Affinage

SH3BP5

SH3 domain-binding protein 5 · UniProt O60239

Length
455 aa
Mass
50.4 kDa
Annotated
2026-06-10
43 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SH3BP5 (Sab) is a mitochondrial outer-membrane scaffold protein that operates as the docking platform converting transient stress-kinase signaling into sustained mitochondrial dysfunction and cell death (PMID:12167088, PMID:26845758). Stress-activated JNK binds Sab through its N-terminal KIM1 motif and is anchored on the outer mitochondrial membrane, where Sab serves as a JNK substrate; this interaction is required for JNK mitochondrial translocation, Bcl-2 phosphorylation, loss of membrane potential, and superoxide generation (PMID:12167088, PMID:21563797). Phosphorylation of Sab by JNK (ATP-dependent) triggers release and activation of intramitochondrial SHP1 (PTPN6), which transfers via the platform protein DOK4 to the inner membrane and dephosphorylates/inactivates mitochondrial Src, impairing electron transport and elevating ROS; the resulting ROS sustains JNK activation, establishing a self-amplifying JNK–Sab–ROS feedback loop (PMID:26845758). This loop is the effector arm of diverse injury settings: ER-stress and PERK-driven lipotoxicity, acetaminophen and TNF/galactosamine liver injury, ischemia/reperfusion and drug cardiotoxicity, and diet-induced steatohepatitis, where genetic deletion or KIM1-peptide/ASO blockade of Sab interrupts the sustained JNK phase and protects against organ injury (PMID:24407242, PMID:25666017, PMID:26845758, PMID:34331779). Sab abundance is a rate-limiting determinant of injury severity, set transcriptionally through a JNK/ATF2 loop and AP-1, and repressed in females via an ERα→p53→miR34a-5p pathway targeting Sab mRNA (PMID:31487267, PMID:34331779). Independently of its mitochondrial role, SH3BP5 functions as a guanine nucleotide exchange factor specific for Rab11, using a coiled-coil architecture to activate Rab11 for receptor recycling, endosomal trafficking, and cytokinesis (PMID:30217979, PMID:28003861). Sab was originally identified as a selective binding partner and negative regulator of the SH3 domain of Bruton's tyrosine kinase (Btk), dampening BCR-induced signaling in B cells (PMID:9571151, PMID:10339589).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1998 Medium

    Established the first molecular partner of Sab, defining it as an SH3-domain ligand with selectivity for Btk over other tyrosine kinases.

    Evidence Protein interaction cloning and SH3-domain binding/immunoprecipitation assays

    PMID:9571151

    Open questions at the time
    • Binding mode to the SH3 domain not structurally resolved
    • Functional consequence of binding not yet shown
  2. 1999 High

    Showed the Btk interaction is functionally inhibitory, placing Sab as a negative regulator of BCR signaling and apoptosis in B cells.

    Evidence Overexpression in B cells with kinase, calcium, IP3, and apoptosis assays

    PMID:10339589

    Open questions at the time
    • Based on overexpression rather than loss-of-function
    • Relationship between the Btk role and later mitochondrial role unexplained
  3. 2002 High

    Reframed Sab as a mitochondrial JNK-interacting protein, identifying the KIM1 motif as the docking determinant and a distinct functional axis from Btk binding.

    Evidence Yeast two-hybrid, in vitro kinase assay with mutagenesis, confocal microscopy and fractionation

    PMID:12167088

    Open questions at the time
    • Downstream mitochondrial consequence of JNK docking not yet defined
    • Whether phosphorylation alters Sab activity unknown
  4. 2004 Medium

    Extended the kinase repertoire docking at Sab by showing SAPK3/p38 also phosphorylates it on Ser321 via KIM1, indicating shared mitochondrial substrate use.

    Evidence In vitro kinase assay, site-directed mutagenesis, subcellular fractionation

    PMID:15158451

    Open questions at the time
    • Cellular significance of Ser321 phosphorylation not established
    • p38-driven outcome via Sab not demonstrated
  5. 2011 High

    Demonstrated that JNK–Sab docking is mechanistically required for mitochondrial JNK actions and that it can be selectively blocked, separating mitochondrial from nuclear (c-Jun/AP-1) JNK signaling.

