Affinage

SASH1

SAM and SH3 domain-containing protein 1 · UniProt O94885

Length
1247 aa
Mass
136.7 kDa
Annotated
2026-04-28
67 papers in source corpus 24 papers cited in narrative 24 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SASH1 is a scaffold/adapter protein that assembles signaling complexes through its SH3, SAM, and intrinsically disordered SPIDER domains to regulate innate immune signaling, cell adhesion, apoptosis, and Hippo pathway output. In endothelial cells, SASH1 scaffolds TRAF6, TAK1, and IKKα/β to drive TLR4-dependent NF-κB/JNK/p38 activation and interacts with β-arrestin 1 to activate eNOS/NO signaling required for alveolar epithelial maturation, as Sash1-knockout mice die perinatally from respiratory distress (PMID:23776175, PMID:31067462). SASH1 co-localizes with cortactin and circumferential actin bundles to maintain cell-matrix and cell-cell adhesion, inhibits CRKL-mediated SRC activation to suppress EMT and metastasis, is phosphorylated by LATS1/2 at S407 to regulate YAP signaling, and is cleaved by caspase-3 to generate a nuclear fragment that promotes NF-κB-dependent apoptosis (PMID:21820526, PMID:30480076, PMID:32523092, PMID:27831555). Its SAM1 domain engages Eph receptor SAM domains—with highest affinity for EphA8—and Caskin1/2 SAM domains, while SASH1 mutations cause dyschromatosis universalis hereditaria through dysregulated melanocyte migration and MITF expression (PMID:37619706, PMID:39688081, PMID:23333244, PMID:32582980).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2003 Medium

    Identification of SASH1 as an SH3/SAM-containing adapter molecule on chromosome 6q24.3 established it as a candidate signaling scaffold, prior to any functional characterization.

    Evidence In silico expression profiling, LOH mapping, and transcript characterization in human tissues

    PMID:12771949

    Open questions at the time
    • No binding partners or signaling function demonstrated
    • Domain functions inferred from homology only
  2. 2011 High

    Demonstration that SASH1 co-localizes with the actin cytoskeleton and cortactin, increases F-actin content, and regulates cell adhesion and migration established a direct cytoskeletal regulatory function.

    Evidence Immunofluorescence, co-distribution assays, F-actin quantification, RNAi knockdown, and domain mapping in cultured cells

    PMID:21820526

    Open questions at the time
    • Direct actin-binding activity not tested biochemically
    • Signaling pathway connecting SASH1 to actin remodeling not identified
  3. 2013 High

    Discovery that SASH1 independently binds TRAF6, TAK1, IKKα, and IKKβ to promote their ubiquitination and activate NF-κB/JNK/p38 downstream of TLR4 defined SASH1 as a bona fide signaling scaffold in innate immunity, while mutations causing dyschromatosis linked SASH1 to IQGAP1/E-cadherin regulation and melanocyte migration.

    Evidence Reciprocal co-immunoprecipitation, ubiquitination assays, cytokine measurement, and migration assays in endothelial cells; patient mutation functional analysis in melanoma cells

    PMID:23333244 PMID:23776175

    Open questions at the time
    • Stoichiometry of the SASH1-TRAF6-TAK1-IKK scaffold complex unknown
    • Whether IQGAP1 binding is direct or bridged was not resolved
  4. 2016 High

    Caspase-3-mediated cleavage of SASH1 generating a nuclear fragment that promotes NF-κB-dependent apoptosis revealed a post-translational activation mechanism linking SASH1 to programmed cell death, while a p53/αMSH/SASH1 feedback loop was placed in melanogenesis.

    Evidence In vitro caspase cleavage, cleavage-site mutagenesis, subcellular fractionation, NF-κB inhibitor epistasis; UV stimulation and pigmentation assays in patient cells

    PMID:27831555 PMID:27885802

    Open questions at the time
    • Chromatin targets of nuclear SASH1 fragment not identified
    • Whether caspase-3 cleavage occurs during non-apoptotic signaling is unknown
  5. 2017 Medium

    Requirement of SASH1 for lumen formation upstream of DLK1-NOTCH1 signaling in 3D breast epithelial culture placed SASH1 in a morphogenetic program beyond simple adhesion regulation.

