML2 is not essential for spermatogenesis and male fertility in mice. Biochemical and biophysical research communications 0 41619509
2026 STOML2 Maintains Pluripotency and Cell Cycle Integrity in Human Pluripotent Stem Cells via PHB-ERK Signaling. International journal of stem cells 0 41709508
2026 Novel mechanism of neuronal hypoxia response: HIF-1α/STOML2 mediated PINK1-dependent mitophagy activation against neuronal injury. Cell death discovery 0 41723145
2026 STOML2 promotes hepatocellular carcinoma cell proliferation, invasion and migration by activating the PI3K/AKT signaling pathway (Review). Oncology letters 0 41743019
2026 STOML2 Alleviates Osteoarthritis by Regulating Mitochondrial Energy Metabolism and Oxidative Stress. Genetics research 0 41995387
2022 Clinical Significance of SLP-2 in Hepatocellular Carcinoma Tissues and Its Regulation in Cancer Cell Proliferation, Migration, and EMT [Retraction]. OncoTargets and therapy 0 36003327
2018 [Silencing of SLP-2 inhibits the migration and invasion of cervical cancer cells in vitro]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 0 33168500
2010 [Expression of SLP-2 protein in esophageal squamous cell carcinoma is associated with cancer invasion]. Zhonghua zhong liu za zhi [Chinese journal of oncology] 0 21223688