    Evidence siRNA, Tat-SabKIM1 peptide, JNK translocation, Bcl-2 phosphorylation, membrane potential and superoxide assays

    PMID:21563797

    Open questions at the time
    • Intramitochondrial relay from Sab to ROS not yet defined
    • Direct substrate of mitochondrial JNK unclear
  6. 2014 High

    Established the JNK–Sab–ROS feedback loop by reconstituting p-JNK/ATP-driven superoxide production in isolated mitochondria and linking it to sustained JNK activation in ER stress.

    Evidence siRNA, isolated-mitochondria respiration and superoxide assays, KIM1 blocking peptide, cellular OCR and apoptosis

    PMID:24407242

    Open questions at the time
    • Molecular intermediates between Sab phosphorylation and respiratory impairment not yet identified
  7. 2016 High

    Resolved the intramitochondrial relay: JNK-phosphorylated Sab releases SHP1 which, via DOK4, inactivates inner-membrane Src to impair electron transport and amplify ROS, with in vivo liver-injury validation.

    Evidence Liver-specific Sab KO, isolated-mitochondria reconstitution, SHP1/DOK4 knockdown, APAP and TNF/galactosamine models

    PMID:26845758

    Open questions at the time
    • Structural basis of SHP1 sequestration by Sab unknown
    • How Src inactivation impairs electron transport mechanistically not fully defined
  8. 2015 High

    Placed the Sab loop downstream of PERK in lipotoxicity, defining pathway epistasis for the sustained JNK phase in hepatocytes.

    Evidence adeno-shSab, blocking peptide, OCR, cell death, PERK/CHOP measurements

    PMID:25666017

    Open questions at the time
    • Link between PERK output and JNK–Sab engagement not molecularly traced
  9. 2017 High

    Generalized the Sab loop beyond liver to cardiomyocyte drug toxicity and showed Sab expression is stress-inducible via AP-1.

    Evidence siRNA, overexpression, KIM1 peptide, Seahorse, ROS/ATP/lipid peroxidation assays, AP-1 reporter (H9c2)

    PMID:28315715

    Open questions at the time
    • In vivo cardiac relevance not tested in this study
  10. 2017 Medium

    Showed Sab is expressed at neuronal mitochondria and that its signaling modulates neuronal excitability, extending its physiology beyond injury contexts.

    Evidence Confocal and electron microscopy, synaptosome purification, neuronal electrophysiology with Tat-SabKIM1

    PMID:28606781

    Open questions at the time
    • Mechanism linking Sab signaling to firing properties unresolved
    • No in vivo neuronal phenotype
  11. 2016 Medium

    Identified a wholly distinct biochemical function: SH3BP5/REI-1 acts as a Rab11 GEF controlling endosomal recycling, Golgi targeting and cytokinesis, conserved from C. elegans to human.

    Evidence GEF assays for worm and human proteins, loss-of-function genetics, co-localization, cytokinesis timing

    PMID:28003861

    Open questions at the time
    • Relationship between mitochondrial and GEF functions in the same cell unknown
    • Subcellular site of GEF activity not pinned to specific membranes
  12. 2018 High

    Provided the structural mechanism of the GEF function, showing a coiled-coil architecture that catalyzes Rab11 nucleotide exchange with specificity over related Rabs.

    Evidence Crystal structure of SH3BP5–Rab11, in vitro GEF assay, mutagenesis, cellular Rab11 activation

    PMID:30217979

    Open questions at the time
    • How the GEF and JNK-docking activities are spatially partitioned within the protein not addressed
  13. 2019 High

    Showed Sab abundance is rate-limiting for injury and is set sex-dependently through an ERα→p53→miR34a-5p axis repressing Sab mRNA.

    Evidence Liver-specific deletion, GalNAc-ASO, p53 knockdown, fulvestrant/ERα agonist, miR34a-5p targeting assays, in vivo injury models

    PMID:31487267

    Open questions at the time
    • Whether this regulation operates in non-hepatic tissues untested
  14. 2019 Medium

    Validated the JNK/Sab/Src/ROS pathway in cardiomyocyte ischemia/reperfusion, confirming Src dephosphorylation and cardiolipin oxidation as downstream events.