    Evidence RNAi knockdown in 3D lumenogenesis assay, gene array, γ-secretase inhibitor epistasis

    PMID:28823832

    Open questions at the time
    • Whether SASH1 directly controls DLK1 transcription or acts post-transcriptionally is unresolved
    • Relevance to in vivo mammary development not tested
  6. 2018 High

    Identification of CRKL as a direct SASH1 binding partner that SASH1 restrains from activating SRC-driven EMT and metastasis provided a mechanistic basis for SASH1's tumor-suppressive role, with in vivo epistasis confirming CRKL dependence.

    Evidence Yeast 2-hybrid, Co-IP/mass spectrometry, domain mapping, site-directed mutagenesis, CRISPR knockout, orthotopic mouse metastasis model

    PMID:30480076

    Open questions at the time
    • Structural basis of SASH1-CRKL interaction not determined
    • Whether SASH1 sequesters CRKL or allosterically inhibits it is unclear
  7. 2019 High

    Sash1 knockout mice dying perinatally from respiratory failure due to defective eNOS/NO/cGMP signaling in endothelial cells—mediated through β-arrestin 1 interaction—established a non-redundant in vivo role for SASH1 in lung maturation via paracrine endothelial-epithelial signaling.

    Evidence Constitutive and endothelial-restricted Sash1 KO mice, Co-IP for β-arrestin 1, eNOS/NO/cGMP pathway dissection, histology

    PMID:31067462

    Open questions at the time
    • Whether SASH1 directly activates Akt or recruits an intermediate kinase is unknown
    • Roles in other vascular beds beyond pulmonary microvasculature not explored
  8. 2019 Medium

    Demonstration that HMGB1 binds SASH1 CpG islands and drives promoter methylation revealed an epigenetic silencing mechanism explaining SASH1 downregulation in disease contexts such as cancer and glioma.

    Evidence ChIP assay for HMGB1 at SASH1 promoter, methylation analysis, siRNA knockdown and overexpression in astrocytes, adhesion/invasion assays

    PMID:31138780

    Open questions at the time
    • Identity of the DNA methyltransferase recruited by HMGB1 to the SASH1 locus not determined
    • Whether HMGB1-mediated silencing occurs broadly across tumor types is unknown
  9. 2020 High

    Placement of SASH1 as a LATS1 substrate phosphorylated at S407 that promotes YAP phosphorylation and suppresses YAP/TEAD-driven invasion integrated SASH1 into the Hippo signaling pathway with direct epistasis evidence, while parallel studies confirmed SASH1's role at adherens junctions and in MITF regulation.

    Evidence Phospho-deficient S407A mutagenesis, YAP inhibitor epistasis, xenograft models; RNAi disruption of linear adherens junctions; SASH1 Y551D knock-in mouse model for MITF

    PMID:32523092 PMID:32582980 PMID:32586229

    Open questions at the time
    • How SASH1 phosphorylation at S407 mechanistically alters YAP phosphorylation—direct substrate relay or scaffold rearrangement—is unresolved
    • Whether LATS1 and LATS2 are redundant for SASH1 phosphorylation in vivo is untested
  10. 2022 High

    NMR characterization revealing that the SAM1 domain exists primarily as a disordered monomer exchanging with a structured oligomer provided the first biophysical framework for understanding how SASH1 SAM-mediated interactions are regulated, while TRAF6 ubiquitination was linked to EZH2 stability in hemangioma.

    Evidence SEC-MALS, NMR relaxation/exchange, site-directed mutagenesis (D663A/T664K); Co-IP and ubiquitination assays in hemangioma endothelial cells

    PMID:35772492 PMID:36341956

    Open questions at the time
    • Full-length SASH1 structure remains undetermined
    • Whether monomer-oligomer equilibrium is regulated by post-translational modifications is unknown
  11. 2023 High

    Crystal structure of the EphA8-SASH1 SAM1 complex, combined with identification of Caskin1/2 as SAM-dependent binding partners and NMR characterization of the disordered SPIDER domain, comprehensively defined the structural basis of SASH1's two major interaction interfaces and showed that cancer mutations disrupt Eph receptor engagement.

    Evidence X-ray crystallography of EphA8-SASH1 complex, Y2H/ITC/SEC/pulldown/TEM for Caskin1/2 interaction, TROSY NMR backbone assignment of SPIDER domain

    PMID:37155029 PMID:37619706 PMID:39688081

    Open questions at the time
    • Functional consequence of SASH1-Caskin1/2 interaction in neurons or other tissues is unknown
    • How SPIDER domain disorder contributes to signaling specificity is not established
  12. 2024 Medium

    Extension of the Hippo pathway model to a MAP4K4-LATS2-SASH1-YAP1 cascade and identification of TNKS2 as a SPIDER domain binding partner (disrupted by the S519N disease variant) added upstream kinase hierarchy and a new interaction node to SASH1 function.

    Evidence Phosphorylation analysis, combinatorial siRNA/overexpression, in vivo tumor models, MAP4K4 inhibition; Y2H, binding kinetics, stem cell assays for TNKS2

    PMID:38657867 PMID:38848986

    Open questions at the time
    • Whether MAP4K4 phosphorylates LATS2 directly or through intermediaries in this cascade is unresolved
    • Cellular context specificity of TNKS2-SASH1 interaction is limited to melanocytes
  13. 2026 Medium

    Discovery that SASH1 sequesters PKM2 in the cytoplasm of astrocytes, preventing nuclear PKM2-driven glycolytic reprogramming, and that a blocking peptide reduces astrocyte activation after traumatic brain injury, extended SASH1's scaffold function to metabolic regulation.

    Evidence Co-immunoprecipitation, nuclear fractionation, glucose uptake/lactate assays, peptide drug in TBI mouse model

    PMID:41690666

    Open questions at the time
    • Whether SASH1-PKM2 interaction occurs outside astrocytes is unknown
    • Structural basis of the SASH1-PKM2 interaction not determined
    • Long-term therapeutic efficacy of blocking peptide not evaluated

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length structure of SASH1, the logic governing pathway selectivity among its numerous scaffold interactions (NF-κB, Hippo, eNOS, Eph, metabolic), and the in vivo relevance of individual interaction nodes beyond lung development remain to be established.
  • No full-length SASH1 structure available
  • How SASH1 selects among its many binding partners in different cell types is unknown
  • Conditional tissue-specific knockout phenotypes beyond lung are not characterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 5
Localization
GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2 GO:0005886 plasma membrane 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1500931 Cell-Cell communication 2 R-HSA-168256 Immune System 2 R-HSA-5357801 Programmed Cell Death 1
Partners
ARRB1CASKIN1CRKLCTTNEPHA8PKMTAK1TRAF6