    Evidence siRNA, JNK and Src inhibitors, confocal colocalization, ROS and cardiolipin oxidation assays (H9c2)

    PMID:31205589

    Open questions at the time
    • Cell-line model only; no in vivo cardiac confirmation in this study
  15. 2020 Medium

    Connected dietary trans-fatty acids to potentiation of the Sab feedback loop during DNA-damage-induced apoptosis.

    Evidence Sab siRNA, JNK/ROS/SHP1 inhibitors, mitochondrial ROS and apoptosis assays, C. elegans UV-lethality

    PMID:32066809

    Open questions at the time
    • How trans-fatty acids prime the loop mechanistically unclear
  16. 2021 High

    Demonstrated therapeutic tractability: inducible Sab deletion or ASO knockdown prevents and reverses diet-induced steatohepatitis and fibrosis via interruption of the JNK/ATF2 loop.

    Evidence Inducible liver-specific KO, GalNAc-Sab-ASO, HFHC diet model, histology, metabolic phenotyping

    PMID:34331779

    Open questions at the time
    • Durability and off-target consequences of chronic Sab suppression not addressed
  17. 2023 Low

    Linked SH3BP5 expression to an m6A regulatory axis (METTL3/YTHDF1) with a tumor-suppressive effect on lung cancer invasion.

    Evidence METTL3/YTHDF1 perturbation, SH3BP5 overexpression, m6A, invasion and mRNA stability assays