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 SASH1 was identified as a member of the SH3/SAM adapter molecule family, encoded on chromosome 6q24.3, with protein domain structure comprising SH3 and SAM domains, suggesting a role in signaling pathways; it is predominantly expressed in breast, lung, thyroid, spleen, placenta and thymus. In silico expression analysis, LOH mapping, transcript characterization Oncogene Medium 12771949
2011 SASH1 localizes to the nucleus, cytoplasm, lamellipodia, and membrane ruffles where it co-distributes with the actin cytoskeleton; it directly interacts with the oncoprotein cortactin; SASH1 overexpression increases filamentous actin content and cell protrusions, inhibits cell migration, and increases cell adhesion to fibronectin and laminin, while SASH1 knockdown reduces cell-matrix adhesion. The actin-regulatory activity maps to the central conserved domain. Immunofluorescence localization, co-distribution assays, structural mutant analysis, F-actin quantification, migration and adhesion assays, RNAi knockdown The international journal of biochemistry & cell biology High 21820526
2013 SASH1 acts as a scaffold molecule in endothelial TLR4 signaling by independently binding TRAF6, TAK1, IκB kinase α, and IκB kinase β; this interaction fosters ubiquitination of TRAF6 and TAK1 and promotes LPS-induced NF-κB, JNK, and p38 activation, resulting in increased proinflammatory cytokine production and increased LPS-induced endothelial migration. Co-immunoprecipitation, ubiquitination assays, NF-κB/JNK/p38 activation assays, cytokine measurement, migration assay Journal of immunology High 23776175
2013 SASH1 mutations found in dyschromatosis patients cause increased cell migration of A375 melanoma cells and induce enhanced binding with IQGAP1 and Gαs; SASH1 mutations lead to uniform loss of E-Cadherin, suggesting SASH1 regulates IQGAP1-E-Cadherin signaling to control melanocyte transepithelial migration. Functional migration assays, co-immunoprecipitation/binding assays, immunofluorescence for E-Cadherin, patient-derived tissue analysis Cellular signalling Medium 23333244
2016 SASH1 is cleaved by caspase-3 following UVC-induced apoptosis; the C-terminal fragment (aa 231–1247) translocates from cytoplasm to the nucleus where it associates with chromatin. Wild-type SASH1 or the cleaved form increases apoptosis; mutation of the caspase-3 cleavage site prevents nuclear translocation and inhibits apoptosis. SASH1 cleavage is also required for efficient nuclear translocation of NF-κB, and the apoptotic effect of SASH1 is NF-κB-dependent. Caspase-3 cleavage assay, site-directed mutagenesis of cleavage site, subcellular fractionation, live-cell imaging, apoptosis assays, NF-κB inhibitor (DHMEQ) treatment Cell death & disease High 27831555
2016 SASH1 is regulated by a p53/POMC/α-MSH/Gαs/SASH1 cascade to mediate melanogenesis upon UV stimulation; a positive feedback loop between SASH1 and p53 is modulated by SASH1 mutations to induce pathological hyperpigmentation in dyschromatosis universalis hereditaria. Reporter assays, expression analysis of pathway components, UV stimulation, functional pigmentation assays in patient cells Journal of cellular and molecular medicine Medium 27885802
2018 SASH1 interacts with the oncoprotein CRKL via direct protein-protein interaction (identified by yeast 2-hybrid and Co-IP/mass-spectrometry, confirmed by domain mapping and site-directed mutagenesis); SASH1 inhibits CRKL-mediated activation of SRC kinase, thereby counteracting EMT; SASH1-deficient cells form significantly more metastases in vivo and this depends entirely on CRKL. Yeast 2-hybrid, Co-IP/mass-spectrometry, domain mapping, site-directed mutagenesis, dynamic mass redistribution assays, CRISPR/Cas9 knockout, orthotopic mouse metastasis model, EMT assays Cellular and molecular gastroenterology and hepatology High 30480076
2019 Endothelial Sash1 interacts with β-arrestin 1 downstream of the TLR4 pathway to activate Akt and endothelial nitric oxide synthase (eNOS) in microvascular endothelial cells; nitric oxide generated downstream of Sash1 affects alveolar epithelial cells in a cGMP-dependent manner, inducing maturation of alveolar type 1 and 2 cells and promoting surfactant production. Sash1-/- mice die perinatally due to respiratory distress caused by delayed alveolar epithelial maturation. Sash1 knockout mice (constitutive and endothelial-restricted), Co-immunoprecipitation (Sash1/β-arrestin 1), eNOS activity assays, nitric oxide measurement, cGMP pathway assays, histology/surfactant protein analysis Cell reports High 31067462
2019 HMGB1 binds to CpG islands in the SASH1 gene promoter and promotes methylation of the SASH1 gene, leading to downregulation of SASH1 expression. In astrocytes, SASH1 knockdown reduces cell adhesion and increases invasion via decreased integrin β8 expression; SASH1 overexpression promotes cell adhesion and decreases invasion. ChIP assay (HMGB1 binding to SASH1 CpG islands), methylation assay, siRNA knockdown, overexpression, adhesion and invasion assays, Western blot for integrin β8 Cell death & disease Medium 31138780
2020 SASH1 knockdown downregulates LATS1 phosphorylation and its effector YAP, upregulating YAP accumulation and its target CYR61; SASH1 expression has the opposite effect. LATS1 phosphorylates SASH1 at S407, and the S407A phosphorylation-deficient mutant fails to rescue altered YAP signaling. YAP upregulates ARHGAP42 via YAP-TEAD, and the YAP-ARHGAP42-actin axis mediates SASH1-regulated TNBC cell invasion. siRNA knockdown, ectopic overexpression, phosphorylation analysis, SASH1-S407A mutant, pharmacological YAP inhibition, YAP knockdown epistasis, in vivo CAM and xenograft models Oncogene High 32523092
2020 SASH1 co-localizes with circumferential actin bundles and linear adherens junctions in normal epithelial cells; SASH1 depletion by RNAi in IAR-20 cells destroys stable linear adherens junctions and induces mesenchymal phenotype, demonstrating SASH1 is required for maintenance of stable cell-cell adhesion. Immunofluorescence, confocal microscopy, RNAi knockdown, adherens junction morphology analysis Biochemistry. Biokhimiia Medium 32586229
2020 The SASH1 c.1761C>G (p.Ser587Arg) mutation downregulates THBS1 expression and inactivates TGF-β1 signaling; SASH1 mutations promote melanocyte migration and invasion while TGF-β1 negatively regulates SASH1 protein expression, establishing a SASH1-THBS1-TGF-β1 signaling cross-talk. Bioinformatics, site-directed mutagenesis in PIG1 cells, Transwell migration and wound-healing assays, Western blot for TGF-β1 pathway components International journal of biological sciences Medium 32174800
2020 In a heterozygous SASH1 Y551D knock-in mouse model, mutated SASH1 increases microphthalmia-associated transcription factor (Mitf) expression in epithelial tissues; increased Mitf-positive epithelial cells were detected in vivo and in affected individuals, indicating SASH1 functions as a scaffold to regulate Mitf expression in the cell nucleus. BALB/c knock-in mouse model, immunohistochemistry, Western blot, in vitro cell assays International journal of molecular medicine Medium 32582980
2022 The SAM1 domain of SASH1 exists primarily as a disordered monomer with a minor oligomer in solution (unlike the dimerizing SAM domain of SASH3); NMR relaxation and exchange experiments revealed exchange between a disordered monomer and a more structured oligomer on multiple timescales; D663A/T664K substitutions in SAM1 increased oligomerization, identifying a key region controlling oligomerization. SEC-MALS, SE-HPLC, NMR (relaxation, exchange experiments), site-directed mutagenesis Journal of structural biology High 36341956
2022 SASH1 knockdown in hemangioma endothelial cells suppresses TRAF6 ubiquitination (reducing TRAF6 degradation) and thereby destabilizes EZH2 (promoting EZH2 ubiquitination and degradation); SASH1 thus regulates EZH2 expression through TRAF6 ubiquitination in hemangioma cells. Co-immunoprecipitation, ubiquitination assays, siRNA knockdown, overexpression, Western blot Experimental cell research Medium 35772492
2023 SASH1 SAM1 domain selectively interacts with Eph receptor SAM domains, with highest affinity for EphA8; the crystal structure of the EphA8-SASH1 complex revealed specific intermolecular interactions; cancer mutations EphA8 R942H or G978D impair this interaction; SAM-SAM interaction is critical for SASH1-mediated regulation of EphA8 kinase activity. Yeast 2-hybrid, biochemical binding assays, X-ray crystallography, co-immunoprecipitation, co-localization, kinase activity assays, cancer mutation analysis Journal of molecular biology High 37619706