    PMID:38141906

    Open questions at the time
    • Single-lab, overexpression-based; direct m6A modification of SH3BP5 not reconstituted
    • Which SH3BP5 function mediates invasion suppression unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the mitochondrial JNK-docking/scaffold function and the cytosolic/endosomal Rab11-GEF function are reconciled within one protein — and whether they are co-active or context-switched in the same cell — remains unresolved.
  • No study tests both activities in the same system
  • Determinants partitioning Sab between mitochondria and recycling endosomes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0060089 molecular transducer activity 2 GO:0098772 molecular function regulator activity 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0005739 mitochondrion 3 GO:0005768 endosome 2
Pathway
R-HSA-5357801 Programmed Cell Death 3 R-HSA-162582 Signal Transduction 2 R-HSA-8953897 Cellular responses to stimuli 2 R-HSA-9609507 Protein localization 2
Partners
BTKDOK4JNKRAB11SAPK3SHP1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 SH3BP5 (Sab) was identified as a novel protein that binds the SH3 domain of Bruton's tyrosine kinase (Btk) through a non-proline-rich structure commonly conserved among SH3 domains, with high preference for Btk over other cytoplasmic tyrosine kinases. Protein interaction cloning, immunoprecipitation, SH3 domain binding assay Biochemical and biophysical research communications Medium 9571151
1999 SH3BP5 (Sab) negatively regulates Bruton's tyrosine kinase (Btk) activity by inhibiting its auto- and transphosphorylation; forced overexpression of Sab in B cells reduced BCR-induced tyrosine phosphorylation of Btk, calcium mobilization, IP3 production, and apoptotic cell death. Overexpression in B cells, in vitro kinase assay, calcium mobilization assay, IP3 measurement, apoptosis assay Proceedings of the National Academy of Sciences of the United States of America High 10339589
2002 SH3BP5 (Sab) is a JNK-interacting protein that binds to and is phosphorylated by JNK in vitro; interaction requires the most N-terminal KIM (KIM1) motif, physical interaction is necessary for phosphorylation, and Sab localizes to mitochondria where it co-localizes with a fraction of active JNK after stress. Yeast two-hybrid, in vitro kinase assay, deletion/site-directed mutagenesis, confocal immunocytochemistry, cell fractionation The Biochemical journal High 12167088
2004 SAPK3 (p38 MAPK subfamily member) localizes to mitochondria and phosphorylates Sab in vitro, primarily on Ser321, dependent on the KIM1 motif of Sab; this reveals a shared mitochondrial substrate between SAPK3 and JNK. In vitro kinase assay, site-directed mutagenesis, subcellular fractionation Biochemical and biophysical research communications Medium 15158451
2004 Sab is a mitochondria-associated JNK-interacting protein; the JNK-Sab interaction occurs via a KIM motif distinct from the Btk-binding domain, and Sab co-localizes with active JNK at mitochondria after stress treatment. Interacting protein screen, confocal microscopy, mitochondrial co-localization Biochemical Society transactions Medium 15506969
2011 JNK-Sab interaction at mitochondria is required for JNK mitochondrial translocation, Bcl-2 phosphorylation, loss of mitochondrial membrane potential, and superoxide generation; a cell-permeable peptide mimicking the KIM1 domain of Sab (Tat-Sab(KIM1)) selectively disrupted mitochondrial JNK signaling without affecting c-Jun phosphorylation or AP-1 transcription. siRNA knockdown, cell-permeable inhibitory peptide (Tat-SabKIM1), JNK translocation assay, Bcl-2 phosphorylation, mitochondrial membrane potential assay, superoxide measurement ACS chemical biology High 21563797
2014 Sab knockdown prevents ER stress-induced sustained JNK activation, impaired mitochondrial respiration, and apoptosis; p-JNK plus ATP added to isolated liver mitochondria promotes superoxide production amplified by calcium and blocked by a KIM1 blocking peptide, establishing that ER stress triggers JNK-Sab interaction at mitochondria leading to impaired respiration and ROS, which sustains JNK activation. siRNA knockdown, isolated mitochondria respiration assay, superoxide measurement, blocking peptide, cellular oxygen consumption rate (OCR) assay, apoptosis measurement Cell death & disease High 24407242
2015 In palmitic acid-induced hepatocyte lipotoxicity, Sab knockdown or a membrane-permeable Sab blocking peptide prevented palmitic acid-induced mitochondrial impairment (decreased OCR) and inhibited the late phase of JNK activation and cell death, placing the JNK-Sab interaction downstream of PERK but upstream of sustained JNK activation and mitochondrial dysfunction. siRNA knockdown (adeno-shSab), cell-permeable blocking peptide, oxygen consumption rate (OCR) measurement, cell death assay, PERK/CHOP activation measurement Journal of hepatology High 25666017
2016 p-JNK interacts with Sab on the outer mitochondrial membrane and phosphorylates it (requiring ATP), leading to release and activation of intramitochondrial SHP1 (PTPN6) from Sab on the inner face of the outer membrane; activated SHP1 transfers to the inner membrane where it dephosphorylates P-Y419Src (inactivating mitochondrial Src) via a platform protein DOK4; inactivation of mitochondrial Src inhibits electron transport, increases ROS, sustains JNK activation, and promotes cell death. Sab liver-specific knockout abrogated sustained JNK activation and liver injury. Liver-specific Sab knockout (Cre-lox), Sab knockdown, isolated mitochondria respiration assay, p-JNK + ATP addition to mitochondria, SHP1/DOK4 knockdown, mitochondrial fractionation, in vivo APAP and TNF/galactosamine models Hepatology (Baltimore, Md.) High 26845758