2023 SASH1 was identified as a novel binding partner of Caskin1/2 through SAM-SAM domain interactions; the SASH1-SAM1/Caskin1-SAMs interaction (characterized by SEC, ITC, GST pulldown, and Co-IP) disrupts Caskin1 tandem SAM homopolymers, as verified by sedimentation, TEM, and immunofluorescence in heterologous cell lines. Yeast 2-hybrid, SEC, ITC, GST pulldown, Co-IP, AlphaFold2 structural modeling, mutagenesis, sedimentation assay, TEM, immunofluorescence The FEBS journal High 39688081
2023 HMGB1 forms a physical complex with SET and HAT1 (HMGB1/SET/HAT1 complex) that inhibits H3K9 and H3K27 acetylation at the SASH1 locus in lung adenocarcinoma cells, thereby suppressing SASH1 expression and facilitating glycolysis and metastasis. Co-immunoprecipitation, ChIP-seq for histone modifications, knockdown/overexpression in vitro and in vivo, transcriptomic analysis Oncogene Medium 37794134
2024 LATS2 phosphorylates SASH1 as part of a MAP4K4-LATS2-SASH1-YAP1 cascade in luminal breast cancer; MAP4K4 negatively regulates LATS2, SASH1 expression, and YAP1 phosphorylation; combined ectopic MAP4K4 expression and SASH1 silencing promote YAP1/TAZ nuclear translocation and downstream transcriptional regulation, mediating ER signaling, tumorigenesis, and metastasis. Expression correlation, siRNA/ectopic expression, phosphorylation analysis, in vitro and in vivo tumor models, targeted MAP4K4 inhibition The Journal of biological chemistry Medium 38657867
2024 SASH1 interacts with TNKS2 (tankyrase 2) via a tankyrase-binding motif located in the SPIDER/SLY domain (around residue S519); the S519N disease variant alters binding kinetics and affinity for TNKS2; TNKS2 interaction is required for SASH1's promotion of stem-like characteristics in human melanocytes. Yeast 2-hybrid screening, biochemical binding assays (kinetics/affinity), cell-based stem cell assays, clinical examination of variant carriers The Journal of investigative dermatology Medium 38848986
2017 SASH1 is required for lumen formation in a 3D breast epithelial culture model; RNAi inhibition of SASH1 prevents lumen formation; SASH1 acts upstream of DLK1 (a NOTCH1 inhibitor), and SASH1 loss leads to DLK1 downregulation, which in turn increases NOTCH1 and its target genes HES1 and HEY1; pharmacological inhibition of NOTCH signaling (γ-secretase inhibitor) also inhibits lumen formation. RNAi knockdown, 3D culture lumenogenesis assay, gene array, γ-secretase inhibitor epistasis Experimental cell research Medium 28823832
2026 SASH1 physically interacts with PKM2 in astrocytes, sequestering PKM2 in the cytoplasm; SASH1 depletion leads to increased nuclear accumulation of PKM2, upregulation of Glut1 and lactate dehydrogenase A, increased glucose uptake and lactate release (shift toward aerobic glycolysis); a peptide blocking SASH1-PKM2 interaction reduces astrocyte activation and promotes tissue repair in a mouse TBI model. Co-immunoprecipitation (SASH1-PKM2), nuclear fractionation, glucose uptake and lactate assays, qPCR for Glut1/LDHA, peptide drug design and in vivo TBI mouse model Brain research Medium 41690666
2015 SASH1 is expressed predominantly in the cytoplasm of human aortic endothelial cells (HAECs); SASH1 knockdown in HAECs results in increased cell migration, proliferation, and angiogenesis, and decreases CYP1A1 expression possibly through inhibition of TP53 activity. siRNA knockdown, immunostaining and subcellular fractionation for localization, wound healing/WST-1/Matrigel assays, transcriptomic and pathway analyses Atherosclerosis Medium 26318107
2023 NMR backbone assignment of the SASH1 SPIDER region (SLy Proteins Associated Disordered Region, aa 400–554) revealed it is intrinsically disordered in solution; the S519N disease variant does not alter the free-form solution structural propensities of SPIDER. Deuteration, TROSY-based 3D NMR, HNN experiments, chemical shift comparison Biomolecular NMR assignments High 37155029