2017 Sab-mediated signaling is required for imatinib mesylate-induced mitochondrial dysfunction in cardiomyocyte-like H9c2 cells; Sab knockdown or KIM1 peptide inhibition prevented ROS production, lipid peroxidation, impaired mitochondrial respiration, ATP loss, and apoptosis; overexpression of Sab increased cardiotoxicity; Sab expression was induced by cardiovascular-like stress in an AP-1-dependent manner. siRNA knockdown, overexpression, KIM1 inhibitory peptide, ROS measurement, Seahorse respiration assay, ATP assay, lipid peroxidation, protein carbonylation, apoptosis assay, AP-1 reporter Toxicology High 28315715
2017 Sab is expressed in the adult mouse brain, enriched in hippocampus, ventral midbrain, and cerebellum; it localizes to mitochondria in neuronal soma, dendrites, and axons (confirmed by electron microscopy in hippocampal sections); inhibiting Sab-mediated signaling with Tat-SabKIM1 peptide decreased firing frequency and spike amplitudes in cultured hippocampal neurons. Confocal microscopy, electron microscopy, synaptosome purification, neuronal culture, electrophysiology with peptide inhibitor Brain research Medium 28606781
2018 Crystal structure of SH3BP5 bound to Rab11 revealed a coiled-coil architecture mediating guanine nucleotide exchange through a unique Rab-GEF interaction; Rab11 switch I adopts a constrained conformation distinct from other Rab-GEF complexes; SH3BP5 functions as a GEF for Rab11 with specificity over evolutionarily similar Rab GTPases; GEF-deficient mutants of SH3BP5 showed greatly decreased Rab11 activation in cellular assays. Crystal structure determination, in vitro GEF assay, mutagenesis, cellular Rab11 activation assay Nature communications High 30217979
2016 REI-1, the C. elegans ortholog of SH3BP5, functions as a GEF for RAB-11; loss of REI-1 impaired RAB-11 targeting to the late-Golgi compartment and recycling endosomes, reduced RAB-11 recruitment to the cleavage furrow, and delayed cytokinesis; human SH3BP5 also exhibits GEF activity toward human Rab11. GEF activity assay (C. elegans and human proteins), loss-of-function genetics, fluorescence co-localization, cytokinesis timing assay Communicative & integrative biology Medium 28003861
2019 SAB expression levels determine severity of JNK-dependent liver injury in a sex-dependent manner; female mice express low hepatic SAB protein due to an ERα→p53→miR34a-5p pathway where miR34a-5p targets the Sab mRNA coding region to repress SAB expression; fulvestrant or p53 knockdown decreased miR34a-5p and increased SAB, enhancing injury, while ERα agonist increased miR34a-5p and decreased SAB and hepatotoxicity in males. Liver-specific Sab deletion, GalNAc-ASO knockdown of Sab, p53 knockdown, fulvestrant/ERα agonist treatment, miR34a-5p measurement, mRNA targeting assay, in vivo liver injury models (APAP, TNF/galactosamine) The Journal of clinical investigation High 31487267
2019 In H9c2 cardiomyocyte-like cells, hypoxia/reoxygenation induces JNK activation, translocation to mitochondria via colocalization with Sab, and subsequent mitochondrial Src dephosphorylation; JNK inhibition or Sab siRNA reduced p-JNK/Sab colocalization, decreased Src dephosphorylation, and reduced mitochondrial ROS and oxidized cardiolipin, validating the JNK/Sab/Src/ROS pathway in cardiomyocyte ischemia/reperfusion injury. siRNA knockdown, JNK inhibitor, Src inhibitor PP2, confocal colocalization, ROS measurement, cardiolipin oxidation assay, mitochondrial membrane potential Oxidative medicine and cellular longevity Medium 31205589
2020 Trans-fatty acids (elaidic acid) facilitate DNA damage-induced apoptosis by driving the mitochondrial JNK-Sab-ROS positive feedback loop; Sab knockdown blocked EA-enhanced mitochondrial ROS generation and JNK activation induced by doxorubicin; pharmacological inhibition of SHP1 (a Sab-associated protein) also suppressed this pathway. siRNA knockdown of Sab, pharmacological inhibitors of JNK/ROS/SHP1, mitochondrial ROS measurement, apoptosis assay, C. elegans UV-lethality assay Scientific reports Medium 32066809
2021 In HFHC diet-fed mice, SAB expression progressively increased through a sustained JNK/ATF2 activation loop; inducible hepatic Sab deletion or ASO knockdown markedly decreased sustained JNK activation, improved energy expenditure, reduced body fat, and prevented or reversed steatohepatitis and fibrosis; reversal of established NASH was achieved by GalNAc-Sab-ASO treatment. Inducible liver-specific Sab KO, antisense oligonucleotide knockdown (ASO, GalNAc-ASO), HFHC diet model, liver histology, p-JNK and p-ATF2 measurement, metabolic phenotyping Hepatology (Baltimore, Md.) High 34331779
2023 METTL3-mediated m6A modification of SH3BP5 mRNA is read by YTHDF1, which maintains SH3BP5 mRNA stability; overexpression of SH3BP5 suppressed invasion of lung cancer cells in an m6A-dependent manner, and METTL3 suppresses lung cancer invasion through this SH3BP5 regulatory axis. METTL3/YTHDF1 overexpression and knockdown, SH3BP5 overexpression, m6A assay, invasion assay, mRNA stability assay Archives of biochemistry and biophysics Low 38141906