Source papers

Stage 0 corpus · 67 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 SASH1: a candidate tumor suppressor gene on chromosome 6q24.3 is downregulated in breast cancer. Oncogene 122 12771949
2004 C-terminal domain of human CAP18 antimicrobial peptide induces apoptosis in oral squamous cell carcinoma SAS-H1 cells. Cancer letters 110 15279899
2011 The candidate tumor suppressor SASH1 interacts with the actin cytoskeleton and stimulates cell-matrix adhesion. The international journal of biochemistry & cell biology 51 21820526
2013 SASH1 is a scaffold molecule in endothelial TLR4 signaling. Journal of immunology (Baltimore, Md. : 1950) 50 23776175
2013 SASH1 regulates melanocyte transepithelial migration through a novel Gαs-SASH1-IQGAP1-E-Cadherin dependent pathway. Cellular signalling 44 23333244
2012 SASH1 regulates proliferation, apoptosis, and invasion of osteosarcoma cell. Molecular and cellular biochemistry 44 23108792
2014 Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma. European journal of human genetics : EJHG 43 25315659
2018 The Tumor Suppressor SASH1 Interacts With the Signal Adaptor CRKL to Inhibit Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer. Cellular and molecular gastroenterology and hepatology 40 30480076
2016 Overexpression of SASH1 Inhibits TGF-β1-Induced EMT in Gastric Cancer Cells. Oncology research 36 27178818
2012 Effects of SASH1 on lung cancer cell proliferation, apoptosis, and invasion in vitro. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 36 22488244
2005 Differential expression and molecular characterisation of Lmo7, Myo1e, Sash1, and Mcoln2 genes in Btk-defective B-cells. Cellular immunology 36 16137664
2012 Overexpression of SASH1 related to the decreased invasion ability of human glioma U251 cells. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 31 22915266
2017 Involvement of PI3K/Akt pathway in the inhibition of hepatocarcinoma cell invasion and metastasis induced by SASH1 through downregulating Shh-Gli1 signaling. The international journal of biochemistry & cell biology 30 28600143
2012 Effects of SASH1 on melanoma cell proliferation and apoptosis in vitro. Molecular medicine reports 28 23023727
2016 Overexpression of SASH1 Inhibits the Proliferation, Invasion, and EMT in Hepatocarcinoma Cells. Oncology research 27 27178819
2015 SASH1, a new potential link between smoking and atherosclerosis. Atherosclerosis 26 26318107
2020 SASH1 suppresses triple-negative breast cancer cell invasion through YAP-ARHGAP42-actin axis. Oncogene 24 32523092
2016 Activation and cleavage of SASH1 by caspase-3 mediates an apoptotic response. Cell death & disease 24 27831555
2016 A novel P53/POMC/Gαs/SASH1 autoregulatory feedback loop activates mutated SASH1 to cause pathologic hyperpigmentation. Journal of cellular and molecular medicine 24 27885802
2021 CircRNA Circ-ITCH Inhibits the Proliferation and Invasion of Glioma Cells Through Targeting the miR-106a-5p/SASH1 Axis. Cell transplantation 22 33571015
2015 SASH1 inhibits proliferation and invasion of thyroid cancer cells through PI3K/Akt signaling pathway. International journal of clinical and experimental pathology 22 26722413
2021 The emerging and diverse roles of the SLy/SASH1-protein family in health and disease-Overview of three multifunctional proteins. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 21 33710696
2016 Lentiginous phenotypes caused by diverse pathogenic genes (SASH1 and PTPN11): clinical and molecular discrimination. Clinical genetics 21 27659786
2020 SASH1 promotes melanin synthesis and migration via suppression of TGF-β1 secretion in melanocytes resulting in pathologic hyperpigmentation. International journal of biological sciences 20 32174800
2019 Endothelial Sash1 Is Required for Lung Maturation through Nitric Oxide Signaling. Cell reports 20 31067462
2019 HMGB1 contributes to SASH1 methylation to attenuate astrocyte adhesion. Cell death & disease 19 31138780
2016 SASH1 inhibits cervical cancer cell proliferation and invasion by suppressing the FAK pathway. Molecular medicine reports 19 26935246
2019 Exosomal and extracellular HMGB1 have opposite effects on SASH1 expression in rat astrocytes and glioma C6 cells. Biochemical and biophysical research communications 18 31421824
2018 MicroRNA-17 promotes osteosarcoma cells proliferation and migration and inhibits apoptosis by regulating SASH1 expression. Pathology, research and practice 17 30396754
2015 Clinical Significance of SASH1 Expression in Glioma. Disease markers 17 26424902
2021 Novel missense mutation of SASH1 in a Chinese family with dyschromatosis universalis hereditaria. BMC medical genomics 15 34174894
2018 MiR-130b promotes the progression of oesophageal squamous cell carcinoma by targeting SASH1. Journal of cellular and molecular medicine 15 30443973
2020 Identification of a Novel Mutation in SASH1 Gene in a Chinese Family With Dyschromatosis Universalis Hereditaria and Genotype-Phenotype Correlation Analysis. Frontiers in genetics 14 32849825