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 c-Jun N-terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)-dependent pathway leading to inactivation of intramitochondrial Src. Hepatology (Baltimore, Md.) 151 26845758
2014 JNK interaction with Sab mediates ER stress induced inhibition of mitochondrial respiration and cell death. Cell death & disease 139 24407242
2006 Simian immunodeficiency virus SIVagm.sab infection of Caribbean African green monkeys: a new model for the study of SIV pathogenesis in natural hosts. Journal of virology 111 16641277
2015 Sab (Sh3bp5) dependence of JNK mediated inhibition of mitochondrial respiration in palmitic acid induced hepatocyte lipotoxicity. Journal of hepatology 108 25666017
1997 Association of polymorphisms of dopamine D2 receptor (DRD2), and dopamine transporter (DAT1) genes with schizoid/avoidant behaviors (SAB). Molecular psychiatry 92 9152988
2002 A new c-Jun N-terminal kinase (JNK)-interacting protein, Sab (SH3BP5), associates with mitochondria. The Biochemical journal 84 12167088
2018 The Regulation of JNK Signaling Pathways in Cell Death through the Interplay with Mitochondrial SAB and Upstream Post-Translational Effects. International journal of molecular sciences 69 30463289
2009 Sab, a novel autotransporter of locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21, contributes to adherence and biofilm formation. Infection and immunity 66 19487483
1999 Bruton's tyrosine kinase activity is negatively regulated by Sab, the Btk-SH3 domain-binding protein. Proceedings of the National Academy of Sciences of the United States of America 60 10339589
1998 Identification and characterization of a novel SH3-domain binding protein, Sab, which preferentially associates with Bruton's tyrosine kinase (BtK). Biochemical and biophysical research communications 46 9571151
2018 Structural determinants of Rab11 activation by the guanine nucleotide exchange factor SH3BP5. Nature communications 43 30217979
2011 Selective inhibition of mitochondrial JNK signaling achieved using peptide mimicry of the Sab kinase interacting motif-1 (KIM1). ACS chemical biology 43 21563797
2019 Expression of mitochondrial membrane-linked SAB determines severity of sex-dependent acute liver injury. The Journal of clinical investigation 37 31487267
2022 N6-methyladenosine-mediated SH3BP5-AS1 upregulation promotes GEM chemoresistance in pancreatic cancer by activating the Wnt signaling pathway. Biology direct 36 36397058
2021 Hepatic Mitochondrial SAB Deletion or Knockdown Alleviates Diet-Induced Metabolic Syndrome, Steatohepatitis, and Hepatic Fibrosis. Hepatology (Baltimore, Md.) 30 34331779
2004 Sab (SH3BP5), a novel mitochondria-localized JNK-interacting protein. Biochemical Society transactions 28 15506969
2008 Phylogeny of Tec family kinases identification of a premetazoan origin of Btk, Bmx, Itk, Tec, Txk, and the Btk regulator SH3BP5. Advances in genetics 27 19161832
2020 trans-Fatty acids facilitate DNA damage-induced apoptosis through the mitochondrial JNK-Sab-ROS positive feedback loop. Scientific reports 26 32066809
2017 Sab mediates mitochondrial dysfunction involved in imatinib mesylate-induced cardiotoxicity. Toxicology 26 28315715
2005 Polyglutamic acid (PGA) production by Bacillus sp. SAB-26: application of Plackett-Burman experimental design to evaluate culture requirements. Applied microbiology and biotechnology 24 15834714
2004 Phosphorylation of the mitochondrial protein Sab by stress-activated protein kinase 3. Biochemical and biophysical research communications 24 15158451
2022 Scoparone Improves Nonalcoholic Steatohepatitis Through Alleviating JNK/Sab Signaling Pathway-Mediated Mitochondrial Dysfunction. Frontiers in pharmacology 23 35592421
2019 N-n-Butyl Haloperidol Iodide Ameliorates Oxidative Stress in Mitochondria Induced by Hypoxia/Reoxygenation through the Mitochondrial c-Jun N-Terminal Kinase/Sab/Src/Reactive Oxygen Species Pathway in H9c2 Cells. Oxidative medicine and cellular longevity 18 31205589
2020 Establishment of a brain cell line (SaB-1) from gilthead seabream and its application to fish virology. Fish & shellfish immunology 15 32771610
2024 Mitochondrial P-JNK target, SAB (SH3BP5), in regulation of cell death. Frontiers in cell and developmental biology 11 38559813
2016 Expressions of SH3BP5, LMO3, and SNAP25 in diffuse large B-cell lymphoma cells and their association with clinical features. Cancer medicine 11 27184832
2023 Phase 2 Safety and Antiviral Activity of SAB-185, a Novel Polyclonal Antibody Therapy for Nonhospitalized Adults With COVID-19. The Journal of infectious diseases 10 36661240
2021 Novel blood-based hypomethylation of SH3BP5 is associated with very early-stage lung adenocarcinoma. Genes & genomics 10 34783986
2018 Sab concentrations indicate chemotherapeutic susceptibility in ovarian cancer cell lines. The Biochemical journal 10 30322886
2023 METTL3 suppresses invasion of lung cancer via SH3BP5 m6A modification. Archives of biochemistry and biophysics 8 38141906
2019 Elevated SH3BP5 Correlates with Poor Outcome and Contributes to the Growth of Acute Myeloid Leukemia Cells. Biomolecules 8 31546831
2024 LncRNA SH3BP5-AS1 promotes hepatocellular carcinoma progression by sponging miR-6838-5p and activation of PTPN4. Aging 7 38761175
2023 SH3BP5-AS1/IGF2BP2/VDAC2 Axis Promotes the Apoptosis and Ferroptosis of Bladder Cancer Cells. Bladder cancer (Amsterdam, Netherlands) 5 38994477
2017 Sab is differentially expressed in the brain and affects neuronal activity. Brain research 5 28606781
2025 The Effective Compound Combination of Bufei Yishen Formula III Improves the Mitochondrial Dysfunction via Inhibiting JNK/Sab Pathway in COPD Mice. Drug design, development and therapy 4 39876989
2025 A sprayable TQ/Ce6@SAB/F-gel for accelerating wound healing via hypoxia-tolerant photodynamic therapy and immune-metabolic pathway. Biomaterials 4 40782448
2008 Coproduction of thermostable amylase and beta-galactosidase enzymes by Geobacillus stearothermophilus SAB-40: aplication of Plackett-Burman design to evaluate culture requirements affecting enzyme production. Journal of microbiology and biotechnology 3 18467863
2016 REI-1, a Novel Rab11 GEF with a SH3BP5 domain. Communicative & integrative biology 2 28003861
2011 [Effects of salviandic acid B (SA-B) on activity of basement membrane-type collagenase and impact of regulatory factors in rats with cardiac hypertrophy]. Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica 2 22121809
1998 Multiply spliced env and nef transcripts of simian immunodeficiency virus from West African green monkey (SIVagm-sab). AIDS research and human retroviruses 1 9566554
2026 Unraveling the mechanism of adventitious bud formation in sugarcane spontaneous adventitious bud (SAB) mutant. Plant physiology and biochemistry : PPB 0 41564701
2026 Screening, validation, and transcriptional regulation analysis of oxidative stress-related biomarkers in gestational diabetes mellitus: SH3BP5, ITGAM, PRRG1, and MIS12. European journal of medical research 0 41787525
2025 Axon termination of the SAB motor neurons in C. elegans depends on pre- and postsynaptic activity. bioRxiv : the preprint server for biology 0 40964322

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