2020 Five novel mutations in SASH1 contribute to lentiginous phenotypes in Japanese families. Pigment cell & melanoma research 14 32981204
2022 Depletion of SASH1, an astrocyte differentiation-related gene, contributes to functional recovery in spinal cord injury. CNS neuroscience & therapeutics 12 36286186
2021 Two novel SASH1 mutations in Chinese families with dyschromatosis universalis hereditaria. Journal of clinical laboratory analysis 12 34028087
2020 SASH1 Suppresses the Proliferation and Invasion of Human Skin Squamous Cell Carcinoma Cells via Inhibiting Akt Cascade. OncoTargets and therapy 11 32547092
2020 Expression of SASH1 in Preeclampsia and Its Effects on Human Trophoblast. BioMed research international 11 33134379
2014 Promoter methylation assay of SASH1 gene in hepatocellular carcinoma. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 11 25536614
2013 Promoter methylation assay of SASH1 gene in breast cancer. Journal of B.U.ON. : official journal of the Balkan Union of Oncology 11 24344014
2023 HMGB1/SET/HAT1 complex-mediated SASH1 repression drives glycolysis and metastasis in lung adenocarcinoma. Oncogene 10 37794134
2020 Involvement of SASH1 in the Maintenance of Stable Cell-Cell Adhesion. Biochemistry. Biokhimiia 10 32586229
2018 Regulatory mechanism of microRNA-128 in osteosarcoma tumorigenesis and evolution through targeting SASH1. Oncology letters 10 29805606
2023 Human Endogenous Retrovirus-H-Derived miR-4454 Inhibits the Expression of DNAJB4 and SASH1 in Non-Muscle-Invasive Bladder Cancer. Genes 8 37510314
2020 Mutated SASH1 promotes Mitf expression in a heterozygous mutated SASH1 knock‑in mouse model. International journal of molecular medicine 8 32582980
2017 Correlation of SASH1 expression and ultrasonographic features in breast cancer. OncoTargets and therapy 8 28138250
2022 SAM1 domain of SASH1 harbors distinctive structural heterogeneity. Journal of structural biology 7 36341956
2017 The adaptor SASH1 acts through NOTCH1 and its inhibitor DLK1 in a 3D model of lumenogenesis involving CEACAM1. Experimental cell research 7 28823832
2023 SASH1: A Novel Eph Receptor Partner and Insights into SAM-SAM Interactions. Journal of molecular biology 6 37619706
2024 Blockade of a novel MAP4K4-LATS2-SASH1-YAP1 cascade inhibits tumorigenesis and metastasis in luminal breast cancer. The Journal of biological chemistry 5 38657867
2023 Uncovering a new SASH1 mutation associated with dyschromatosis universalis hereditaria using whole-exome-sequencing: A case report. Medicine 5 37543808
2023 SASH1 contributes to glial cell migration in the early development of the central nervous system. Developmental biology 5 37741309
2022 SASH1 knockdown suppresses TRAF6 ubiquitination to regulate hemangioma progression by mediating EZH2 degradation. Experimental cell research 4 35772492
2024 SASH1 S519N Variant Links Skin Hyperpigmentation and Premature Hair Graying to Dysfunction of Melanocyte Lineage. The Journal of investigative dermatology 3 38848986
2024 The downregulation of SASH1 expression promotes breast cancer occurrence and invasion accompanied by the activation of PI3K-Akt-mTOR signaling pathway. Scientific reports 3 39300116
2023 Solution NMR backbone assignment of the SASH1 SLy proteins associated disordered region (SPIDER). Biomolecular NMR assignments 3 37155029
2021 AAV1-Mediated shRNA Knockdown of SASH1 in Rat Bronchus Attenuates Hypoxia-Induced Pulmonary Artery Remodeling. Human gene therapy 3 33297837
2025 SASH1 Mutations and Hereditary Disorders of Pigmentation: Review of Literature. Pigment cell & melanoma research 2 40511878
2023 SASH1 interacts with TNKS2 and promotes human melanocyte stem cell maintenance. bioRxiv : the preprint server for biology 2 37808724
2024 SASH1 is a novel binding partner to disassemble Caskin1 tandem SAM homopolymer through heterogeneous SAM-SAM interaction. The FEBS journal 1 39688081
2026 A peptide drug targeting SASH1-PKM2 interaction promotes recovery of traumatic brain injury in mice. Brain research 0 41690666
2026 Therapeutic Targeting of miR-21 Restores SASH1 and Sensitizes HBV-HCC to Sorafenib. Cancers 0 41899638
2025 Sam-Sam Association Between EphA2 and SASH1: In Silico Studies of Cancer-Linked Mutations. Molecules (Basel, Switzerland) 0 39942820
2025 Case report: Clinicopathological characteristics of SASH1 mutation-related dyschromatosis: a rethinking of the classification of dyschromatosis. Frontiers in genetics 0 40115815
2025 Dyschromatosis universalis hereditaria with SASH1 mutation improved with picosecond laser treatment. Skin health and disease 0 40584949
2025 SASH1 Modulates Melanin Synthesis and Melanoma Cell Metastasis via Suppression of the TGF-β Signaling Pathway. Pigment cell & melanoma research 0 41284354
2024 Gastric cancer cell-derived exosomal miRNA-128-3p promotes angiogenesis by targeting SASH1. Frontiers in oncology 0 39664191